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Practical Periodontics
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Practical Periodontics
Second Edition
Edited by
Kenneth Eaton
PhD, MSc, BDS, MGDSRCS, FFGDP(UK) Hon.,
FCGDent, FFPH, FHEA, FICD, FNCUP, DHC
Specialist in Periodontics and Dental Public Health,
Visiting Professor University College London; Honorary
Professor University of Kent, Advisor to the Council of
European Chief Dental Ocers
Philip Ower
MSc, BDS, FFGDP(UK) Hon., MGDSRCS (Eng & Ed)
Formerly Specialist in Periodontics and Director,
PerioCourses Ltd, UK
For additional online content visit Elsevier eBooks+

© 2023, Elsevier Limited. All rights reserved.
First edition © Elsevier Limited 2015
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(other than as may be noted herein).
Notices
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and
using any information, methods, compounds or experiments described herein. Because of rapid advances
in the medical sciences, in particular, independent verication of diagnoses and drug dosages should
be made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or
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contained in the material herein.
ISBN: 978-0-3238-7845-6
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Design: Ryan Cook
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Last digit is the print number: 9 8 7 6 5 4 3 2 1

Contents
Foreword, vii 2.4 Periodontitis and Systemic Diseases, 102

Preface, viii Marilou Ciantar and Kenneth Eaton
Contributors, ix
2.5 Determining Periodontal Prognosis, 116
Section 1: Aetiology of Periodontal Monica Lee
Diseases
Section 3: Periodontal Treatment Planning
1.1 The Macro- and Microanatomy of Periodontal
Tissues, 3
Iain Chapple and Mike Milward 3.1 Treatment Planning – Gingivitis and
Periodontitis, 125
Paul Baker
1.2 The Pathogenesis of Periodontal Diseases, 11
Mike Milward, John Matthews, and Iain Chapple
3.2 The Management of Mucogingival Conditions
(Gingival Recession), 135
1.3 Epidemiology of Periodontal Diseases, 23 David Gillam and Wendy Turner
Kenneth Eaton
3.3 Treatment Planning: Periodontal Problems in

1.4 Host Response and Susceptibility, 31 Children and Adolescents, 146
Paul Cooper and Martin Ling Valerie Clerehugh and Aradhna Tugnait
1.5 The Role of Biolms in Health and Disease, 41 3.4 Referral to a Periodontal Specialist, 161
Philip D Marsh Alan Woodman
1.6 Periodontal Risk – Modifying and Section 4: The Role of Self-Care and Oral
Predisposing Factors, 56
Iain Chapple and Mike Milward Hygiene Methods
Section 2: Periodontal Diagnosis and 4.1 Patient Education and Self-Performed Biolm
Control, 171
Prognosis Elaine Tilling
2.1 Classication and Diagnosis of Periodontal 4.2 Clinical Imaging in Patient Assessment and
Diseases, 71 Motivation, 182
Philip Ower Ulpee Darbar
2.2 Periodontal Assessment and Monitoring, 80 4.3 Patient Adherence, 193

Philip Ower and Leo Briggs Philip Ower
2.3 Gingival Enlargement, 93

Alan Woodman
v
vi Contents
Section 5: Non-surgical Periodontal 7.2 The Periodontal–Orthodontic Interface, 264

Ian Dunn
Management
7.3 Dental Implants – Anatomy, Complications,
5.1 The Diseased Root Surface in Periodontitis, 205 Management of Peri-Implant Diseases, 271
Philip Ower Colin Priestland and Neil Meredith
5.2 Periodontal Instrumentation, 212

Philip Ower Appendix 1 World Workshop on Classication of
Periodontal and Peri-implant Diseases
and Conditions 2017 - Staging and
5.3 Antibiotics in the Management of Periodontal Grading of Periodontitis, 285
Diseases, 222
Andrew Walker Appendix 2 Implementing the 2017 Classication of
Periodontal Diseases to Reach a Diagno-
sis in Clinical Practice, 287
5.4 Assessment of Treatment Outcomes and
Supportive Periodontal Therapy, 230 Appendix 3 European Federation of Periodontology
Valerie Clerehugh S3-Level Clinical Treatment Guidelines -
Stepwise Approach, 290
Appendix 4 BSP UK Clinical Practice Guidelines
Section 6: Surgical Periodontal Therapy for the Treatment of Periodontal
Diseases, 291
6.1 Rationale for Periodontal Surgery, 243
José Zurdo
Index, 294
Section 7: Interaction with Other Dental

Disciplines
7.1 The Periodontal–Restorative Interface, 257

Ewen McColl
Foreword
After the success of the rst edition, Practical Periodontics is e authors, led by Professor Kenneth Eaton and
now released as a second edition with fully updated chap- Dr Philip C. Ower, together with many contributors, are
ters. is new edition maintains its scientic rigour, com- not only well respected in the United Kingdom but also
bining the introduction of new knowledge with a detailed throughout Europe and beyond. eir contribution to this
description of current therapeutic concepts and the advent work clearly demonstrates not only excellent preparation
of new technologies. is work continues to focus on edu- but also the academic spirit and the teaching abilities that
cating students with evidence-based concepts and acquisi- are needed to produce a book such as this with scientic
tion of relevant professional competences. e information rigour and practical relevance for students and professionals.
provided is clear, well organized and very practical, but In summary, this book continues to provide useful and rel-
at the same time it has been rigorously reviewed and is evant content in line with contemporary educational concepts
updated with current knowledge, comprehensively covering and with a practical approach to modern periodontology.
modern periodontology from the basic knowledge necessary Mariano Sanz
to understand aetiology and pathogenesis to the most rel- Professor and Chairman of Periodontology
evant aspects of the prevention and therapy of periodontal Faculty of Odontology, University Complutense of
diseases. Madrid (Spain)
vii
Preface
We were honoured when Elsevier approached us with an on the nature of root surface contamination, periodontal
invitation to edit a second edition of Practical Periodon- instrumentation, the use of antimicrobials, the assessment
tics. We were tasked with producing a textbook for dental of treatment outcomes and supportive therapy. e sixth
hygiene and therapy undergraduates and general dentists section covers surgical periodontal therapy and the ratio-
that is in the same style as other recent textbooks published nale for a surgical approach. e seventh and nal sec-
by Elsevier. We chose the title to reect the fact that we tion explains the interaction of periodontology with other
wanted this text not only to be a useful learning resource dental disciplines, and there is a new chapter on dental
but also to have practical application. As a result this new implants – monitoring, maintenance and management of
book contains numerous gures and tables to illustrate the complications.
text and also the key points, highlighted in every chap- There is increasing emphasis nowadays on the role of
ter. It is hoped that this layout will help dental, hygiene evidence-based healthcare. It is therefore essential that
and therapy undergraduates when they are preparing for from the outset undergraduate clinicians are prepared
examinations, as well as provide a resource for qualied to question everything they read or are told. The ques-
clinicians. tions “Who says so?”, “Is it true?” and “Where is the
We have also provided additional aids for revision and evidence?” are key. For this reason all chapters contain
understanding in the form of questions, cases and videos. several citations to lead the reader to the source texts for
ese resources can be found on the following website the statements made, and as a result there is an exten-
using the pin code in the front of this book for access: sive reference list for most chapters. It is hoped that
http://ebooks.health.elsevier.com/. the reader will refer to the source papers when wanting
e sections of the new edition follow a logical pro- to challenge any statement in the textbook, as deeper
gression starting with the aetiology of periodontal diseases. understanding comes from challenge and debate and
In the rst section, the chapters cover the basic sciences not from rote learning.
relevant to periodontology and are on the anatomy of the We are deeply indebted to our colleagues who have
periodontal tissues, periodontal pathogenesis, the epide- either written or contributed to chapters in the textbook
miology of periodontal diseases, host response and sus- or who have made video or case reports available for the
ceptibility, the role of bacterial biolm and systemic and online part of this publication. ey come from academia,
local risk factors for periodontitis. In the second section, specialist practice, general practice and industry. All have a
the chapters cover classication of periodontal diseases, passion for periodontology that we hope shines through in
periodontal assessment of patients, gingival overgrowth, their chapters. Our sincere thanks to all of them. In addi-
periodontal/systemic disease relationships and determin- tion we would like to thank Professors Peter Heasman and
ing prognosis. e chapter on assessment is supplemented Philip Preshaw for permission to use the Newcastle Uni-
with an extensive video on the subject. e third section versity online material on assessing the periodontium and
on treatment planning covers treatment planning for gin- Dr Anastasiya Orishko and Professor Francesco D’Auito for
givitis and periodontitis, gingival recession, periodon- permission to use the radiographs and periodontal charts for
tal problems in children and young adults and specialist four cases. We would also like to thank the team at Elsevier
referrals. e fourth section deals with patient education for their support and for guiding us through the publica-
and self-performed biolm control. Its chapters are on the tion process, in particular Alexandra Mortimer and Supriya
role of self-care and oral hygiene methods, clinical imag- Barua Kumar.
ing and patient adherence. At a simplistic level this is We dedicate this book to the late Graham Smart and to
perhaps the key section, as without excellent communica- the late Bernie Kieser, who was such an inspiration to us and
tion with patients and total cooperation on their part to Graham during our postgraduate training and subsequent
control their biolm, the eorts of a clinician are likely careers in periodontology.
to be doomed to failure. e fth section details non-
surgical periodontal management and includes chapters Kenneth Eaton and Philip Ower
viii
Contributors
Paul Baker, MSc, BDS, MClinDent, FDSRCS(Eng), Monica Lee, MSc, BDS, MFDSRCPS (Glas), MClinDent,
MRDRCS MRDRCPS (Glas)
Specialist in Periodontics, PerioLondon, UK Specialist in Periodontics, Cambridge, UK
Leo Briggs, MSc, BDS Martin Ling, BDS, MFDS, MFGDP, FHEA
Specialist in Periodontics and Deputy Head, Dental Lecturer in Periodontology, University of Birmingham, UK
Defence Union, UK
Philip D. Marsh PhD, BSc
Iain Chapple, PhD, BDS, FDSRCS, FDSRCPS, CCST (Rest Professor Emeritus in Oral Microbiology, Department of
Dent) Oral Microbiology, School of Dentistry, University of
Professor of Periodontology, Consultant in Restorative Leeds, UK
Dentistry and Director of Research, Institute of Clinical
Sciences, University of Birmingham, UK John Matthews, PhD
Professor and Honorary Consultant in Periodontology,
Marilou Ciantar, PhD(Hons), MSc, BChD(Hons), ILTM, University of Birmingham, UK
MFDSRCS, MFDRCSI, FFDRCSI
Senior Clinical Lecturer in Periodontology, University of Ewen McColl, BSc(Hons), BDS, MFDS, FDSRCPS,
Edinburgh, UK MCGDent, MRDRCS Ed, MClinDent, FDSRCS, FHEA,
FDTF(Ed)
Valerie Clerehugh, PhD, BDS, FDSRCS, FHEA Director of Clinical Dentistry, Peninsula Dental School,
Emeritus Professor of Periodontology, School of Dentistry, University of Plymouth, UK
University of Leeds, UK
Neil Meredith, PhD, MSc, BDS, FDSRCS, LDSRCS, FICD
Paul Cooper, PhD, BSc Professor in Prosthodontics and Head of Dental School,
John Arnaud Bell Professor of Oral Biology, University of James Cook University, Queensland, Australia
Otago, Dunedin, New Zealand
Mike Milward, PhD, BDS, MFGDPRCS, MFDSRCPS,
Ulpee Darbar, MSc, BDS, FDSRCS (Rest Dent) Ed, FHEA (UK)
FDSRCS Eng, FHEA Professor and Honorary Consultant in Periodontology,
Consultant in Restorative Dentistry & Honorary Associate University of Birmingham, UK
Professor, Eastman Dental Hospital & Institute,
University College, London Philip Ower, MSc, BDS, FFGDP(UK) Hon., MGDSRCS
(Eng & Ed)
Ian Dunn, MSc, BChD, MCGDent Formerly Specialist in Periodontics and Director,
Specialist in Periodontics, UK PerioCourses Ltd, UK
Kenneth Eaton, PhD, MSc, BDS, MGDSRCS, FFGDP(UK) Colin Priestland, MSc, BDS, MGDSRCS
Hon., FCGDent, FFPH, FHEA, FICD, FNCUP, DHC Private Practice, Townsville, Queensland, Australia
Specialist in Periodontics and Dental Public Health,
Visiting Professor University College London, Elaine Tilling, MSc, RDH, DMS MIPHE
Honorary Professor University of Kent, Advisor to the Education and Projects Manager, TePe Oral Hygiene Projects,
Council of European Chief Dental Ocers UK
David Gillam, BA, BDS, MSc, DDS, FRSPH, MICR Aradhna Tugnait, PhD, MDEntSci, BChD, FDSRCS (Ed),
Clinical Reader in Oral Bioengineering, Institute of FHEA
Dentistry, Barts and the London School of Medicine Associate Professor in Restorative Dentistry, School of
and Dentistry, Queen Mary University London Dentistry, University of Leeds, UK
ix
x Contributors
Wendy Turner, BDS, FDS Alan Woodman, MSc, BDS, DGDP(UK), MRDRCS(Eng)
Clinical Professor, Centre for Dentistry, School of Formerly Specialist in Periodontics and Tutor, University
Medicine, Dentistry and Biomedical Science, Queen’s of Portsmouth Dental Academy, UK
University Belfast
José Zurdo, MBBS, BDS, Cert.Perio MSc
Andrew Walker, BDS, MFDS (Edin), MClinDent (Perio), Specialist in Periodontics
DLM
Specialist in Periodontics, Dentolegal Consultant, Dental
Protection, Tutor, University of Liverpool Dental
School, UK
SECTION 1
Aetiology of Periodontal Diseases
1
1.1
THE MACRO- AND
MICROANATOMY OF
PERIODONTAL TISSUES
IA I N C H A P P L E A N D M I K E M I LWA R D
CHAPTER OUTLINE
Introduction Periodontal Ligament
Embryological Origins of the Periodontal Tissues Cementum
Microanatomy of the Alveolar Bone
Microanatomy of the Gingival Tissues
Acknowledgement
Microanatomy of the Periodontal Ligament and Cementum
OVERVIEW OF THE CHAPTER

This chapter provides a description of basic periodontal anatomy and outlines the functions of the periodontal tissues.
By the end of the chapter the reader should be able to: • Describe the microscopic features of normal anatomy and
• Describe the macroscopic anatomy of the periodontal understand how they are related to normal structure and
tissues and their embryological origins function, as well as how they change during disease.
• Identify key features of applied periodontal anatomy, visible e chapter covers the following topics:
during clinical examination • The embryological origins of the periodontium
• Recognize how anatomical landmarks are related to • The tissues comprising the periodontium
deönitions of health, gingivitis and periodontitis • The microanatomy of the gingival tissues
• Recognize the changes in anatomical relationships that • The microanatomy of the periodontal ligament and cementum
occur during disease processes • The microanatomy of alveolar bone.
Introduction of periodontal anatomy at both macroscopic and micro-

scopic levels. e latter is complex, being of mixed ectoder-
Inammatory periodontal diseases are among the most mal and mesodermal origins. Periodontal anatomy includes
prevalent chronic diseases of humans and are a major cause the gingival, alveolar bone and dental tissues.
of tooth loss.
ey can also be risk factors (see Chapter 1.6 for deni-
tion) for other systemic inammatory diseases such as ath- Embryological Origins of the Periodontal
erogenic cardiovascular disease, type 2 diabetes, rheumatoid
arthritis, chronic obstructive pulmonary disease, chronic Tissues
kidney disease, neurodegenerative diseases and certain other
inammatory conditions. e gingival epithelium is of ectodermal origin.
In addition, many systemic conditions can present in and e periodontal ligament and cementum are of neural crest
around the periodontal tissues, and their diagnosis and/or (ectomesenchymal) origin.
symptomatic management is aided by a detailed knowledge e alveolar bone is of mesodermal origin (Figure 1.1.1).
3
4 SECTION 1 Aetiology of Periodontal Diseases
Gingival epithelium
Ectodermal
Peridontal ligament
Neural crest
(ectomesenchyme)
Alveolar bone
Mesodermal
Cementum
Neural crest
(ectomesenchyme)
• Figure 1.1.1 The embryological origins of the periodontal tissues.
Microanatomy of the Gingival Tissues rates of cell division and shedding are balanced so that
the thickness of the epithelium is constant. e epi-
e microanatomy of the gingival tissues is shown in Fig- thelium is attached to the underlying connective tissue
ure 1.1.2, and the appearance of healthy gingival tissues is by a basal lamina consisting of two layers of a protein/
shown in Figure 1.1.3 polysaccharide complex, the lamina lucida and the
e key elements of the normal gingival tissues are: lamina densa.
1. Outer gingival epithelium: the outer gingival epithe- 2. Gingival connective tissue: the gingival connective tis-
lium is an orthokeratinised, stratied squamous epithe- sues consist of a mesh of collagen bres in an extracel-
lium. e keratinisation makes it resistant to abrasion lular matrix made up of noncellular ground substance of
from rough and hard food particles. A histological sec- glycosaminoglycans (such as hyaluronic acid), proteogly-
tion of the outer gingival epithelium is shown in Figure cans, and glycoproteins (such as bronectin), all of which
1.1.4. e gingival epithelium covers a core of brous are synthesized by the principal cell type in the gingival
connective tissue, which was dened in the 2017 world connective tissues, the broblast. e matrix contains
workshop classication system as the “supracrestal con- blood vessels, nerves and cells, most of which are bro-
nective tissue attachment”, replacing the term “biologi- blasts (which also synthesize collagen), but immune
cal width”. Like all stratied squamous epithelia, the system cells are also found, including neutrophils, lym-
gingival epithelium undergoes constant renewal with phocytes, tissue macrophages (called Langerhans cells)
shedding of the surface cells as they are replaced by and plasma cells. e gingival connective tissue is highly
cell proliferation from the deeper layers. Keratinocytes vascular, allowing for the entry of circulating inamma-
make up the majority of the cells of the gingival epi- tory cells that perform “immune surveillance”. e col-
thelium, which comprises basal cells (stratum basale), lagen bres run in dierent directions in groups (Figures
prickle cells (stratum spinosum), granular cells (stratum 1.1.5 and 1.1.6), and the groups are interlinked, giving
granulosum) and keratinised cells (stratum corneum). the gingival tissues both strength and resilience. e
e cells at the surface lose their nuclei and form a solid collagen is initially secreted in the form of inactive pro-
layer of protective keratin. Cell division takes place in collagen, which is converted into tropocollagen. is is
the basal layer, and the cells produced travel through polymerized into collagen brils that are then combined
the gingival epithelium where they are eventually into collagen bundles by the formation of cross linkages.
shed. During this process, the cells increase in size and e collagen in gingival connective tissue is mostly type
become attened, producing more and more keratin as I but types III and V are also found.
they do so. It is the keratin that results in the mechani- 3. e dentogingival, circular and transeptal bres form a
cal toughness of the most supercial epithelium. e physical barrier to the spread of gingival inammation
CHAPTER 1.1 The Macro- and Microanatomy of Periodontal Tissues 5
Enamel
Gingival margin
Sulcular epithelium
Outer gingival epithelium
Free gingivae
Junctional epithelium
Cemento-enamel junction
Connective tissue
Gingival groove
Attached gingivae
Mucogingival junction
Alveolar mucosa
A
Gingival margin
Outer gingival epithelium
Sulcular epithelium
Free gingivae
Gingival groove
Enamel
Attached gingivae
Connective tissue
B
• Figure 1.1.2 Microanatomy of normal gingival tissues.
toward the alveolar crest, thus aording some protec- 7. e free gingiva: this is a mobile cu of keratinised
tion from alveolar bone loss around teeth: these bres gingival tissue lying above the alveolar crest. It extends
are absent in peri-implant mucosa, and peri-implant from the gingival margin to the gingival groove (when
bone loss thus progresses in a more rapid concentric present), which is at the level of the CEJ. e free
manner. gingiva forms a cu around the neck of the tooth, and
4. e gingival margin: the visible edge of the gingivae, 1.5–2 its surface is smooth. It is separated from the attached
mm coronal to the cemento-enamel junction (CEJ). gingiva by the free gingival groove. Between the teeth,
5. e gingival groove: in health, this line separates the the free gingiva forms the cone-shaped interdental
free from the attached gingiva at the level of the CEJ. It papilla, and it forms the interdental “col” beneath
is only present in 30–40% of adults. the contact points of the abutting teeth. e col area
6. e sulcular epithelium: this lies between the oral and has very thin, nonkeratinised epithelium that makes
junctional epithelium. It has rete ridges. is tissue dis- this area more vulnerable. is is often a site of bac-
plays rapid turnover and para-keratinisation (cell nuclei terial accumulation, which explains why periodontal
still present). It is thinner and less keratinised than the diseases (gingivitis or periodontitis) usually start in
outer gingival epithelium. this area.
Gingival
groove
Stippling
Attached
gingiva
Interdental
papilla
Gingival
margin Mucogingival
junction
Alveolar
mucosa
• Figure 1.1.3 Healthy gingival tissues (Reproduced with kind permission by Quintessence from Chapple,
I.L.C., Gilbert A.D., 2002. Understanding Periodontal Diseases: Assessment and Diagnostic Procedures in
Dental Practice. Quintessence, London. ISBN: 1-85097-053-X).
8. e attached gingiva: this is a band of between 1 and 9

mm of keratinised gingival tissue that is tightly bound
Keratin down to the underlying alveolar bone/periosteum by the
layer
collagen bres of the dentogingival complex. It is pale
pink compared with the deeper red colour of the alveo-
Stratum lar mucosa. ese dierences in colour are due to the
corneum
alveolar mucosa being more vascular and the overlying
epithelium being thinner and nonkeratinised. It extends
Stratum
granulosum
from the free gingival groove apically to the mucogingi-
val junction (MGJ) where it becomes continuous with
Stratum
the nonkeratinised and mobile alveolar mucosa. e
spinosum attached gingiva has a “stippled” appearance (depressions
on the surface) because of epithelial rete ridges.
9. e mucogingival junction: the MGJ is a well delin-
eated line that marks the boundary between the pink
keratinised attached gingiva, which is tightly bound
Stratum down to the alveolar bone, and the darker red, nonke-
basale ratinised alveolar mucosa, which is only loosely bound
down to alveolar bone.
10. e enamel space: this is a demineralised section (as a
• Figure 1.1.4 The histology of the outer gingival epithelium. result of histological preparation) in which the enamel is
absent and indistinguishable from the gingival crevice.
Enamel
Dentogingival fibres
Circular fibres
Transeptal fibres
Cementum
Alveolo gingival fibres
Dentine
Alveolar bone
Oblique principal
fibres
• Figure 1.1.5 The interdental periodontal tissues in health.
tooth is also known as the “epithelial attachment”.

Unlike the sulcular epithelium the JE has no rete ridges.
Enamel
It is fragile and is 20 to 30 cells thick with the most api-
cal cells positioned at the CEJ (unless there has been
Dentine recession, in which case the JE lies on cementum). e
length of the JE is about 40 cells, or about 1 mm. e
cells of the JE are larger than other oral epithelial cells
Dentogingival and oriented parallel to the tooth surface. ey also
fibres have wider intercellular spaces resulting in increased
permeability of the JE to bacteria (and their products),
gingival crevicular uid (GCF) and inammatory cells.
Circular fibres Neutrophils are often seen in the JE, even in health.
ese cells pass through the JE into the gingival crev-
Transeptal
fibres
ice where they form part of the host’s immune defence
against bacteria in the biolm. Cell turnover in the JE
Cementum is rapid. When the most apical cell of the JE migrates
Alveolar bone
apically below the CEJ, this denes periodontal true
pocket formation.
Oblique principal Figure 1.1.7 shows the microanatomy of the dento-gin-
fibres gival junction.
• Figure 1.1.6 Histological longitudinal section of the interdental peri-
odontal tissues in health.
Microanatomy of the Periodontal
Ligament and Cementum
11. e junctional epithelium (JE): the JE provides the Periodontal Ligament
contact between the gingiva and the tooth and attaches
to enamel via hemidesmosomes, forming a tight attach- e periodontal ligament forms the brous attachment
ment to the tooth surface. A thin basement lamina lies between the tooth and bone. It is mostly made up of col-
between the JE and connective tissue and also between lagen bres that insert into the root cementum and also into
the JE and the tooth surface. is attachment to the the alveolar bone in an acellular matrix that is similar to that
Sulcular epithelium
Gingival sulcus
Rete ridges
Circular fibres
of PDL
Gingival connective
tissue
Alveolo gingival
fibres
Principal fibres of
periodontal ligament
• Figure 1.1.7 Microanatomy of the dento-gingival junction.
found in the gingival connective tissues. e ligament has movements, providing a hydraulic “cushion” eect. is is
the following functions: provided by the ability of the matrix components (glycos-
• Maintains the tooth in a functional position aminoglycans, proteoglycans and glycoproteins) to bind
• Resists occlusal loading water.
• Protects dental tissues from excessive loading Fibroblasts are the main cell type of the periodontal liga-
• Maintains and repairs alveolar bone and cementum ment, producing and degrading collagen through a process
(contains stem cells) of repair and regeneration. ey have phagocytic capabilities
• Controls the neurological functions of mastication via that enable them to remove damaged collagen and replace
mechanoreceptors. it with new collagen, thus maintaining the integrity of the
e ligament varies in thickness (0.3–0.1 mm), being periodontal ligament. e ligament also contains stem
wider coronally and apically, and is at its narrowest at the (mesenchymal) cells that can dierentiate into osteoblasts
axis of rotation of the tooth. Its main collagen bres (the (bone-forming cells) and cementoblasts (cementum-form-
“principal bres”) run obliquely from bone to tooth in an ing cells). is allows the periodontal ligament to maintain
apical direction (Figure 1.1.8). and repair itself and its insertions into bone and cementum.
e bres are not straight but follow a wavy course, Osteoblasts, osteoclasts, cementoblasts and cementoclasts
which allows for tooth movement during mastication. e are found lining the bone and cementum surfaces within
bres that are embedded in bone and cementum are known the ligament, all these cell types being derived from stem
as Sharpey’s bres. e main types of collagen are types I, cells within the periodontal ligament. e ligament also
III and V, but there is more type III than in the gingival contains the cell rests of Malassez, which are the odonto-
connective tissue. Type III collagen is more extensible than genic remnants of the epithelial root sheath of Hertwig, and
other types of collagen and may be important in maintain- which can dierentiate into cementoblasts during guided
ing the integrity of the periodontal ligament during tooth tissue regeneration.
movements in mastication. e ligament also contains e periodontal ligament has a rich blood and nerve sup-
oxytalan bres that are not found elsewhere in the body; ply that is derived from the neural supplies to the pulp (which
these are elastic bres that insert into cementum and run branch o before entering the tooth’s apical foramina) and
more longitudinally. ey are more numerous in teeth that also from the blood supply to the alveolar bone. e liga-
are subject to high loading, such as bridge abutments. ment’s nerve supply, which has both sensory and autonomic
e periodontal ligament matrix also plays an impor- bres, permits the monitoring of loading during mastica-
tant role in the absorption of functional stress during tooth tion through proprioceptive bres and mechanoreceptors.
Alveolar crest
Horizontal
Oblique
Apical
• Figure 1.1.8 Periodontal ligament bres.
ere are two types of cementum: cellular and acellular.

Cementum
Cellular cementum is found near the apex of the root.
e cemental layer of the root provides an anchorage site It contains cementocytes in lacunae that communicate
for the collagen bres of the periodontal ligament. It is a through a network of canaliculi (channels).
calcied connective tissue, which is a highly mineralised Acellular cementum covers most of the root surface of the
tissue, similar to bone, and it is tightly bound to the tooth and contains no cementocytes, but its surface is popu-
underlying dentine. It comprises collagen bres in a calci- lated with cementoblasts.
ed organic matrix and is about 65% inorganic (mostly Cementoblasts are similar to osteoblasts and are respon-
hydroxyapatite), 23% organic (mostly type I collagen) sible for the synthesis of the organic components of the
and 12% water. Unlike bone, cementum is less readily matrix and for their calcication. As cementum formation
resorbed. is may be because a layer of uncalcied matrix occurs, the cementoblasts become trapped in the calcifying
(precementum) is laid down by cementoblasts before matrix and become cementocytes.
calcication and remains on the surface of the mature e inserting Sharpey’s bres are arranged at right angles
cementum. As cementum formation occurs throughout to the cementum surface. In acellular cementum, the bres
life, there is always a layer of precementum present on the are closely packed and mostly calcied; in cellular cemen-
cementum surface. tum, they are only partially calcied and are more loosely
At the cementoenamel junction, the cementum usually arranged.
abuts onto enamel but, occasionally, it may either overlap
enamel or stop short, leaving a band of exposed dentine. Microanatomy of the Alveolar Bone
ere is no direct blood or nerve supply to cementum.
Cementum formation is continuous throughout life to Alveolar bone is part of the mandible and maxilla, but
accommodate changes within the periodontal ligament. its existence depends on the presence of teeth and, in the
e thickness of cementum coronally is 16 to 60 μm and, if absence of teeth, it gradually resorbs. ere is, however, no
exposed (for example, in recession), it can be easily removed identiable boundary between the alveolar bone and the
by a toothbrush, resulting in dentinal sensitivity (see Chap- bones of the jaws.
ter 3.2). In the apical third of the root, the cementum can be Alveolar bone comprises cancellous bone covered by a
up to 200 μm thick. e thickness of cementum increases thin layer of cortical bone. e Sharpey’s bres of the peri-
throughout life. odontal ligament insert into the alveolar bone in what is
referred to as “bundle bone”. is cortical bone layer is

perforated (it is also called the “cribriform plate”) to allow
vascular and neural communication between the periodon-
tal ligament and the alveolar bone for periodontal ligament
remodelling.
Anatomically, the alveolar bone structure is identical to
other bones of the skeleton with haversian canals, Volk-
mann’s canals and Howship’s lacunae. e alveolar bone
crest usually lies 1 to 2 mm apical to the CEJ, but this
may vary depending on tooth position. When the root of a
tooth is displaced out of the arch, for example in a crowded
mouth, the overlying alveolar bone may be absent from the
root surface, creating a dehiscence or fenestration in the
alveolar bone that may in turn result in gingival recession
defects (see Chapter 3.2 and Figure 1.1.9). A
Like cementum, alveolar bone is about 60% inorganic,
25% organic and 15% water.
Alveolar bone undergoes constant deposition and resorp-
tion, just like other skeletal bones, in response to functional
demands. Osteoblasts line the bone surface and regulate
bone remodelling, recruiting osteoclasts when necessary.
Acknowledgement
is chapter is based on a session within e-Den that Pro-
fessors Chapple and Milward produced in 2011. Acknowl-
edgement is given to the Faculty of Dental Surgery of the
Royal College of Surgeons of England for giving permis
sion for material from the e-Den session to be used in this
chapter. B
Multiple Choice Questions on the contents of this chap-
• Figure 1.1.9Upper incisors showing localized recession as a result
ter are available online at Elsevier eBooks+ of underlying bone dehiscences that have developed as a result of
overcrowding during tooth eruption. (A) Labial view; (B) incisal view.
1.2
THE PATHOGENESIS OF
PERIODONTAL DISEASES
MI K E M I LWAR D, J O H N M AT T H E WS , A N D I A I N C H A P P L E
CHAPTER OUTLINE
Periodontal Disease or Diseases? Inammasomes
Introduction Neutrophils (Polymorphonuclear Leucocytes [Pmnls])
Mast Cells
Bacterial Factors Immune Responses to Bioölm Antigens
Colonisation T Lymphocytes (T Cells)
How Do Bacteria Cause Disease? B Lymphocytes
Host Factors Antibodies/Immunoglobulins
Inøammatory Response to the Bacterial Bioölm Bacteria Versus Host
The Epithelial Barrier Does Gingivitis Inevitably Lead to Periodontitis?
Complement Acknowledgement
Cytokines

Inammatory periodontal diseases are among the most prevalent of human chronic diseases and are a major cause of tooth loss. Much
research has been directed at unravelling the complex processes underpinning their aetiology and pathogenesis.
This chapter will provide key information on the pathogenesis of chronic periodontal diseases, including the bacteria involved, host/
bacterial interactions, and the role of host responses, with particular emphasis on hyper-responsive neutrophils and the role of
antioxidants.
By the end of the chapter the reader should understand: This chapter covers the following topics:
• The concept of disease pathogenesis • Periodontal disease or diseases?
• Inøammatory and immune responses to bioölm bacteria and • Introduction
their products • Bacterial factors
• The role of periodontal bacteria in provoking damaging host • Host factors
responses • Inøammatory response to bioölm bacteria
• The potential for reactive oxygen species–mediated tissue • Immune responses to bioölm antigens
damage and the role of antioxidants • Bacteria versus host
• The critical factors in the pathogenesis of periodontal • Does gingivitis inevitably lead to periodontitis?
diseases.
Periodontal Disease or Diseases? widely used, this term causes much confusion. It (periodon-
tal disease in the singular) will therefore not be used in this
ere are many forms of disease that can aect the peri- book; instead, throughout the book the terms gingivitis and
odontal tissues, including gingivitis, necrotising periodontal periodontitis will be used. e former implies that the dis-
diseases and periodontitis. All manifest as an inammatory ease process is limited to the gingiva and that there has been
and an immune response to bacterial biolm (also known as no destruction of the periodontal ligament or alveolar bone.
plaque). erefore the term “periodontal disease” does not e latter implies that there has been destruction of the
describe a single disease entity but is a general term encom- periodontal ligament and alveolar bone and that this pro-
passing all diseases of the periodontal tissues. Although cess is generally concurrent with the presence of gingivitis.
11
Health
Bacteria Host
Time exposed Modifiable and

to risk factors non-modifiable
Disease
• Figure 1.2.1 Interactions that are responsible for disease.
Introduction Bacteria
20%
Pathogenesis describes how a disease develops. It includes the
origin of the disease and the events that take place leading
to that disease. Whether periodontitis develops in a patient
depends on the interaction between biolm bacteria and the
host’s inammatory and immune responses. is interaction
can be modied by a variety of complex factors, collectively Host
80%
called “risk factors” (Figure 1.2.1 and see Chapter 1.6).
• Figure 1.2.2 Most of the damage seen in periodontitis is host mediated.
KEY POINT 1
Periodontitis is the result of complex interactions between
plaque bacteria and the host response.
Bacterial Factors
In many mouths and at many sites in a mouth, the long- Colonisation
term presence of bacterial biolm results in gingivitis but
does not progress to periodontitis. Periodontitis is in part Bacteria need to colonise (become established) in the gingi-
due to direct damage of the periodontal tissues by certain val sulcus/periodontal pocket for periodontitis to develop.
bacteria in the biolm and also by bacterial activation of the e stages in this process are:
host’s immune/inammatory responses. Grossi etal. (1994) • Acquisition—occurs predominantly at birth from paren
have suggested that, on average, the relative direct eect tal or environmental sources and on tooth eruption (i.e.,
from biolm bacteria contributes to 20% of the tissue dam- appearance of new habitats such as enamel surfaces and
age seen in periodontitis and the other 80% comes from an the gingival crevice)
aberrant host response (Figure 1.2.2). • Adherence/retention—the ability of bacteria to attach
Periodontitis is regarded as a condition that is seen in to a surface or occupy a site not aected by saliva ow,
susceptible patients who have an exaggerated inamma- essential for bacterial survival
tory/immune response to bacterial biolm and/or reduced • Initial survival—after adherence/retention the bacteria
levels of antioxidant defence (intracellular molecules pres- have to acquire essential nutrients to survive
ent in cells that oer protection from excess inammatory • Prosperity—the ability of bacteria to be able to survive in
response). is leads to chronic collateral damage of the a biolm with other microorganisms in the long term
periodontal tissues because the host response is unable to • Avoidance of elimination—bacterial strategies to help
successfully remove the biolm, resulting in propagation of bacteria evade host defence mechanisms
the periodontal lesion. Over the years there has been much • Multiplication—division to ensure a critical mass for
debate over whether the change to a pathogenic microbial survival
biolm comes before or after the inammatory response. • Virulence factors—factors expressed by certain bacteria
A review by Van Dyke etal. (2020) has proposed that the for their benet that concurrently cause tissue damage
inammatory response is the key factor that modulates the and disease
change to a pathogenic biolm, and it is only in the lat- • Maturation of bioëlm—as the bioëlm develops the ìora
ter stages that the microbial pathogenicity becomes impor- will change and, in disease, Gram-negative anaerobic
tant. ese ndings oer the potential that management of motile bacilli will predominate
inammation can result in a shift to a healthy microbial • Invasion—to cause tissue damage and elicit an inìam
balance. matory/immune response.
CHAPTER 1.2 The Pathogenesis of Periodontal Diseases 13
Quantity Quality
Species-specific virulence factors
Enzymes Toxins Metabolic products
Local gingival • Collagenase Exotoxins Endotoxins • Hydrogen sulphide

inflammation due to • Elastase • Ammonia
“general” properties/ • Other proteases, • Volatile fatty acids
products of e.g. gingipains
plaque bacteria • Hyaluronidase
Gingivitis Potential periodontal tissue damage
• Figure 1.2.3 Overview of periodontitis pathogenesis.
KEY POINT 2 periodontitis), Aggregatibacter actinomycetemcomitans is

strongly associated.
Certain key bacteria are implicated in periodontal tissue
breakdown, but the nature of the host response appears to be
the most important feature in disease progression. Host Factors
Damage to the periodontal tissues from the products of the
bacterial biolm may be direct (via bacterial toxicity) or
How Do Bacteria Cause Disease?
indirect (by stimulation of the host response). Figure 1.2.4
Both the quantity and the quality of bacteria that have colo- summarises possible direct and indirect damage mecha-
nised the gingival sulcus/periodontal pocket can contribute nisms that may be operating.
to disease. e quantity causes local gingival inammation A summary of how the host response can cause plaque-
(gingivitis). e quality (species of bacteria) can produce induced disease is shown in Figure 1.2.5
specic virulence factors, especially enzymes, toxins and
other metabolic products, all of which have the potential Inflammatory Response to the Bacterial
to damage the periodontal tissues (and activate the host’s Biofilm
inammatory/immune response).
Specic enzymes, toxins and metabolic products that e host’s innate inammatory response is the rst line of
are involved in the pathogenesis of periodontal diseases are defence against bacterial challenge; it is rapid and nonspe-
shown in Figure 1.2.3 cic. If this response is excessive, it can cause collateral tissue
e bacterial ora changes from health to disease. us damage. It involves the epithelial barrier, the complement
Gram-positive, aerobic, nonmotile species of bacteria such cascade, cytokines, neutrophils and mast cells. ese fea-
as Streptococcus sanguis, Actinomyces viscosus and Streptococ- tures will now be considered in further detail.
cus oralis are associated with health, and Gram-negative,
anaerobic, motile bacteria such as Porphyromonas gingivalis The Epithelial Barrier
are associated with disease. e epithelial barrier provides an interface between the
Because there are frequently more than 400 species external environment of the gingival crevice or the pocket
of microorganisms present in the mouth, it is often dif- and the underlying connective tissues. It is not an inert
cult to know exactly which species or combinations of barrier, and both cells and uids pass across it. Evidence
species are responsible for periodontitis. However, in the suggests that it has a role in initiating and propagating the
ora for acute necrotising ulcerative gingivitis (ANUG), a inammatory response via cytokine release after stimulation
fusospirochetal complex can be seen with a predominance by bacterial products such as lipopolysaccharides (LPS). In
of Treponema vincenti, Fusobacterium nucleatum and P. addition, stimulated epithelium also releases antibacterial
gingivalis, and, in patients with periodontitis Grade C in peptides such as beta-defensins, which help maintain its
the absence of risk factors (previously termed aggressive integrity to bacterial attack.
Bacteria
Inflammatory
signals/mediators
Inflammation Tissue damage Neutrophils Immune response
Damage by plaque bacteria/products

Direct Indirect (involves host response)
• Figure 1.2.4 Direct and indirect bacterial effects in periodontitis.
Inflammatory response Immune response

to plaque bacteria to plaque antigens
• Rapid • Relatively slow

• First-line defence • Modifiable
• Crude and nonspecific • Specific
• Can be excessive • Can be excessive causing
causing “collateral “collateral damage”
damage”
Involves Involves
• Epithelial barrier • Antigen-presenting cells
• Gingival crevicular fluid • Helper T cells
• Complement cascade • Cytotoxic T cells
• Cytokines • Lymphokine-producing T cells
• Adhesion molecules • B cells and plasma cells
• Neutrophils / PMNs • Antibodies
• Mast cells • Complement cascade
• Macrophages
Gingival inflammation Chronic inflammation
Occur together: chronic stimulation because plaque not

removed by host responses
• Figure 1.2.5 Host response mechanisms in biolm-induced periodontitis.
Complement • Cell lysis (both of the host’s cells and bacteria)
Complement consists of 20 serum glycoproteins that are • Mast cell degranulation with the release of vasoactive
inactive in circulating blood/tissue uid. ey can be acti- amines, resulting in increased vascular permeability
vated via two pathways—the alternate pathway (activated e “cascade” is shown in Figure 1.2.6
by bacterial endotoxin/proteases) or the classical pathway Cytokines
(activated by antibody–antigen interaction).
When activated, these glycoproteins initiate a range of Cytokines are signalling molecules released by a variety of
proinammatory eects (a “cascade”) that ultimately cause: cells that have a range of actions that include proinamma-
• Neutrophil recruitment (movement of neutrophils to the tory activity, for example, neutrophil chemotaxis.
damaged site) e types of cytokine and their eects are shown in Table
• Phagocyte binding to bacteria 1.2.1
Antibody Microbial
binding polysaccharide
C1
B
Classical Alternative
C2
pathway pathway
D
C4
Cleavage of C3
Coating of microbes C5
and induction C6
of phagocytosis
C7
C8
C9
Vasodilation Recruitment of neutrophils
Cell lysis
• Figure 1.2.6 The complement cascade.
Inflammasomes • contain numerous granules that are released after mild
One of the key cytokines in the periodontitis is interleukin 1 mechanical or chemical stimulation;
(IL-1), which causes a proinammatory response including • have granules that include neutrophil chemotactic factor,
activation of osteoclasts and neutrophil recruitment (see Table histamine, and heparin;
1.2.1). IL-1 expression is controlled via central regulators of • can be activated and caused to degranulate by mild
innate immunity called inammasomes. A number of these chemical or physical trauma, complement activation,
multiprotein complexes have been identied that trigger the and cross-linking IgE receptors; and
host’s response after detection of bacteria or tissue damage • degranulate and cause a local increase in vascular per
(Lamkan & Dixit, 2017). Research has identied dysregula- meability with dilation of blood capillaries, which aids
tion of this system in periodontitis, which may contribute to neutrophil migration from blood into the tissues.
the aberrant host response characteristic of periodontitis. Table 1.2.2 shows the chemicals that are released from an
activated mast cell, together with the actions.
Neutrophils (Polymorphonuclear Leucocytes
[Pmnls])
Immune Responses to Biofilm Antigens
Neutrophils:
• are the most commonly occurring white blood cells and Immune responses have three basic characteristics:
the most abundant and important inammatory cell in • speciëcity to particular antigens
periodontitis, • the ability to distinguish between self and nonself
• play a key role in the ërst-line defence of these tissues, • a memory to produce a modiëed response (faster and
• move toward the site of infection through the process of bigger) on secondary exposure to a specic antigen.
chemotaxis, e immune response involves T lymphocytes, B lym-
• kill bacteria either through intra- or extracellular methods, phocytes, and antigen-presenting cells.
• kill by means of enzymes and free radicals as well as neu ese cells will now be discussed in more detail.
trophil extracellular traps (NETS) and
• may produce an exaggerated response that can lead to T Lymphocytes (T Cells)
collateral local tissue damage (periodontitis).
A diagrammatic example of how neutrophils kill bacteria 1. Make up the so-called cell-mediated immune response,
is shown in Figure 1.2.7 as the antigen-specic molecule is not secreted (like an
antibody) and remains bound to the cell surface (the
Mast Cells T-cell antigen receptor).
Mast cells: 2. Direct contact between the T cell and its associated anti-
• are resident in all connective tissues, including gingiva gen is required to initiate an immune response and to
and periodontal ligament; destroy the antigen.
TABLE
1.2.1 Cytokines, their cells of origin, and eects on the inammatory/immune response
Cytokine Cell of origin Effects upon inflammatory/immune response

Interleukin 1 (IL-1) Macrophage (MØ), broblast, Activation of osteoclasts
monocytes upon stimulation by ↑ PMNL margination
endo/exotoxins, epithelial cells ↑ Prostaglandin PGE2 by broblasts
↑ IL-6 synthesis by periodontal broblasts
↑ TNF-α production and release
Interleukin 6 (IL-6) MØ, broblasts, epithelial cells ↑ Acute phase protein synthesis by liver
↑ Bone resorption
↑ B-cell differentiation and Ig production
↑ T-cell activation
Interleukin 8 (IL-8) MØ, endo/epithelial cells, LPS- Potent PMNL chemotaxin
stimulated broblasts, platelets
Interleukin 10 (IL-10) Suppression of cytokines (anti-inammatory)
Transforming growth Anti-inammatory (at high concentrations) stimulates
factor beta (TGF-β) collagen synthesis and repair
Tumour necrosis factor Activated MØs, monocytes, epithelial ↑ MØ production IL-1
alpha (TNF-α) cells ↑ MØ production of PGE-2
↑ ICAM-1 expression/PMNL margination
↑ PMNL oxygen radical production
↑ PMNL degranulation of enzymes
Prostaglandin E2 (PGE2) Activated MØs, monocytes, PMNLs, ↑ Vascular permeability
mast cells, epithelial cells ↑ Vasodilation
↑ PMNL chemotaxis
Stimulates bone resorption
Granulocyte–macrophage Epithelial cells, monocytes, endothelial ↑ Release of PMNLs from bone marrow
colony stimulating cells, broblasts ↑ PMNL chemotaxis
factor (GM-CSF) ↑ Apoptosis
↑ Degranulation
↑ Oxygen radical formation
Bacterium
Phagocyte
1 2 3 4
Membrane Initiation of
Chemotaxis Adherence
activation phagocytosis
Granules
5 6 7 8
Phagosome Killing and Release of

Fusion
formation digestion degradation products
• Figure 1.2.7 Diagram of a neutrophil phagocytosing a bacterium and the subsequent degranulation.
TABLE
1.2.2 Substances released from an activated mast cell and their actions
Preformed Effect
Granule release ▸ Histamine Vasodilation, increased capillary permeability
chemokinesis, bronchoconstriction
Proteoglycan Binds granule proteases
Neutral proteases Activates C3
β-Glucosaminidase Splits off glucosamine
ECF Eosinophil chemotaxis
NCF Neutrophil chemotaxis
Platelet-activating factor Mediator release
Interleukins 3,4, 5, & 6 Multiple, including macrophage activation, trigger
GM-CSF, TNF acute phase proteins, etc.
Newly synthesized Effect
Lipoxygenase pathway ▸ Leukotriene C4, D4 (SRS-A) Vasoactive, bronchoconstriction, chemotaxis,
Leukotriene B4 and/or chemokinesis
Cyclo-oxygenase pathway ▸ Prostaglandins Affect bronchial muscle, platelet aggregation, and
Thromboxanes vasodilation
3. Antigen-specic T cells can only interact with antigens secondary (non–antigen binding) biological functions such
when present on a host cell surface. that only IgG and IgM antibodies can activate complement.
4. Helper T cells start immune responses by interacting Normally, a B-cell response to antigen will result in the
with specic antigens displayed on the surface of an anti- production of specic antibodies including all ve classes.
gen-presenting cell. However, the IgG class usually predominates.
5. Eector T cells interact with specic antigens displayed Dimeric IgA is predominant in responses to antigen that
on host cell surfaces and either lyse the cell (cytotoxic is swallowed (not via the gingival sulcus) and is present in
T cells) or release soluble mediators (lymphokines) that saliva where it aggregates antigens/bacteria/viruses, prevent-
attract macrophages and/or other inammatory cells to ing them from harming the body.
the area. In terms of periodontal diseases, IgG class antibodies to
6. A diagrammatic representation of the T-cell response is plaque antigens are of most importance. ey are within
shown in Figure 1.2.8 periodontal tissues and present within gingival crevicular
uid.
B Lymphocytes e mechanism for the removal or destruction of antigen
by an antibody is shown in Figure 1.2.10
7. Form part of the so-called humoral immune response. Antibody–bacteria aggregation is shown in Figure 1.2.11
8. When activated by its associated antigen, the B cell
proliferates and dierentiates into antibody-secreting Bacteria Versus Host
cells (plasmablasts and plasma cells).
9. B-cell responses to most antigens will not occur with- If there is an ongoing imbalance between the host’s inam-
out the help of T cells and the mediators they produce matory/immune response and biolm bacteria then disease
(e.g. IL-2, IL-4). will occur. is is demonstrated in patients with periodon-
10. Antibodies are released into the tissue/circulation where titis by an aberrant inammatory/immune response with
they can bind soluble and insoluble antigens that do excess nonresolving inammation, resulting in collateral
not have to be associated with host cells. tissue damage. Although the aberrant host response is the
11. Antibody–antigen binding, with or without comple- major cause of tissue damage, bacteria are required to initi-
ment activation, allows removal and destruction of the ate and propagate the host response and have the ability
antigen via phagocytosis. to cause some tissue damage directly. e quantity of the
e B-cell response is shown in Figure 1.2.9 bacteria in the biolm and the specic species present are
the two most important bacterial factors that can lead to
Antibodies/Immunoglobulins periodontal destruction. Both the host and plaque factors
are modulated by risk factors (Figure 1.2.12).
In humans, there are ve main classes of antibody (immuno- An excessive host response can cause periodontal break-
globulin): IgG, IgA, IgM, IgD, and IgE. ɨese diêer in their down. e mechanism for this is thought to be due to
T-cell response
Antigen
Presentation to
CD4+ antigen-specific T cell
Macrophage
IL-2 R Proliferation
expression
T cells factors
Dendrite cell e.g. IL-2
Differentation
IL-4
IL-6
Naive T cells
Antigen-presenting cells Effector T cells Memory T cells
“process” antigen and
then display on their
membranes associated with
HLA-DR (HLA class II)
Cytotoxic Lymphokine Helper/
producing suppressor
Kill/lyse Lymphokine Regulate

cells produce and attract response
macrophages, etc.
When effector T cell responds to antigen associated

with HLA-class I on cell membranes
• Figure 1.2.8 The T-cell response.
Soluble or cell Activation and

membrane–associated proliferation
antigen
Many antigen-
specific B cells
T-cell factors,
e.g. IL-4, IL-2
Differentation
Recruitment of Th T cell factors and “class switching”
T helper cells e.g. IL-4, IL-6, IFNγ
Naive B cells
(many different
specificities)
Helper T cells
(many)
Plasma cells
Plasma cells (later antibody
(early antibody Memory B cells
formation—higher
formation) binding affinity)
• Figure 1.2.9 The B-cell response.

All antibodies cross-link antigens and

make them more easily phagocytosable
Antigen binding to IgE

Antibody binding to antigen will IgG or IgM antibodies
antibody on mast cell
not normally harm the antigen BUT react with antigen and
membrane results in
“labels” it for removal/destruction activate complement
mast cell degranulation
IgG antibodies opsonise

Dimeric IgA antibodies prevent
antigen (phagocytes have
antigen entering tissues
Fcγ receptors on their surface)
• Figure 1.2.10 The removal/destruction of antigen by antibody.
IgM Antigen
Bacteria
Bacterium
• Figure 1.2.11 Antibody–bacteria aggregation (mainly a function of polymeric antibodies—IgM and dimeric
secretory IgA).
periodontal pathogens in the biolm stimulating a proin- not the case. e risk for the progression to periodontitis
ammatory response, resulting in neutrophil recruitment is greatest in individuals who are susceptible, representing
leading to the local release of reactive oxygen species (free between 5% and 15% of the population. At the other end
radicals) and enzymes capable of damaging host tissue. of the scale, about 10% of the population are resistant to
Although host tissue antioxidants can neutralize reactive oxy- periodontal breakdown, despite persistent long-term plaque
gen species, if the latter predominate (due to either low local accumulation, and disease progression in these individuals
levels of antioxidants and/or excess reactive oxygen species is rare.
production), oxidative stress can result in an excessive and Clinically, there are some shared signs of disease between
aberrant response leading to tissue damage (Figure 1.2.13). gingivitis and periodontitis: biolm accumulation, bleed-
e action of the excess free radicals and enzymes on the ing, inamed gingivae, loss of stippling and loss of a knife-
periodontal tissues is summarised in Figure 1.2.14 edge gingival margin.
e critical role that oxidative stress and reactive oxygen In addition to these signs, in periodontitis the following
species play in local tissue damage is shown in Figure 1.2.15 signs may be seen: pocket formation, suppuration, attach-
ment loss, bone loss and furcation exposure. Furthermore
Does Gingivitis Inevitably Lead to when periodontitis is present, teeth may become mobile
Periodontitis? and drift and diastemas (spaces between the teeth) may
develop. However, these last three signs can also be due to
In the past, it was thought that gingivitis inevitably led aberrant occlusal forces or a combination of periodontitis
to periodontitis. However, it is now accepted that this is and aberrant occlusal forces.
Host Plaque bacteria
Aberrant inflammatory/ Bacterial Bacterial

immune response load pathogens
Risk factor modulation

(modifiable and non-modifiable)
Periodontitis
• Figure 1.2.12 Host and bacterial factor modulation by risk factors.
Periodontal
pathogens in plaque
Normal host defence
Neutrophils recruited
and activated
Excess ROS moderated

Tissue damage Free radicals (ROS)
by innate
(periodontal diseases) and enzymes
Aberrant antioxidant defences
response
• Figure 1.2.13 How an excessive host response can contribute to disease.

Free radicals (ROS) and enzymes
Bone Epithelium Connective tissue

• Reduced osteoclast • Stimulation of NF κB and • Direct tissue damage
apoptosis downstream production of Neutrophils to fibroblasts
• Increased differentiation pro-inflammatory cytokines
of osteoclasts • Direct cell damage
• Reduction in osteocytes • Loss of connective
tissue
• Recruitment and activation
of neutrophils
• Apoptosis of epithelial cells
Loss of bone
Periodontal attachment loss
• Figure 1.2.14 Tissue damage caused by free radicals and enzymes.
Sucular / pocket
Recruited neutrophils epithelium Bacteria
Pro-inflammatory mediators
e.g. chemokines and cytokines
Reactive oxygen
species (ROS)
Pro-inflammatory mediators
Normal host innate defence response
Aberrant host response

Excess ROS production
Oxidative stress
Local tissue damage
Sucular / pocket
epithelium Fibroblasts Bone
• Figure 1.2.15 The role of oxidative stress in local tissue damage.

Acknowledgement References
is chapter is based on a session within e-Den that Pro- Grossi SG, Zambon JJ, Ho AW, Koch G, Dunford RG, Machtei EE,
fessor Milward and Dr. Matthews produced in 2011. etal. Assessment of risk for periodontal disease. 1. Risk indicators
Acknowledgement is given to the Faculty of Dental Surgery for attachment loss. J Periodontol. 1994;65:260–267.
of the Royal College of Surgeons of England for giving per- Lamkanë M, Dixit VM. In Retrospect: e inammasome turns 15.
mission for material from the e-Den session to be used in Nature. 2017;548(7669):534–535.
Van Dyke TE, Bartold PM, Reynolds EC. e nexus between peri-
this chapter.
odontal inammation and dysbiosis. Frontiers in immunology.
Multiple Choice Questions on the contents of this chap 2020;11:511.
ter are available online at Elsevier eBooks+
1.3
EPIDEMIOLOGY OF
KE N N E T H E ATO N
CHAPTER OUTLINE
Introduction How to Measure
Principles of Descriptive Epidemiology Probes
Use of Radiographs in Epidemiological Surveys
Why is There a Need for Data on Periodontal Health/ What to Measure – Full Versus Part Mouth Assessment
Disease? Examiner consistency
Periodontal Epidemiology National Surveys
Indices used in Epidemiological Surveys
Positive Developments
Problems with Periodontal Epidemiology
Possible Future Developments
What to Measure

This chapter explains the principles of epidemiology and why clinicians need to be aware of the epidemiology of diseases and conditions that
they treat. It then outlines the current deciencies in periodontal epidemiology and gives brief details of two national studies and a positive
development.
By the end of the chapter the reader should: e chapter covers the following topics:
• Understand the principles of epidemiology and periodontal • Introduction
epidemiology • The principles of descriptive epidemiology
• Be able to describe indices that have been used in • Why is there a need for data on periodontal diseases?
periodontal epidemiology • Indices that have commonly been used in periodontal
• Recognise the problems in periodontal epidemiology epidemiology
relating to: what to measure, how to measure, examiner • Problems with periodontal epidemiology – what to measure,
training and consistency how to measure, examiner consistency
• Describe the major öndings of the periodontal aspects • National surveys
of the National Health and Nutrition Examination Survey • A positive development
(2002/2013) and the Adult Dental Health Survey (2009). • Possible future developments.
Introduction are therefore based on the need to nd information about a

population, which may be the entire population of a town,
Porta and Last (2008) have dened epidemiology as the region or country or a subset with problems of interest.
study of the distribution and determinants of health-related
states or events in specied populations and the application KEY POINT 1
of the study to control health problems. Epidemiology can In practical terms, where commonly occurring diseases such
also be dened as the science of epidemics. as dental caries or periodontal diseases are concerned, it is
In healthcare, epidemiological techniques are used to inves- not possible to investigate/examine the entire population, so
tigate, at a specic time, the proportion of people in a popula- only a sample is examined. The selection of a representative
sample is therefore of paramount importance.
tion that is aected by a disease. e principles of epidemiology
23
MacMahon et al. (1960) suggested that epidemiol- Why is There a Need for Data on
ogy should be more than just counting numbers of people
within the population with disease but should also try to
Periodontal Health/Disease?
clarify the factors contributing to, or causing, the disease in Leroy etal. (2010) suggested that accurate epidemiological
question. ey therefore suggested that there are four stages: data on periodontal health/disease are needed to:
• Descriptive epidemiology: in which the distribution of • identify people at risk of periodontal diseases in the
the disease under investigation is described, with a com- population
parison of its frequency in dierent populations and dif- • assess the eïcacy of preventive strategies and curative
ferent subsets of the population. e description is based therapies at a population level
on prevalence, incidence and severity. • inform workforce planning
• Formulation of hypotheses: which sought to explain • evaluate the interplay with risk factors for periodontitis
specic factors relating to the disease in question. • assess the interaction between periodontal health/disease
• Analytical epidemiology: in which observational stud- and systemic diseases
ies were designed and performed to examine these • assess the eêect of periodontal diseases on the quality of
hypotheses. life.
• Experimental epidemiology: in which experimental
studies were performed in human populations to test the
hypotheses that had been proved in observational and Periodontal Epidemiology
analytical studies. Techniques for periodontal epidemiology have evolved over
In practice, oral epidemiology, including periodontal the last 60 years. As will be seen later in this chapter, there
epidemiology, has been largely descriptive. have been problems deciding exactly which variables to
measure and how to measure them.
Principles of Descriptive Epidemiology Until the 1950s, both clinically and in epidemiologi-
cal surveys, periodontal health was frequently classied as
As mentioned in the introduction, descriptive epidemiology good, moderate or poor. ese were very subjective assess-
is based on prevalence, incidence and severity. ments, which were not based on any specic criteria and,
as a result, were frequently interpreted dierently by dif-
KEY POINT 2 ferent examiners or by the same examiner from 1 day to
Descriptive epidemiology is based on prevalence, incidence another. As a result, a series of periodontal indices were
and severity. developed to achieve greater consistency of assessment,
both during the clinical examination of patients and in
Prevalence is the amount of disease present in a popula- epidemiological surveys. e indices used in clinical prac-
tion at a given time (measured as a percentage) and depends tice for assessing and monitoring patients are described in
on the duration of a disease and its previous incidence. Chapter 2.2. Additional ones have been used in epidemio-
Incidence is the number of new cases or events that occur logical surveys.
during a specied time period.
Severity has been dened as the quality of being severe
in the disease, or in the extent and severity index (Carlos
Indices used in Epidemiological Surveys
et al. 1986), as “the stage of advancement of periodontal e rst was Russell’s Periodontal Index (PI) (Russell 1956).
destruction”. is involved assessing the periodontal tissues around each
e basic principles for a descriptive epidemiological tooth and awarding a score to the tooth. e scores used in
study are that: “eld” studies (where no radiographs were available) were:
• ɨe methods should be described clearly with a detailed 0 Neither overt inammation in the investing tissues, nor
explanation and should be easily reproducible by any cli- loss of function due to destruction of supporting tissue
nician or scientist who works in the same discipline. 1 Mild gingivitis: an overt area of inammation in the free
• ɨe assessment of the variables should be performed in gingiva but the area does not circumscribe the tooth
an objective manner and follow the documented meth- 2 Gingivitis: inammation completely circumscribes the
ods for data collection precisely and consistently. tooth but there is no apparent break in the epithelial at-
• ɨe environment in which the data are collected should tachment
be controlled and standardised. 4 ere is early, notch-like resorption of the alveolar crest.
• ɨe examiners should be well trained and calibrated so Not used in eld studies
that they are consistent in their assessments. 6 Gingivitis with pocket formation: the epithelial attach-
• ɨe size of the sample should be determined using a power ment has been broken and there is a pocket (not merely a
calculation, be of adequate size and be representative. deepened gingival crevice due to swelling of the free gin-
• ɨe data should be collected in such a manner that they givae). ere is no interference with normal masticatory
can easily be analysed. function, the tooth is rm in its socket and not drifted
CHAPTER 1.3 Epidemiology of Periodontal Diseases 25
8 Advanced destruction with loss of masticatory function:

the tooth may be loose, may have drifted, may sound
dull on percussion with a metallic instrument and may
be depressed in its socket.
All the resulting scores were added together and divided
by the number of teeth to give an overall score.
e next index to be devised for periodontal epidemiol-
ogy was Ramord’s Periodontal Disease Index (PDI) (Ramf-
jord 1959). Ramord highlighted two signicant weaknesses
of the Russell’s Periodontal Index: it did not involve probing
to assess periodontal pocket depth and did not “orientate
pockets to the cemento-enamel junction”. He claimed that, • Figure 1.3.1 Picture of WHO epidemiological probe. Note the round
as a result, it underestimated the true extent of periodontitis. tip, rst band (silver) from 0 to 3.5 mm, second band (black) from 3.5
e Ramord PDI was based on the assessment of six teeth to 5.5 mm.
which were: the upper right rst molar, the upper left central
incisor, the upper left rst premolar, the lower left rst molar, rather than periodontal status and not specically as an
the lower right central incisor and the lower right rst pre- epidemiological index. However, it has been used (or mis-
molar. e following assessments took place at each tooth: used) for this purpose for the last 30 years. A simplied
• Four-point pocket probing (mid-buccal, mid-palatal/lin periodontal probe was designed to be used with the index
gual, mesio-buccal, disto-buccal) relating the crest of the (Figure 1.3.1).
gingiva and the bottom of the pocket to the cemento- For adults, 10 teeth (all upper and lower ërst and second
enamel junction (CEJ) molars and the upper right and lower left central incisors)
• Recording of gingivitis, calculus, plaque, attrition, mobil are assessed for:
ity and lack of contact using a four-point scale (0–3) for • Gingival bleeding after probing
each of these variables • Supragingival calculus
• If the gingival crevice had migrated apically from the CEJ • Subgingival calculus
by no more than 3 mm at any of the probing sites, the • Pocket depths of 4 or 5 mm
score for the tooth was 4. If this migration was between 3 • Pocket depths of 6 mm or more.
mm and 6 mm, it was 5, and if it was more than 6 mm, e following scores are given:
it was 6. e six scores were added together and divided 0 = periodontal health (no bleeding, calculus or pockets)
by 6 to give an overall score for periodontitis. e other 1 = gingival bleeding but no calculus or pockets
scores were treated individually to give scores for gingivi- 2 = supra- or subgingival calculus present
tis, plaque, etc., but not amalgamated with the score for 3 = a 4 or 5 mm pocket
pocket depth/attachment loss. 4 = a 6 mm or deeper pocket present.
e worst score for each sextant (Figure 1.3.2) is
KEY POINT 3 recorded, and the overall score is taken as the worst score
Ramfjord highlighted two signicant weaknesses of the from the sextants.
Russell’s Periodontal Index which were that it did not involve
probing to assess periodontal pocket depth and did not After a few years, CPITN was redesignated as CPI to
“orientate pockets to the cemento-enamel junction”. He denote its use as an epidemiological tool rather than to
claimed that, as a result, it underestimated the true extent of assess treatment need. Its use in epidemiological surveys has
periodontitis. been recommended by WHO in both the third (1989) and
fourth (1997) editions of Oral Health Surveys: Basic Methods
e advantage of the Ramord index was that it did However, in the light of growing evidence that CPITN
measure pocket depth and loss of attachment. However, it underestimates the extent of periodontal breakdown in a
was complicated to record and did not assess all teeth. ere mouth and that from an epidemiological standpoint, calculus
was therefore a need for a simpler index. is an irrelevance (Leroy etal. 2010), WHO has revised their
recommendations in the fth edition of Oral Health Surveys:
KEY POINT 4 Basic Methods, as will be described later in this chapter.
The advantage of the Ramfjord index was that it did measure
pocket depth and loss of attachment. However, it was
complicated to record and did not assess all teeth. KEY POINT 5
However, in the light of growing evidence that CPITN
underestimates the extent of periodontal breakdown in a
To address this need, the Community Periodontal Index mouth and that from an epidemiological standpoint, calculus
of Treatment Need (CPITN) was devised for the World is an irrelevance (Leroy etal. 2010), WHO has revised their
Health Organization (WHO) (Ainamo etal. 1982). As its recommendations in the fth edition of Oral Health Surveys:
name implies, it was designed to assess treatment needs Basic Methods
A modied version of CPITN, known as the basic subsequently. However, like the PDI and CPITN, it does
periodontal examination (BPE), has been developed as not assess all teeth in a mouth.
a screening tool by the British Society of Periodontology
and Implant Dentistry. It is widely used in the UK and is KEY POINT 6
described in Chapter 2.2 The advantage of the ESI is that it is simple to use and can
e Extent and Severity Index (ESI) was proposed by provide a measurement against which to compare when it is
Carlos etal. (1986). It involves assessing half the mouth – repeated subsequently. However, like the PDI and CPITN, it
does not assess all teeth in a mouth.
the upper right and lower left quadrants. Mid-buccal and
mesio-buccal sites and all the teeth other than third molars
are assessed for attachment loss (Figure 1.3.3). Attachment
loss is thought to be a more reliable indicator of past peri- Problems with Periodontal Epidemiology
odontal breakdown than pocket depth.
In the ESI, attachment loss is considered to be due to e problems with periodontal epidemiology arise from
disease if it is greater than 1 mm. three main areas. ese are:
Extent is measured by the percentage of sites where such • What to measure
a measurement was found, e.g. if it was found at 7 of the • How to measure
28 sites assessed in a half mouth, then the extent would be • How to ensure that examiners measure consistently.
25%. e severity is calculated as the mean loss of attach-
ment at all the sites. us if the total attachment loss for the What to Measure
half mouth was 56 mm, the severity score would be 2.0 and
the extent and severity score would be 25, 2.0. e advan- As explained in Chapter 1.2, it is currently recognised that
tage of the ESI is that it is simple to use and can provide a the presence of gingivitis at a site does not necessarily mean
measurement against which to compare when it is repeated that it will progress to periodontitis. A number of stud-
ies have also shown that the presence of calculus does not
necessarily lead to either gingivitis or periodontitis. is
3 0 3 is not to say that patients with gingivitis or calculus do
1 2 1
not need advice on oral hygiene and professional clean-
ing. From a periodontal epidemiological point of view, the
most important consideration is the life expectancy of a
Overall score = 3
tooth; if periodontal attachment (periodontal ligament and
• Figure 1.3.2 Example of CPITN scores for each sextant and the over- alveolar bone) has been lost, then a tooth is at a greater
all score.
risk than if the attachment level is normal. Historically, a
Enamel
CEJ
Recession
GM
Pocket Loss of
attachment
JE
Key
CEJ Cemento-enamel
junction
GM Gingival margin
JE Junctional epithelium
• Figure 1.3.3 Diagram showing loss of attachment (LOA) which is the sum of recession plus pocket
depth.
TABLE American Academy of Periodontology and Centre for Disease Control case denitions for
1.3.1 periodontitis
Disease category Attachment loss (AL) Pocket depth (PD)
Severe periodontitis At 2 or more interproximal (IP) sites with AL And 1 or more IP site(s) with PD ≥5 mm
≥6 mm (not on the same tooth)
Moderate periodontitis At 2 IP sites with AL ≥4 mm (not on same tooth) Or 2 or more IP sites with PD ≥5 mm (not
on same tooth)
No or mild periodontitis Neither “moderate” nor “severe”
Reprinted from Journal of Periodontology, 78(7S):13, Page & Eke (2007), with permission from John Wiley & Sons.
healthy attachment level has been taken to be when the TABLE European Federation of Periodontology
base of the gingival sulcus is no more than 1 mm apical 1.3.2 case denitions for periodontitis
to the cemento-enamel junction. However, this is a rather Incipient periodontitis IP attachment loss of ≥3 mm
simplistic assumption because, with age, teeth erupt, and in ≥2 non-adjacent teeth
as long as the teeth are not mobile and there is no ongoing
Periodontitis with IP attachment loss of ≥5 mm
periodontitis, an 80-year-old can happily live with a gener- substantial extent and in ≥30% of teeth
alised 25% attachment loss, whereas this would be a cause severity
for concern in an 18-year-old. Nevertheless, the measure-
ment of attachment loss is taken to be the gold standard Reprinted from Journal of Clinical Periodontology, 32(S6):4,
Claffey (2005), with permission from John Wiley & Sons.
for periodontal epidemiology. Pocket probing depth is also
an important variable to assess but in combination with
attachment loss.
KEY POINT 7 KEY POINT 9

If its periodontal attachment (periodontal ligament and alveolar There are a number of potential inaccuracies which can occur
bone) has been lost, then a tooth is at a greater risk than if the when measuring pocket depth. These may be due to:
attachment level is normal. • The extent to which a probe penetrates into a
pocket, which can vary depending on the degree of
inammation at the base of the pocket. If the tissues
are very inamed, then there will be less resistance to
KEY POINT 8 pressure and the probe tip will penetrate further than in
The measurement of attachment loss is the gold standard a pocket without an inamed base.
for periodontal epidemiology. Pocket probing depth is also • The diameter of the probe tip. The smaller the tip the
an important variable to assess but in combination with greater its potential to penetrate.
attachment loss. • The thickness (width) of the tine (the part of the probe
with markings).
• The probing force used.
Unfortunately, there is no consensus on a “case” deni- • The angulation of the probe to the pocket wall.
tion for periodontitis in epidemiological studies (Savage • The accuracy of the markings on the probe.
etal. 2009), i.e. the threshold at which loss of attachment • Presence of overhanging restorations or calculus.
and pocket depth should be considered a threat to the
teeth and the number of sites where this threshold has been
crossed. is makes meaningful comparisons between stud-
Apart from measuring attachment loss and pocket prob-
ies impossible. Two case denitions have been suggested by
ing depth, the exposure of furcations, tooth mobility, gin-
Page and Eke (2007) for the American Academy of Peri-
gival bleeding, gingival recession, plaque and calculus have
odontology/Centre for Disease Control (AAP/CDC) (Table
frequently been recorded. Details of the techniques for
1.3.1) and Tonetti and Claey (2005) for the European
recording these variables are in Chapter 2.2. Finally, non-
Federation of Periodontology (EFP) (Table 1.3.2).
clinical details such as frequency of toothbrushing and use
of oral hygiene aids, such as interdental brushes and dental
How to Measure oss, may be recorded.
Probes
Both attachment loss and pocket depth are measured with Use of radiographs in epidemiological surveys
a periodontal probe. Ideally, a probe with 1 mm markings, It is considered unethical to take oral radiographs for the
such as the North Carolina 15 (Figure 1.3.4), should be used. population en masse. e needs of the individual must be
National Surveys
e results of two national surveys, NHANES 2009/2010
in the United States and the UK Adult Dental Health
Survey (ADHS) 2009, have raised some interesting issues
which will need to be addressed in the future.
In previous NHANES surveys, part mouth assessments
were performed. e results of NHANES III, which was
performed in the late 1990s and used a part mouth assess-
ment, indicated that 53.1% of Americans aged 30 years or
older who were examined had attachment loss of ≥3 mm
• Figure 1.3.4 A picture of a North Carolina (NC) 15 periodontal probe. and 23.1% pocket depth of ≥4 mm. When full mouth
Note the 1 mm markings. assessment was used in the 2009/2010 survey, these gures
increased to 85.9% and 40.9% respectively (Eke etal. 2012).
assessed prior to taking a radiograph, and there must be a e survey conrmed previous ndings that the periodontal
good clinical indication to do so. For this reason and for health of those with lower socio-economic status was worse
reasons of time and cost, radiographs are not usually taken than that of those with higher socio-economic status.
during epidemiological surveys.
KEY POINT 12
What to Measure – Full Versus Part Mouth Eke etal. (2012) concluded that the higher burden of
periodontitis in the adult US population and the prevailing
Assessment disparities among socio-demographic segments detected
from this survey, coupled with the potential economic cost
Because a periodontal assessment is usually part of a larger for prevention and treatment, suggest periodontitis as an
oral or other epidemiological survey, there are often con- important dental public health problem, especially among our
straints on the time available to perform this assessment. ageing population.
As a result, historically, part mouth rather than full mouth
assessments have been performed, and indices such as those In the ADHS (2009), pocket depth, gingival bleeding,
described earlier in this chapter have been employed. How- calculus and plaque were recorded at two teeth in each sex-
ever, the publication of the results of the periodontal section tant. However, in the South Central area of England, the
of the National Health and Nutrition Examination Survey BPE was used. Loss of attachment was only recorded for
(NHANES) (2009/2010) has reinforced the fact that part those over 55 years of age. e WHO probe (see Figure
mouth assessment underestimates the true level of disease 1.3.1) was used.
(Eke etal. 2012, Papapanou 2012). Overall, it was found that 55% of the adults examined
had no pocketing, 37% had a pocket or pockets of between
Examiner Consistency 4 mm and 5.5 mm and 8% had a pocket or pockets of 6
mm or deeper. e methodology used makes it impos-
ɨe potential diïculties in assessing pocket depth accu
sible to compare these results with those obtained in the
rately were discussed earlier in this chapter.
NHANES 2009/2010 survey. ere were wide variations
KEY POINT 10 in the percentage of adults assessed as having a healthy peri-
odontium with a range from 9% in the West Midlands to
There are also difculties in assessing and scoring variables
such as plaque and gingivitis accurately and consistently. 36% in the East of England. Two examiners recorded over
These difculties may be due to variation between examiners 70% of those they examined as periodontally healthy. It is
(inter-examiner variability) or variation by one examiner (intra- entirely possible that these apparent variations were due to
examiner variability) such that he/she scores the same site with examiner inconsistency and did not reect the true picture.
the same amount of plaque or gingivitis inconsistently.
To try to overcome lack of consistency, examiners for epi- KEY POINT 13

As the report of the survey points out, this could reect inter-
demiological surveys undergo training and calibration prior
examiner variation (an under recording of disease) rather than
to performing the survey and perform repeat scores on a pro- a difference in the pattern of disease (NHS Information Centre
portion of subjects each day during the survey. Oral Health 2009).
Surveys: Basic Methods, 4th Edition (1997) recommended
that after 4 or 5 days of training inter- and intra-examiner
agreement on assessments should be in the 85–95% range. KEY POINT 14
In other countries, it is rare to nd periodic national oral health
KEY POINT 11 surveys, let alone periodontal surveys. Furthermore, when they
Examiners who are persistently inconsistent during training and have been performed, they used a variety of techniques, both
calibration should not take part in the survey concerned. to recruit the population sample and in the clinical assessment.
TABLE Modied from WHO periodontal and will doubtless continue to do so. In the next 10 years
1.3.3 examination criteria 0 changes may occur as a result of two developments; the rst
is the newest classication scheme for periodontal and peri-
Score Criteria
implant diseases and conditions (Caton et al. 2018). is
0 Healthy periodontium may lead to changes in the case denitions used and the data
1 Gingival bleeding but no pocket depth recorded in periodontal epidemiology. However, because
greater than 3.5 mm the new scheme requires the availability of radiographs for
2 Pocket of between 3.5 mm and 5.5 mm
all subjects/patients, there may be no immediate changes
in periodontal epidemiological methods. e second is that
3 Pocket greater than 5.5 mm in depth Papapanou and Susin (2017) have suggested that additional
dimensions should be included in periodontal epidemiol-
ogy, such as the assessment of impaired function, aesthet-
ics and the eect on general health and quality of life. e
ese problems were highlighted in a systematic review authors believe that such a multidimensional approach
of published studies which concluded that as far as Europe would lead to improved understanding of the epidemiology
was concerned, more comparable and representative data on and eects of periodontitis and its consequences.
periodontal disease and tooth loss from all major countries Multiple choice questions on the contents of this chapter
are needed to get a clear picture on periodontal health in are available online at Elsevier eBooks+
Europe (König etal. 2010).
References
Positive Developments
Ainamo J, Barmes D, Beaggrie G, Cutress T, Martin J, Sardo-Inrri
e fth edition of Oral Health Surveys: Basic Methods J. Development of the World Health Organisation (WHO) Com-
(WHO 2013) recommends that a full mouth assessment munity Periodontal Index of Treatment Need (CPITN). Int Dent
should be performed using the WHO probe and the record- J. 1982;32:281–291.
ing criteria and scores in Table 1.3.3 Carlos JP, Wolfe MD, Kingman A. e extent and severity index: a
In addition, at a minimum, loss of attachment should be simple method for use in epidemiologic studies on periodontal
assessed at all upper and lower rst and second molars and disease. J Clin Periodontol. 1986;13:500–505.
the upper right and lower left central incisors (WHO 2013). Caton JG, Armitage G, Berglundh T, Chapple ILC, Jepson S, Korn-
man KS, Mealey BL, Papapanou PN, Sanz M, Tonetti MS. A new
classication scheme for periodontal and peri-implant diseases and
KEY POINT 15 conditions - introduction and key changes from the 1999 classi-
WHO has suggested the need for full mouth examination of the cation. J Periodontol. 2018;89(suppl 1):S1–S8.
periodontium when epidemiological studies are performed and
Eke PJ, Dye BA, Wei L, ornton-Evans GD, Genco RJ, etal. Preva-
also indicated the irrelevance of assessing calculus in these
studies, as it is not a disease. lence of periodontitis in adults in the United States: 2009 and
2010. J Dent Res. 2012;91:914–920.
Holtfreter B, Albandar JM, Dietrich T, Dye BA, Eaton KA, Eke PI,
A group of North American and European periodontal Papapanou PN, Kocher T. Joint EU/USA Periodontal Epidemiol-
epidemiologists (Holfreter etal. 2015) have published stan- ogy Working Group. Standards for reporting chronic periodontitis
dards for reporting chronic periodontitis prevalence and prevalence and severity in epidemiologic studies: proposed stan-
severity in epidemiological studies – proposed standards dards from the Joint EU/USA Periodontal Epidemiology Working
from the Joint EU/USA Periodontal Epidemiology Working Group. J Clin Periodontol. 2015;42(5):407–412.
Group. Among other things, this publication recommends König J, Holtfreter B, Kocher T. Periodontal health in Europe: future
that, when conducting periodontal epidemiological surveys, trends based on treatment needs and the provision of periodon-
the key indicators to record are the prevalence and extent of tal services – position paper 1. Eur J Dent Educ. 2010;14(suppl
clinical attachment loss, probing depth and bleeding on prob- 1):1–20.
Leroy R, Eaton KA, Savage A. Methodological issues in epidemiologi-
ing at site and tooth level using the Centre for Disease Con-
cal studies of periodontitis – how can it be improved? BMC Oral
trol/American Academy of Periodontology case denition. Health. 2010;10:8.
MacMahon B, Pugh TF, Ipsen J. Epidemiologic Methods. Boston:
KEY POINT 16 Little and Brown; 1960.
In order to achieve comparable data, there is a need for all NHS Information Centre for Health and Social Care. Adult Dental
future periodontal epidemiological studies to use the same Health Survey 2009. London, Health and Social Care Information
standardised methods. Centre; 2011. Available from https://digital.nhs.uk/data-and-
information/publications/statistical/adult-dental-health-
survey-2009-summary-report-and-thematic-series. (accessed
Possible Future Developments 31.05.21).
Page RC, Eke PI. Case denitions for use in population-based
As has been demonstrated in this chapter, periodontal epi- surveillance of periodontitis. J Periodontol. 2007;78:1387–
demiology has developed and evolved over the last 70 years 1399.
Papapanou PN. e prevalence of periodontitis in the US: forget been used to identify the disease. J Clin Periodontol. 2009;36:
what you were told. J Dent Res. 2012;91:907–908. 458–467.
Papapanou PN, Susin C. Periodontitis epidemiology: is periodontitis Tonetti MS, Claey N. Advances in the progression of periodontitis
under-recognised, over-diagnosed, or both? Periodontology 2000. and proposal of denitions of a periodontitis case and disease pro-
2017;75:45–51. gression for use in risk factor research. Group C consensus report
Porta M, Last JT. Dictionary of Epidemiology. 5th ed. USA: Oxford of the 5th European Workshop in Periodontology. J Clin Periodon-
University Press, Oxford United Kingdom; 2008. tol. 2005;32(suppl 6):210–213.
Ramord SP. Indices for the prevalence and incidence of periodontal World Health Organization. Oral Health Surveys: Basic Methods. 3rd
disease. J Periodontol. 1959;30:51–59. ed. Geneva: WHO; 1989.
Russell AL. A system of classication and scoring for prevalence sur- World Health Organization. Oral Health Surveys: Basic Methods. 4th
veys of periodontal disease. J Dent Res. 1956;35:350–359. ed. Geneva: WHO; 1997.
Savage A, Eaton KA, Moles DR, Needleman I. A systematic World Health Organization. Oral Health Surveys: Basic Methods. 5th
review of denitions of periodontitis and methods that have ed. Geneva: WHO; 2013.
1.4
HOST RESPONSE AND
SUSCEPTIBILITY
PAU L CO O P E R A N D M A R T I N L I N G
CHAPTER OUTLINE
Introduction Cell Signalling
Denitions Innate Immunity
Host Susceptibility Acquired Immunity
Host Response to the Bacterial Biolm The Contribution of Genes to Host Responses
Normal Host Response Acknowledgements
The Pathogenesis of Periodontal Lesions

This chapter explains the factors that contribute to a susceptible host response and the host’s innate immune response to the plaque biolm.
It then goes on to describe the immunopathology of the host response in periodontitis and to explain the contribution of genes to host
susceptibility.
By the end of the chapter the reader should be able to: The chapter covers the following topics:
• Describe the factors which contribute to a susceptible host • Introduction
response • Deönitions
• Explain the host’s innate immune response to the plaque • Host susceptibility
bioölm • Host response to the bacterial bioölm
• Describe the immunopathology of the host response in • Normal host response
periodontitis • The pathogenesis of periodontal lesions
• Explain the contribution of genes to host susceptibility. • Cell signalling
• Innate immunity
• Acquired immunity
• The contribution of genes to host responses
Introduction KEY POINT 1

Periodontitis is an inammatory disease initiated by bacteria,
Periodontal diseases, as a group, are one of the most preva- but it is the host response that causes the majority of the
lent of human chronic inammatory conditions, and they damage to the periodontium.
are a major cause of tooth loss, particularly in developed
countries. ey are also one of the most complex of human Whereas bacteria in the biolm trigger the disease pro-
diseases, involving a range of aetiological factors, including cess and are part of the causal pathway of periodontal
microbial, genetic and environmental factors. destruction, the response of the host to the bacteria is key
Without bacteria there would be no periodontitis, but to the development of periodontitis and to disease pro-
bacteria are also important to oral health with over 1200 gression (Figure 1.4.1). In the past, it was thought that
species (including uncultivable species) described in the the presence of bacteria, and their toxins, were principally
mouth. However, certain key bacteria, which are referred responsible for the tissue damage seen in periodontitis and
to as “periopathogenic” organisms, such as Porphyromonas that the host response had only a relatively small part to
gingivalis and Aggregatibacter actinomycetemcomitans, are play in this destructive process. at understanding is now
strongly associated with periodontitis progression. reversed, and it is now thought that the host response is
31
the principal determinant of disease progression. It has been Periodontitis results from an imbalance between the oral
estimated that 20% of the tissue destruction in periodontitis bacterial ora and the host response (Figure 1.4.2). ere
is explained directly by bacterial action (Grossi etal. 1994) is a delicate balance between host and bacterial factors in
and that about 80% of the damage occurring in periodontal health, and there is the potential for dysregulation of this
diseases is attributable to the host response. balance which can result in disease. Genetic and environ-
mental factors are key to upsetting this balance.
KEY POINT 2 Overall, the host response to the oral microbial biolm
Merely 20% of the tissue destruction in periodontitis is is designed to be protective, but underactivity, or indeed
explained by direct bacterial action, the remainder being overactivity, of specic aspects of the response can lead to
attributed to the host response. tissue destruction. e host response is largely determined
by genetics, and some individuals display an inappropriate
e host response includes both inammatory and or dysregulated host response. In addition, and rarely, cer-
immune components, comprising innate and acquired tain inherited conditions may aect the periodontal tissues
immunity. and act as a systemic risk factor for periodontitis.
Evidence now suggests that most of the damage seen in
periodontitis is the direct result of the inammatory and
immune response of the individual to the bacterial biolm
and that over 50% of susceptibility to periodontitis can be
explained by genetic factors (Michalowicz etal. 2000). us
it has been stated that “periodontitis is an inammatory dis-
ease initiated by the oral microbial biolm. However, it is
the host response to the biolm that destroys the periodon-
tium” (Van Dyke 2008).
It is probably inaccurate therefore to describe periodontitis
as an “infection” in the traditional sense, mainly because the
causative organisms are mostly commensal and rarely invade
the tissues; instead it is “. . . more accurately categorised as
a non-resolving inammation that is ineective in eliminat-
ing the initiating pathogens” (Chapple 2009). It should be
thought of as a disease that is initiated by the accumulation of
pathogenic bacteria, but one that is propagated by a dysregu-
• Figure 1.4.1 A patient with untreated chronic periodontitis. lated immune response and includes aspects of autoimmunity.
Tissue damage Host Bacterial Tissue damage

response virulence
Health Health
Tissue damage Tissue damage
Host Bacterial
response virulence
Health Health

response virulence
Health Health
• Figure 1.4.2 The interaction between bacteria and the host response.
CHAPTER 1.4 Host Response and Susceptibility 33
Definitions poor diet. In health, a balance is achieved between the oral

bacteria and the host response, but such equilibrium may
Pathogen: An organism that causes disease. easily be disrupted in a susceptible host, leading to inam-
Commensal: Non-disease-causing microorganism that is mation and tissue damage.
part of the resident ora. Bacterial virulence can increase as a result of an increase
Opportunistic pathogen: Microorganism not normally patho- in bacterial load and/or change in composition. e bacteria
genic (can be commensal) but can become pathogenic if present may express virulence factors and toxins. ese mol-
the local environment changes. ecules may be expressed by the pathogens to:
Virulence factors: Molecules expressed and/or secreted by • enable colonisation and multiplication
pathogens to enable colonisation, evasion of the host’s • evade the host’s immune response
immune response, cellular entry/exit or derive nutrition • enable intracellular entry/exit
from the host. • derive nutrition from the host.
e host inammatory and immunological response to
oral bacteria will ultimately determine how the individual
Host Susceptibility responds to these bacterial factors and whether this response
is inappropriate in such a way as to cause collateral tissue
A susceptible host is an individual who is at risk of develop- damage.
ing disease if he or she is exposed to a causative agent; in In addition to these host-related factors, there may also
the case of periodontitis this is the bacterial biolm. Host be local site-based factors within the mouth, usually in the
susceptibility results from a number of risk factors that are form of plaque retention factors, such as the presence of
involved in the host response (Figure 1.4.3). calculus or overhanging restorations. Although such local
risk factors may contribute to the accumulation of bacterial
KEY POINT 3 biolm, remember that this alone is insucient to progress
A susceptible host is someone who is at greater risk of gingivitis to a form of periodontitis; it is necessary for the
developing a disease when exposed to a causative agent. host to be susceptible for this to happen.
ere are thus many factors related to both the host and
Such factors include genetic factors, including those that bacteria in the mouth that can contribute to periodontal tis-
contribute to impaired neutrophil function, or environmen- sue destruction. Most commonly, it is factors on both sides
tal factors, such as smoking, poorly controlled diabetes or a of the equation that lead to periodontitis.

response virulence
Health Health
Inflammatory Immunological Bacterial Bacterial

response response load composition
Modulators of the above Virulence factors, toxins,

(e.g. drugs, diabetes, smoking) cell-signalling molecules
- +
or Subject-based Site-based
+ risk factors risk factors
Modulation by
e.g. neutrophil function e.g. plaque
retention factors
Periodontal tissue
destruction
• Figure 1.4.3 Bacterial/host factors that can affect the delicate balance between the host and the oral
microora.
Host Response to the Bacterial Biofilm Normal Host Response

A normal host response to the accumulation of bacterial ere are two main components of the normal host response
biolm invariably results in gingivitis, which is ubiquitous to plaque bacteria:
in all populations. is is a reversible inammatory con- Innate or natural immunity: is is the rst line of
dition and can be resolved with clinical intervention and defence. It is rapid but may cause collateral tissue damage if
does not lead to any periodontal tissue loss. Sometimes, the not regulated or controlled correctly.
host response to the bacterial biolm may be inappropri- Acquired or specic immunity: is occurs at the same
ate (hypo-responsive or, more likely, hyper-responsive), and time as the innate immune response but takes longer to
host-mediated damage occurs in the periodontal tissues develop and is more specic and more ecient.
(Figure 1.4.4). Both types of immunity are involved in the host’s response
to the biolm and occur at the same time. e innate sys-
tem is constantly in function and more rapidly mobilised in
response to a bacterial threat, whereas the acquired system
involves specic cell–cell interactions, which take more time.
KEY POINT 4
The normal host response involves both innate and acquired
immunity.
Early gingival inammation largely involves the innate

system, whereas the acquired system becomes involved in
moderate-to-advanced gingivitis and periodontitis (i.e. lon-
ger-term, chronic disease).
In a less periodontally susceptible host, the response to
the microbial biolm may be minimal and results only in
A gingivitis, which is a reversible condition. However, in the
presence of systemic and local risk factors, gingivitis may
progress to periodontitis, in which irreversible tissue damage
occurs (Figure 1.4.5). e more susceptible the host the more
damage that will occur and the more advanced the resulting
periodontitis. In most cases, periodontitis is chronic but, in
the most susceptible individuals, aggressive periodontitis
may develop (see Chapter 2.1 and Figure 1.4.5).
The Pathogenesis of Periodontal Lesions

Within the gingival crevice (Figure 1.4.6), the host tissues
detect the presence of the bacterial biolm and respond to
B bacterial components and toxin production by the bacte-
• Figure 1.4.4 Gingivitis (A) does not necessarily lead to periodontitis ria within the biolm (Figure 1.4.7). is initiates both the
(B).
Low Moderate High
Host susceptibility component
Chronic Aggressive
Health Gingivitis periodontitis periodontitis
Periodontitis resistance Periodontitis Periodontal susceptibility

(no host susceptibility component), susceptibility in the and tissue destruction
plaque biofilm driven presence of risk factors inconsistent with
(local or systemic) local risk factors
• Figure 1.4.5 Factors affecting the progression of gingivitis to periodontitis.
Enamel
External oral
epithelium
Oral sulcular
epithelium
Gingival sulcus
Rete ridges
Circular fibres
Gingival connective
tissue
Alveologingival
fibres
Cementum
Alveolar bone
Principal fibres
of PDL
Neutrophils Resident periodontal cells

(e.g. fibroblasts/macrophages)
• Figure 1.4.6 The microanatomy of the dentogingival area.
Dentine
Enamel
Epithelial tissue
Cytokines/chemokines
Host epithelial cells

Neutrophils/macrophages
Gingival connective tissue
Plaque biofilm
Cementum
• Figure 1.4.7 Bacterial interaction with host epithelial cells.

innate and acquired immune responses. is process of rec- When the innate immune response becomes dysregulated,
ognition is achieved through a variety of key components: the collateral tissue damage is signicant.
• Bacteria form a bioëlm within the gingival crevice adja Innate immunity involves:
cent to root dentine and associated cementum. 1. Epithelial barriers provided by the oral, sulcular and
• Bacterial components (such as lipopolysaccharide [LPS]/ junctional epithelium.
endotoxin) alert the host to the presence of the biolm. 2. Fluid lubrication: this takes the form of both saliva
• ɨe host releases neutrophilic polymorphonuclear leuco and GCF, both of which possess antibacterial properties.
cytes (neutrophils or PMNLs) from the blood circulation Saliva contains antibacterial enzymes such as lysozyme
and adjacent gingival tissues as the rst line of defence in and immunoglobulins (antibody) which bind to bac-
the host response. teria. GCF carries all components of serum, including
• Various resident cells are involved in the recognition complement and immunoglobulins.
of biolm bacteria and subsequently promote the host 3. Complement cascade: this is a series of 20 serum gly-
response through a number of key cell signalling mol- coproteins that circulate in inactive forms in the blood-
ecules initially via the junctional epithelium (JE) and stream. When activated, complement components have
sulcular epithelium (SE). profound and powerful eects in stimulating inamma-
tion.
Cell Signalling e main role of complement activation is:
• to recruit phagocytes to the area (diapedesis and
e unique features of the JE are its rapid rate of turnover chemotaxis)
and permeability to both gingival crevicular uid (GCF) • to facilitate binding of phagocytes (e.g. neutrophils) to
and PMNLs (diapedesis). ɨe JE thus helps to defend the bacteria, thereby aiding phagocytosis – a process called
host against bacterial invasion (Figure 1.4.7). Junctional opsonization
and sulcular epithelium and other resident periodontal • to cause bacterial killing (cell lysis).
cells, such as broblasts, detect bacteria via receptors for ere are two possible routes for complement activation
molecules derived from the outer cell wall or internal to (Figure 1.4.8):
the bacteria. ese molecules include bacterial components • Classical pathway – only activated by the formation of
such as LPS, lipoteichoic acids and bacterial DNA and are antigen–antibody complexes (i.e. after initiation of the
known collectively as pathogen-associated molecular pat- acquired immune response)
terns (PAMPs). PAMPs can be detected by bacterial-sensing • Alternate pathway – activated directly by bacterial endo-
receptors, known as pathogen recognition receptors (PRRs), toxin (LPS) when it enters the periodontal tissues and
on human cells, such as those of the JE. One important from the cementum reservoir.
example of PRRs is the Toll-like receptor (TLR) family. Both pathways stimulate the activation of complement
component C3, which leads to the activation of C5 and
KEY POINT 5 later forms C5–C9, which is also termed the membrane
In general, chemokines are cell signalling molecules that recruit attack complex (MAC). is is responsible for the destruc-
other inammatory cells whereas cytokines are molecules that tion of Gram-negative bacteria, but it is also thought to be
activate inammatory cells. responsible for collateral host cell damage.
4. Cell signalling: epithelial cells release cell-signalling
Binding of a PAMP to a TLR can activate intracellular sig- molecules that orchestrate the inammatory response
nalling pathways (e.g. nuclear factor-kappaB), which results resulting in key vascular changes in early inammation.
in the release of chemokines and cytokines (such as inter- Signalling includes detection of bacteria (e.g. by TLRs
leukins). Chemokines recruit other immune cells to the area on JE cells and other resident periodontal cells such as
where they are needed whereas cytokines activate the immune broblasts) and subsequent release of cytokines and che-
cells, stimulating them to release other proinammatory mol- mokines. One of the most important cytokines in peri-
ecules, which perform key proinammatory functions. odontal diseases is interleukin-1 (IL-1) as it stimulates
After the detection of the bacterial bioëlm by TLRs on bone resorption and is a powerfully proinammatory
the host’s oral epithelial cells, cytokines and chemokines regulator.
are produced and are released into the underlying gingival ɨe gene that codes for IL-1 has diêerent forms (poly-
connective tissue. e gradient of these molecules gener- morphisms) that may be involved in host susceptibility (see
ated results in recruitment of immune system cells, such as later).
neutrophils, which are attracted from the vasculature and Examples of cell signalling molecules are listed in Table
migrate towards the bacterial biolm. 1.2.1. in Chapter 1.2.
is is an example of a component of innate immunity. 5. Vasoactive peptides: vasoactive peptides such as his-
tamine play an important role in the development of
Innate Immunity inammation.
Histamine is released from mast cells on stimulation
Innate immunity, although rapid, remains crudely indis- (by either complement C3a and C5a or prostaglandin E2
criminate relative to the specicity of the acquired system. [PGE2]) and causes vasodilation to recruit more blood cells
Classical pathway Common pathway Alternate pathway
Antigen-antibody
complex Proteolytic enzymes
e.g. plasmin (via
tissue plasminogen
activator after vascular
C1 C1 active C3 endothelial damage)
C4 C4 active
Endotoxin/
lipopolysaccharide
C2 C2 active
C3 active
C3a C3b
C5-C9 MAC
• Figure 1.4.8 Complement activation pathways.
and plasma proteins (e.g. complement and antibody) to the KEY POINT 6
area of infection.
The neutrophil (PMNL) is the most abundant and important cell
Histamine also increases vascular permeability and, in the innate host defence system.
because vasodilation slows down blood ow within the ves-
sels, this allows defence cells to migrate out of midstream e sequence of neutrophil activity is as follows:
circulation, contact the endothelial cells lining the blood • Rolling – slowing down of neutrophils (PMNLs) within
vessels and then leave the circulation and enter adjacent tis- the bloodstream occurs due to vasodilation after the
sues (diapedesis and subsequently chemotaxis). release of vasoactive peptides. Selectins on the neutro-
6. Adhesion molecule expression facilitates inamma- phils then make initial “make and break” contacts with
tory cell contact with vascular endothelial cells and complementary ligands on the endothelial cells lining
migration to infected areas. is is a tightly controlled the vessel wall.
process directed by signalling molecules in very specic • Margination – as the neutrophil slows down, the receptor
sequences and pathways. binding increases and eventually the neutrophils become
Examples of important adhesion molecules are intercel- immobilized on the vascular endothelium by adhesion of
lular adhesion molecules I and II (ICAM-I and II), endothe- integrins on the neutrophil to integrin receptors on the
lial adhesion molecule 1 (ELAM-I) and leucocyte function endothelium.
antigen-1 (LFA-1). • Diapedesis – other cell-to-cell adhesions allow the neu
7. Neutrophils (PMNLs): the neutrophil is an immune trophil to pass through the “leaky” blood vessel wall and
defence cell that destroys invading bacteria, ideally by enter the tissues.
internalizing them (phagocytosis) prior to destroying • Chemotaxis – the neutrophil then moves along a chemi
them. cal gradient through the tissue towards the area of
It is the most abundant and important defence cell in the infection.
periodontal tissues. Neutrophil intracellular killing: after intracellular killing
Once the neutrophils arrive at the site of infection, of bacteria, the neutrophils go through a process of pro-
they kill bacteria by either intra- or extracellular methods. grammed cell death (apoptosis) whereby they essentially
Intracellular killing involves the same methods as extracel- self-digest to prevent harmful contents entering the host
lular killing, except the neutrophils release their enzymes tissues.
and oxygen radicals (a process called degranulation) safely e enzymes and oxygen radicals, if released by neutro-
within themselves and inside special membrane-bound phils, may damage host tissue and bacteria, and the PMNL
structures called phagosomes. therefore contains:
Extracellular Neutrophil
degranulation (polymorphonuclear
leucocyte)
Opsonised
cocci
Filamentous
bacteria
• Figure 1.4.9 Extracellular killing by neutrophils.
• Enzyme inhibitors – for example, α-1 antitrypsin, which IgG IgE IgD
neutralize enzymes such as elastase
• Antioxidants – these are powerful scavengers of oxygen
radicals (e.g. glutathione) and involve enzyme systems
(e.g. superoxide dismutase and catalase) to prevent dam- IgM IgA
age to the neutrophils during oxygen radical release.
Neutrophil extracellular killing (Figure 1.4.9): when
the bacterial mass is too large for the neutrophil to
phagocytose, it degranulates extracellularly and releases
its enzymes, oxygen radicals and neutrophil extracellular
• Figure 1.4.10 Immunoglobulins.
traps (NETs) over the bacterial mass in an eort to kill
and contain it. If this occurs in the gingival crevice, it may
cause damage to the crevicular epithelium. Where a mas- • B lymphocytes – form humoral immune response as they
sive neutrophil response is present in the tissues, inadver- produce immunoglobulins (Ig) which, with complement
tent release of these chemicals is believed to be the major and phagocytes, kill bacteria (Figure 1.4.10)
cause of periodontal tissue damage and subsequently con- • Immunoglobulins – include ëve main classes: IgG, IgA,
tributes to bone loss. Notably, NETs are relatively newly IgM, IgD and IgE.
described and are formed from the release of the neutro- In periodontitis, IgG (in gingival crevicular uid) and
phil’s DNA, which is decorated with antimicrobial pro- IgA (in saliva) are considered the most important.
teins and enzymes derived from the granules. Whereas
these DNA webs entrap and lead to the killing of the bac-
teria, they can also cause further damage to the host peri- The Contribution of Genes to Host
odontal tissues (Cooper et al. 2013). Responses
8. Macrophages: macrophages not only scavenge dead cells
(bacteria and neutrophils) but also play an important role e host response to the bacterial biolm depends not only
in bridging the gap between innate and acquired immu- on the nature and virulence of the bacterial pathogens but
nity. As phagocytes, they function in a similar manner to also on genetic factors. Because the pathogenesis of peri-
neutrophils, but they also act as antigen presenting cells odontitis largely involves host responses to periodontal
(APCs), thereby stimulating acquired, or specic, immu- microorganisms, it follows that genetic variations modulate
nity. host responses which can inuence disease progression.
Genetic variation inuencing the host response to envi-
Acquired Immunity ronmental or systemic risk factors for periodontitis could
also inuence the eects of such factors on disease.
Acquired immunity occurs at the same time as the innate e host’s response to the biolm is complex, and the
immune response but is more specic and ecient. host’s innate and acquired immune response can lead to the
Cell mediators include: development of periodontitis. Local factors can be managed
• T lymphocytes – require direct contact with bacteria for to reduce risk, but there is usually a signicant genetic factor
killing involved in the host’s susceptibility to periodontitis.
TABLE
1.4.1 Inherited conditions with additional risk for the development of periodontitis
Condition Associated gene Underlying defect of periodontal relevance

Down’s syndrome Chromosome 21 Defects of neutrophil chemotaxis, killing and
phagocytosis. Depressed T-cell antigen-induced killing
Chronic granulomatous Gp91 protein p91-PHOX on Failure of the “respiratory burst” in phagocytosis. Oxygen
disease chromosome b558 radicals are not produced, and bacteria survive
Insulin-dependent juvenile IDDM1 gene located on chromosome Hyperglycaemia reduces neutrophil function. Monocytes
diabetes 6 are hyper-reactive and excess IL-1, PGE2, TNF-α and
oxygen radicals are produced. Collagen solubility and
vascularity changes negatively affect the healing ability
Papillon–Lefèvre syndrome Cathepsin C gene on chromosome 11 Defects of neutrophil chemotaxis and phagocytosis
Ehlers–Danlos syndrome Gene mutation encoding for brous Altered collagen structure and function. Type VIII is
proteins (e.g. COL1A1) or enzymes associated with severe periodontal destruction
Chediak–Higashi syndrome Lysosomal trafcking regulator gene on Defects of phagocyte chemotaxis, degranulation and
chromosome 1 membrane fusion results in loss of the adult dentition
Job syndrome STAT3 gene on chromosome 17 Excessive IgE and histamine release by mast cells and
IgE immune complex formation. Results in abnormal
neutrophil chemotaxis as a result of an altered cytokine
prole
KEY POINT 7 be controlled or managed. A host’s genetic susceptibil-

There is understood to be a signicant genetic contribution to ity cannot easily be controlled. However, genetics could
the host’s susceptibility to periodontitis. help identify those patients who are more susceptible
and therefore help with prevention, early diagnosis, and
management of the disease. Ultimately, susceptible indi-
Twin, sibling pair and family studies demonstrate that
viduals could be targeted with preventative treatments to
periodontitis has a signicant genetic component (Micha-
minimise disease risk.
lowicz etal. 2000).
Genetic single nucleotide polymorphisms (SNPs) have
been linked to risk of periodontal tissue breakdown. ere KEY POINT 8
is extensive research aimed at identifying the association Periodontitis is the result of a complex interaction between the
between gene polymorphisms and periodontitis suscep- bacterial biolm, the host’s lifestyle and genetic factors.
tibility. IL-1 gene polymorphisms are examples of SNPs
that have been shown to be associated with periodonti-
tis in some people. IL-1 is a key cytokine in periodontal Acknowledgements
disease pathogenesis, and “overproduction” of this cyto-
kine has been identied in chronic periodontitis patients. is chapter is based on a session within e-Den which Profes-
In the future, it may be possible to develop “periodonti- sor Cooper and Dr. Ling produced in 2011. Acknowledge
tis susceptibility tests” based on screening SNPs that may ment is given to the Faculty of Dental Surgery of the Royal
identify patients at risk of developing periodontitis. Such College of Surgeons of England for giving permission for
a test already exists for IL-1 but is not widely employed material from the e-Den session to be used in this chapter.
because of a lack of generalizability of results from IL-1 Multiple choice questions on the contents of this chapter
SNP studies. are available online at Elsevier eBooks+
In addition to SNPs, certain inherited conditions may
aect the periodontal tissues and act as risk factors for peri-
odontitis. ese are shown in Table 1.4.1 References
Ultimately, periodontitis is the result of a complex Chapple ILC. Periodontal diagnosis and treatment – where does the
interaction between the bacterial biolm, the environ- future lie? Periodontol. 2009;51:9–24.
ment, the host’s lifestyle and genetic factors. e envi- Cooper PR, Palmer LJ, Chapple IL. Neutrophil extracellular traps as
ronmental factors can be eectively controlled by oral a new paradigm in innate immunity: friend or foe? Periodontol
hygiene, and, to some extent, lifestyle factors can also 2000. 2013;63(1):97–165.
Grossi SG, Zambon JJ, Ho AW, Koch G, Dunford RG, Machtei EE, Further reading
etal. Assessment of risk for periodontal disease. 1. Risk indicators
for attachment loss. J Periodontol. 1994;65:260–267. Chapple ILC, Gilbert AD. Understanding Periodontal Diseases: Assess-
Michalowicz BS, Diehl SR, Gunsolley JC, Sparks BS, Brooks CN, ment and Diagnostic Procedures in Practice. Quintessence London;
Koertge TE, et al. Evidence of a substantial genetic basis for 2002.
risk of adult periodontitis. J Periodontol. 2000;71:1699–1707. Henderson B, Curtis M, Seymour R, Donos N. Periodontal Medicine
Van Dyke TE. e management of inammation in periodontal dis- and Systems Biology. Wiley-Blackwell Chichester; 2009.
ease. J Periodontol. 2008;79:1601–1608.
1.5
THE ROLE OF BIOFILMS IN
HEALTH AND DISEASE
PH I L I P D M A R S H
CHAPTER OUTLINE
Introduction Stage 5. Secondary Colonisation
What are Biolms? Stage 6. Bioölm Maturation
Stage 7. Detachment From Surfaces
Biolms in the Mouth
Reduced Sensitivity of Biolms to Antimicrobial Agents
Methods to Determine the Microbial Composition of Dental
Benets of the Resident Oral Microbiome
Biolms
Microbial Composition of Dental Biolms in Periodontal
Microbial Composition of Dental Biolms in Health
Diseases
Fissures
Gingivitis
Approximal Surfaces
Periodontitis
Gingival Crevice
Necrotizing Periodontal Diseases
Stages in the Formation of Necrotizing ulcerative gingivitis (NUG)
Dental Biolms Necrotizing ulcerative periodontitis
Stage 1. Conditioning Film formation Contemporary Perspectives on the Aetiology of Periodontal
Stage 2. Transport of Microorganisms Diseases
Stage 3. Reversible Attachment
Stage 4. Irreversible Attachment Concluding Remarks

This chapter describes the role of dental biolms previously referred to as dental plaque in periodontal health and disease. The chapter
discusses the signicance of a biolm lifestyle on the properties of oral microorganisms and explains why clinicians need to be aware of this
when they plan their treatment.
• Understand the signiöcance of the term “bioölm” • Introduction
and appreciate the beneöts to the host of the • What are bioölms?
microorganisms found naturally in the mouth (the oral • Bioölms in the mouth
microbiome) • Methods to determine the microbial composition and
• Be aware of the main groups of microorganisms found in the function of dental bioölms
healthy mouth • Microbial composition of dental bioölms in health
• Describe the shifts in composition of the subgingival • Stages in the formation of dental bioölms
microbiome that occur in periodontal diseases • Reduced sensitivity of bioölms to antimicrobial agents
• Understand the mechanisms by which these • Beneöts of the resident oral microbiome
subgingival bioölms cause disease and are more diócult to • Microbial composition of dental bioölms in periodontal
treat. diseases
• Contemporary perspectives on the aetiology of periodontal
diseases
• Concluding remarks
41
Introduction rectied. us oral care should involve eective plaque

control techniques that maintain dental biolms at levels
e mouth, like all other surfaces in the body, is colonised compatible with oral health to retain the benecial proper-
by a characteristic and natural community of microorgan- ties of the resident microbiome, while reducing the risk of
isms, termed the oral microbiome or the oral microbiota dental disease from excessive plaque accumulation (Marsh
(Kilian etal. 2016), which is composed predominantly of 2012). ese levels may vary between individual patients.
bacteria but can also include viruses, fungi, mycoplasmas,
Archaea and even protozoa. e oral microbiome is normal KEY POINT 2
and confers important benets to the host (see later) and The resident oral microbiome and the host exist in a natural
exists on surfaces as structurally organised, multispecies bio- and mutually benecial relationship (symbiosis). Disease results
lms (Marsh etal. 2016). from a breakdown of this relationship after a deleterious shift in
the composition of the microbiome (dysbiosis).
KEY POINT 1
The mouth harbours characteristic communities of What are Biofilms?
microorganisms, the presence of which are normal and
benecial to the host. These microbial communities grow on In nature, microorganisms preferentially attach to surfaces
oral surfaces as biolms. (inanimate and living) usually as multispecies communi-
ties. is is a fundamental survival stratagem for microbes
e resident oral microbiome plays a direct and active (Nobbs et al. 2011). Once attached, microbes grow and
role in the normal development of the physiology, nutrition form three-dimensional structures, termed biolms, embed-
and defence systems of the host (Kilian etal. 2016, Marsh ded in an extracellular matrix of sticky polymers (Zijnge
etal. 2016). A dynamic balance exists between the resident etal. 2010, 2012, Mark Welch etal. 2016, 2019, Bowen
microbiome and the host in health (symbiosis), whereas et al. 2018). Biolms are ubiquitous and are found in
disease results from a breakdown (dysbiosis) of this delicate water distribution pipes and machinery, on contact lenses,
relationship (Curtis etal. 2020, Hajishengalis etal. 2020). implants and catheters, as well as on oral surfaces, especially
erefore it is important that the factors that regulate and teeth (dental plaque), dentures and implants (Figure 1.5.1).
inuence this intimate relationship between the host and e signicance of dental plaque as an example of a biolm
their microorganisms are understood, and those that are is that discoveries made on biolms in general may also be
driving dysbiosis in individual patients are identied and applicable to dental plaque.
A Biofilm
B
• Figure 1.5.1 Examples of biolms. (A) A biolm forming on a hospital tap outlet and (B) a dental biolm on
a tooth surface. (Courtesy Dr. Jimmy Walker, PHE.)
CHAPTER 1.5 The Role of Biolms in Health and Disease 43

Biolms are: Biolms develop on all surfaces in the mouth (mucosal and
• Spatially and functionally organised multispecies dental). Each surface harbours a distinctive microbiome which
microbial communities reects, and is a consequence of, the biological and physical
• Environmentally heterogeneous, enabling organisms to properties of each site. A change to the oral habitat can result,
coexist that appear incompatible with one another therefore, in a shift in the composition of the biolm.
• More tolerant of environmental stresses, the host
defences and antimicrobial agents, and therefore more
difcult to treat. Biolms that form on mucosal surfaces are restricted
by desquamation, whereas non-shedding surfaces, such as
teeth (or dentures, implants and restorations, etc.), permit
Dental plaque is a classic example of both a biolm and extensive biolm development. Dental plaque preferentially
a microbial community. Plaque is composed of numerous forms at retention and stagnant sites because these provide
interacting microbial species; on average, there are 20 to 50 protection from removal forces in the mouth, e.g. saliva
species present in even a small sample of dental biolm (Aas ow, mastication, and such sites are also the most suscep-
et al. 2005). ere are numerous advantages for microor- tible to disease.
ganisms to exist as a biolm and as a microbial community.
ese include:
• Bioëlms are more tolerant of environmental stresses, the Methods to Determine the Microbial
host defences and antimicrobial agents Composition of Dental Biofilms
• Microbial communities have a greater tolerance of anti
microbial agents and the host defences because of cross- e method of sampling dental biolms depends on the
protection, i.e. one species can protect a neighbouring anatomy of the site. When plaque is processed, care must
species, for example, by producing a neutralizing enzyme be taken to disperse the biolm, which, by denition, is a
• Microbial communities display an enhanced pathogenic diverse collection of interacting microorganisms that are
potential; groups of dierent bacteria can combine to tightly bound to one another, without adversely killing
pool their weak virulence determinants in order to cause fastidious bacteria, such as obligate anaerobes, that may be
disease (“pathogenic synergism”) present in the sample. Fissures can be sampled with a ne
• Microorganisms that exist within a community exhibit probe or toothpick. Dental oss, abrasive strips or dental
a broader habitat range (e.g. obligate anaerobes can sur- probes can be used for approximal surfaces whereas the gin-
vive in an overtly aerobic environment) and increased gival crevice can be sampled with a paper point, curette or
metabolic diversity and eciency (e.g. they can catabo- scaler.
lize substrates collectively which individual organisms are ere are three main approaches to determine the micro-
unable to utilize) bial composition of plaque biolms; these are: microscopy,
• ɨerefore the properties of a microbial community such conventional culture techniques and molecular biology–
as dental plaque are greater than the sum of the activities based (culture-independent) methods. Microscopy can
of the component species. give a rapid and cheap assessment of the microbial diversity
within the biolm, e.g. the enumeration of motile bacte-
KEY POINT 4 ria such as spirochaetes, but generally cannot identify the
Microbial communities display:
microbes unless specic stains are available, e.g. antibody-
• a broader habitat range or nucleotide-based probes labelled with a signalling mol-
• increased metabolic diversity and efciency ecule such as a uorescent dye (for example, uorescent in
• cross-protection to antimicrobial agents and host situ hybridization [FISH]) (Mark Welch etal. 2016, 2019).
defences Confocal laser scanning microscopy enables biolms to be
• an increased pathogenic potential.
viewed in their natural hydrated state and has shown that all
biolms, including dental plaque, have a more open archi-
Biofilms in the Mouth tecture than thought from previous electron microscopy
images and a functionally organised structure (Mark Welch
Biolms are found on all surfaces in the mouth, but the etal. 2016, 2019).
largest and most diverse biolms are found on teeth (dental As stated previously, bacteria are the most abundant
plaque). e composition and structure of the biolms are group of microorganisms in the oral microbiome, but sig-
directly inuenced by the anatomy and biological properties nicant numbers of fungi can be present too (Dewhirst
of the surface to which they attach. erefore each surface etal. 2010, Hong etal. 2015, Marsh etal. 2016). Initially,
will have a biolm with a characteristic microbial compo- bacteria and fungi were characterised using traditional
sition that reects, and is a product of, the local environ- approaches which involved prolonged culture on selective
ment (Aas etal. 2005, Marsh etal. 2016, Papaioannou etal. and nonselective agar plates, under dierent atmospheric
2009). conditions; the microbial colonies that grew then had to
be further cultured in pure culture and undergo additional the whole diversity of the microbiome is revealed (Wade &
biochemical tests to obtain an identication. ese steps Prosdocimi 2020) (Figure 1.5.2). ese culture-independent
are laborious, time consuming and expensive, and over approaches are not without their own bias, however, as it can
time it became apparent that there was a large discrepancy be more dicult to lyse and extract DNA from some organ-
between the number of microorganisms in a sample that isms, and because the primers used for amplication are not
could be grown by these conventional methods and those optimised for all species (Wade etal. 2016, Wade & Prosdo-
that were observed directly by microscopy. Only about cimi 2020). Nevertheless, the introduction of these culture-
50% of the resident oral microbiome can currently be independent approaches has changed our understanding of
grown in pure culture in the laboratory (Wade & Pros- the richness and diversity of the oral microbiome in health
docimi 2020). e "missing” microbes have been referred and disease (Marsh etal. 2016, Wade etal. 2016) and could
to as “unculturable”’, but our inability to culture them is lead eventually to chairside kits and services to help diagnose
due mainly to our ignorance of the growth requirements oral diseases and monitor the outcome of treatment (Meuric
of some species and our naivety in attempting to isolate etal. 2017, Belibasakis etal. 2019, Chen etal. 2021).
microbes in pure culture as these have evolved over mil- Rather than just cataloguing the types of microorgan-
lennia to grow with other species as part of a community ism that are present at a site, complementary molecular
(Wade etal. 2016). approaches are also being used to monitor gene expression
Contemporary approaches are using molecular (i.e. cul- so as to determine the metabolic and functional activity in a
ture-independent) methods to detect and identify micro- sample (e.g. by using metatranscriptomics, proteomics and
organisms (Diaz et al. 2017, Wade & Prosdocimi 2020). metabolomics). In the future, more emphasis may be placed
ese rely on detecting the nucleic acid signatures that are on what microorganisms are “doing” (i.e. their function and
specic to each species and range from targeted approaches activity) rather than providing a list of merely “who” is pres-
such as PCR, DNA–DNA checkerboard systems or microar- ent (Takahashi 2015, Espinoza etal. 2018). It is likely that
rays that identify preselected microbial groups to the more dierent combinations of species within a microbial com-
current and preferable open-ended approaches in which all munity will perform similar tasks, and this might explain
of the microbial DNA in a sample is digested, amplied, why there is not always a clear consensus when comparing
sequenced, reassembled and nally mapped against a refer- the composition of dental biolms in health and disease
ence database of relevant genomes (metagenomics), so that from dierent studies.
Colony counts Subculture to Physiological tests Data analysis

obtain pure culture
- Sugar fermentaon paern Compare test
- Acid end product profile profile to idenficaon
- Cell wall structure schemes & databases
- Angen profile / serology
- Anbioc sensivity
- Blood agar - Selecve agar blood agar - etc MICROBIAL COMMUNITY
COMPOSITION
CULTURE
ORAL
MICROBIOME
METAGENOMIC [culture independent]
DNA extracon DNA sequencing Metagenome Bioinformac

sequences pipeline & data analysis
GTCAGTTTA…..
AACTGCATAT…
TTATGCCACCGAA….
GGATTCCTGGGAAA..
TATCCACGACGGGGTTAATTGGC…
• Figure 1.5.2 Schematic to show the stages in determining the microbial composition of dental biolms
using traditional culture or contemporary molecular-based (metagenomic) approaches. Theoretically, a
metagenomic approach can be quicker than conventional culture as many species grow slowly; also
approximately half of the oral microbiome cannot be cultured at present.
e accumulated data from numerous studies of dierent and streptococci. Obligately anaerobic bacteria are common
oral surfaces and sites from around the world have resulted (e.g. Veillonella, Prevotella and Fusobacterium spp.) and pres-
to date in the identication of around 770 dierent types ent in relatively high proportions, although spirochaetes are
of microorganism (sometimes referred to as dierent taxa usually absent.
or phylotypes) from the mouth; of these, 57% are ocially
named, 13% unnamed but cultivable and 30% are known Gingival Crevice
only as currently “unculturable” phylotypes. A single indi-
vidual may harbour between 50 to 300 species. It is beyond is site contains biolms with the highest species diver-
the scope of this chapter to describe the properties of mem- sity in the healthy mouth and with the greatest numbers
bers of the resident oral microbiome, and the reader is rec- of obligately anaerobic bacteria, many of which are Gram
ommended to refer to specialist texts for more detail (for negative or are Eubacterium-like. Many of the currently
example, Marsh etal. 2016), or to the two curated oral 16S “unculturable” bacteria are found subgingivally. Common
rRNA databases: the Human Oral Microbiome Database bacteria associated with the healthy gingival crevice are
(HOMD; http://www.homd.org) and the Core Oral Micro- members of the mitis and anginosus groups of streptococci
biome Database (CORE; http://microbiome.osu.edu). and Gram-positive rods such as species of Actinomyces,
Molecular (culture-independent) approaches are being Rothia and Corynebacterium. Gram-negative genera that
adopted because: are commonly detected include Neisseria, Lautropia, Hae-
• there is less bias compared with culture mophilus, Capnocytophaga, Fusobacterium, Prevotella and
• “unculturable” and novel species can be detected; these Veillonella (Abusleme etal. 2013, Hong etal. 2015, Diaz
can account for >50% of the microorganisms that are et al. 2016). e ecology of the crevice is inuenced by
present, especially at subgingival sites the ow and properties of gingival crevicular uid (GCF).
• the techniques can be comparatively quick and are not as GCF introduces not only components of the host defences
labour intensive as traditional culture (neutrophils, complement, antibodies), but also host mol-
• microbial signatures of health and disease can be identi ecules that can be degraded and used as important sub-
ed (Meuric etal. 2017, Chen etal. 2021). strates. Many of the microbial residents are proteolytic and
A limitation of molecular approaches is that: derive their energy from the hydrolysis of these host pro-
• they are semiquantitative at best teins and peptides and from the catabolism of amino acids;
• viable bacteria are not isolated, from which to determine others also require heme as an essential cofactor for growth,
their properties, including antibiotic sensitivities which can be obtained from haemoglobin and other host
• some approaches will detect dead as well as viable cells. molecules in GCF.
Stages in the Formation of

Microbial Composition of Dental Biofilms Dental Biofilms
in Health
e formation of dental plaque can be subdivided into a
e microbial composition of biolms on distinct surfaces series of arbitrary stages although, as biolm formation is a
on teeth varies markedly because of dierences in local envi- dynamic process, some of these stages will occur simultane-
ronmental conditions (nutrition, pH, O2, host defences, etc.) ously (Figure 1.5.3).
(Aas etal. 2005, Papaioannou etal. 2009, Marsh etal. 2016).
KEY POINT 6
Fissures Stages in the formation of dental plaque:
1. conditioning lm formation: adsorption of host
e microbiota of ssures is composed mainly of Gram-pos- molecules on to dental surfaces (the acquired pellicle)
itive and facultatively anaerobic bacteria that have a saccha- 2. transport of microbes to surface: passive or active
3. reversible phase: long-range, weak, physicochemical
rolytic metabolism (i.e. gain energy from the catabolism of forces
carbohydrates including dietary sugars); the majority of the 4. irreversible phase: strong, short-range adhesin-receptor
bacteria are streptococci, especially extracellular polysaccha- interactions
ride-producing species. Obligately anaerobic Gram-negative 5. secondary colonisation: co-aggregation/co-adhesion
bacteria are either absent or detected only rarely and in low 6. biolm maturation: growth and extracellular matrix
formation
numbers; Veillonella species are the most commonly isolated 7. detachment: facilitates colonisation at other sites.
Gram-negative organism from this site. Saliva has a large
inuence on the properties of the microbiota of ssures.
Stage 1. Conditioning Film Formation
Approximal Surfaces
Microorganisms rarely come into contact with clean enamel.
ese surfaces have high numbers of Gram-positive and fac- Within seconds of being cleaned, molecules are adsorbed
ultatively anaerobic bacteria, particularly Actinomyces spp. onto the tooth surface, forming a surface-conditioning lm
Stage 2. Microbial transport–

passive/active
Some oral bacteria are motile, 2. Transport
but most are swept passively – passive/active
Bacteria towards the tooth surface by the
in saliva flow of saliva.
1. Conditioning Weak, long range,

film formation van der Waals forces
Surface Surface
Stage 1. Conditioning film formation Stage 3. Reversible attachment

The conditioning film (also referred Once bacteria are close to the tooth surface, weak
to as the acquired pellicle) starts to form long-range (>10–20 µm) forces between the
within seconds immediately after a surface molecules on the microbial cell surface and those
is cleaned. It is composed of salivary proteins, in the conditioning film can hold the cell reversibly
glycoproteins and bacterial glucans and enzymes. near to the tooth.
A B
Stage 5. Secondary colonisation Stage 7. Detachment
Later colonisers attach via adhesin If conditions become sub-optimal,
receptor interactions to the already bacteria can detach and
attached bacteria (co-adhesion/ colonise elsewhere.
co-aggregation).
Secondary
coloniser
Primary
colonisers
Adhesin
Receptor
Surface Surface
Stage 4. Irreversible attachment Stage 6. Biofilm maturation

Attachment can become irreversible if specific The attached bacteria grow, form micro-colonies,
molecules on the bacterial cell surface (termed and interact both synergistically (e.g. food webs,
“adhesins”) are able to bind to complementary cell–cell signalling, etc.) and antagonistically (e.g.
molecules in the acquired pellicle inhibitor production, etc.). The metabolism of the
(termed “receptors”). early colonisers modifies the environment in the
biofilm, thereby making conditions suitable for the
C attachment and growth of later colonisers (e.g.
obligate anaerobes). An extracellular matrix is
synthesised.
D
• Figure 1.5.3 Stages in the development of dental biolms. (A) Stage 1: A conditioning lm (the acquired
pellicle) forms immediately on a cleaned tooth surface. Stage 2: Microorganisms are generally transported
passively to the tooth surface. (B) Stage 3: Microorganisms may be held reversibly close to the tooth
surface by weak, long-range physicochemical forces of attraction. (C) Stage 4: Attachment becomes
more permanent if specic and stronger stereochemical molecular interactions occur between adhesins
on the bacterium and receptors in the acquired pellicle. Stage 5: Secondary colonisers attach to primary
colonisers, also by adhesin-receptor interactions (co-adhesion), thereby increasing the diversity of the
developing biolm. (D) Stage 6: Growth of attached cells results in biolm maturation, facilitating interbac-
terial interactions (synergistic and antagonistic) and biolm matrix formation. Stage 7: If conditions become
sub-optimal, cells can detach and colonise elsewhere.
(termed the acquired enamel pellicle). is lm contains biolm development, as this species can coadhere to most
salivary glycoproteins, phosphoproteins and lipids, includ- oral bacteria and acts, therefore, as an important bridging
ing statherin, amylase, proline-rich peptides (PRPs), host organism between early and late colonising species. Co-
defence components and bacterial components such as glu- adhesion may help ensure that bacteria are co-located with
cosyltransferases and glucan (Figure 1.5.3A) (Hannig etal. other organisms with complementary metabolic functions.
2005); it is to these molecules that the early microbial colo- us the composition of the biolm changes over time due
nisers (predominantly bacteria) attach. Depending on the to a series of complex interactions; these changes are termed
site, pellicle can also contain components from GCF. microbial succession.
Stage 2. Transport of Microorganisms Stage 6. Biofilm Maturation

Microorganisms are generally transported passively to the e microbial diversity of the biolm increases still further
tooth surface by the ow of saliva (see Figure 1.5.3A); a few over time because of consecutive waves of microbial succes-
oral bacterial species are motile (e.g. possess agella), and sion and subsequent growth, eventually leading to a stable
these are mainly located subgingivally. “climax microbial community” and a “mature” biolm (see
Figure 1.5.3D). e metabolism of the early colonising bac-
Stage 3. Reversible Attachment teria can modify the biolm environment (e.g. consumption
of oxygen and production of reduced fermentation prod-
Long-range, relatively weak physicochemical forces of attrac- ucts), which can increase the probability of colonisation by
tion are generated as the cell approaches the pellicle-coated more fastidious species (e.g. obligate anaerobes). Some of
surface. ese are generated by the interactions between the the attached bacteria can synthesize extracellular polymers
electrical charge on the molecules on the surface of the colo- (the plaque matrix) that can consolidate attachment of the
nising bacteria and the charge on the conditioning lm and biolm (Bowen et al. 2018). e matrix is more than a
can hold the cell reversibly close to the tooth (see Figure mere scaold for the biolm; the matrix can bind and retain
1.5.3B) (Busscher etal. 2008). molecules, including enzymes, and retard the penetration
of charged molecules (including antimicrobial agents) into
Stage 4. Irreversible Attachment the biolm (Bowen et al. 2018). e matrix can contain
extracellular DNA (eDNA) (Jakubovics & Burgess 2015),
e adherence of the reversibly attached cells can become soluble and insoluble polysaccharides (glucans, fructans,
stronger, and more likely to be permanent, if molecules etc.) (Koo etal. 2013) and lipoteichoic acid, the diering
(adhesins) on early bacterial colonisers (mainly streptococci, proportions of which will inuence the biological properties
e.g. Streptococcus mitis, Streptococcus oralis) can bind to com- of the biolm (Koo etal. 2013, Bowen etal. 2018).
plementary receptors in the acquired pellicle (Busscher etal. Biolms are spatially and functionally organised, and the
2008, Nobbs et al. 2011) (see Figure 1.5.3). Actinomyces, heterogeneous conditions within the biolm induce novel
Haemophilus and Neisseria spp. are also commonly isolated patterns of bacterial gene expression, whereas the close
early on, but obligately anaerobic species are detected only proximity of dierent species provides the opportunity
rarely at this stage and are usually in low numbers. Indi- for multiple types of synergistic and antagonistic interac-
vidual species express multiple adhesins; in Gram-positive tion (Jakubovics 2015, Marsh & Zaura 2017, Bowen etal.
bacteria, several families of surface proteins can act as adhes- 2018). Examples of these interactions include:
ins, including serine-rich repeat, antigen I/II and pilus
families. Adhesins in Gram-negative bacteria include auto- (a) e development of food chains (in which the terminal
transporters, extracellular matrix–binding proteins and pili product of metabolism of one organism is used as a pri-
(Nobbs etal. 2011). Once attached, these early colonisers mary nutrient by secondary feeders) and metabolic coop-
divide and form microcolonies, and their metabolism starts eration among species to catabolize structurally complex
to modify the local environment in the biolm. host macromolecules. ese interactions increase the
metabolic eciency of the microbial community and
Stage 5. Secondary Colonisation contribute to the stability and resilience of oral biolms
(Marsh & Zaura 2017, Rosier etal. 2018).
Over time, the composition of the biolm becomes more (b) Cell–cell signalling. Plaque bacteria can communicate
diverse; there is a shift away from dominance by strepto- with one another in a cell density–dependent manner
cocci to increasing proportions of Actinomyces, other Gram- via small diusible molecules. Gram-positive bacteria se-
positive bacilli and obligate anaerobes. Some organisms that crete small peptides to coordinate gene expression among
were unable to colonise the pellicle-coated tooth surfaces are cells of a similar species, whereas autoinducer-2 (AI-2)
able to attach to already adherent pioneer species by further is produced by several genera of oral Gram-positive and
adhesin-receptor interactions (termed co-aggregation or co- Gram-negative bacteria, implying that AI-2 may signal
adhesion) (see Figure 1.5.3C) (Kolenbrander et al. 2006, across a broader species range (Jakubovics 2010, Leung
2010). Fusobacterium nucleatum is a key organism in dental etal. 2015, Nobbs & Jenkinson 2015). Several putative
periodontal pathogens (Fusobacterium nucleatum, Pre- referred to as “tolerance”. Microorganisms can become truly
votella intermedia, Porphyromonas gingivalis, Aggregati- “resistant” to antimicrobial agents because of the increased
bacter actinomycetemcomitans) secrete a signal related to probability of gene transfer occurring in biolms. Recipi-
AI-2. ents of an antibiotic resistance gene are truly resistant to the
(c) Physically close cell-cell associations, such as “corn-cob” agent irrespective of whether they are in a biolm or not
(in which coccal-shaped cells attach along the tip of la- (Uruen etal. 2020).
mentous organisms), and “test-tube brush” structures
(rod-shaped bacteria sticking out perpendicularly from KEY POINT 7
bacterial laments), develop (Zijnge etal. 2010). Lacto- • Oral biolms are difcult to treat
bacilli formed the central axis of some of the “test-tube • Biolms are many times more tolerant of antimicrobial
brushes”, with organisms such as Tannerella, F. nucleatum agents than the same cells in planktonic liquid culture.
and Synergistes spp. radiating from this central cell. Corn-
cobs can form between streptococci and Corynebacterium e mechanisms that underpin this enhanced tolerance
matruchotii and between Veillonella spp. and Eubacteri- of biolms to antimicrobial agents include:
um spp. (Zijnge etal. 2010). • limited penetration of charged molecules, e.g. due to the
(d) Horizontal gene transfer, including the sharing of anti- binding of antimicrobials to the biolm matrix
biotic resistance genes (Marsh & Zaura 2017). • inactivation by production of neutralizing enzymes (e.g.
(e) Antagonism between competing species, for example, by cross-protection by neighbouring cells that secrete cata-
the production of inhibitory molecules (bacteriocins, hy- lase or β-lactamase that degrade hydrogen peroxide or
drogen peroxide, organic acids, etc.). e production of penicillin, respectively)
such inhibitory molecules will also contribute to “coloni- • quenching of the agent, e.g. by binding to cells at the
sation resistance” in which the resident oral microbiome biolm surface
is able to prevent the growth of potentially invading or- • unfavourable environments for the antimicrobial to
ganisms (Marsh & Zaura 2017). function in the depths of the biolm
• expression of a novel phenotype, e.g. the drug target is no
As the biolm matures, bacterial metabolism results
longer expressed during growth in the biolm
in the development of gradients within dental biolms in
• the slow growth rates of bacteria in bioëlms (slow-grow
parameters that are critical to microbial growth (nutrients,
ing organisms are generally less susceptible than faster-
pH, oxygen, etc.). Such environmental heterogeneity will
growing cells)
allow fastidious bacteria to survive in plaque and enable
• horizontal gene transfer (e.g. drug resistance plasmids;
microorganisms to coexist that would be incompatible with
this is an example of increased “resistance” to an antimi-
one another in a more homogeneous environment.
crobial agent). In a biolm, cells are close to one another,
which facilitates eective gene transfer (Uruen et al.
Stage 7. Detachment From Surfaces 2020).
Bacteria can “sense” adverse changes in environmental con-
ditions, and these may act as “cues” to induce genes involved Benefits of the Resident Oral Microbiome
in active detachment from the biolm, for example, by the
upregulation of proteases to cleave their adhesins from the e resident oral microbiome confers important benets to
cell surface (see Figure 1.5.3D). the host and plays an essential role in the normal develop-
ment of the physiology, nutrition and defences of the host
(Sanz etal. 2017).
Reduced Sensitivity of Biofilms to
Antimicrobial Agents KEY POINT 8
The oral microbiome provides signicant benets to the host
All biolms display a reduced sensitivity to antimicrobial by:
• Resisting colonisation (in which the resident microbiome
agents compared with the same cells growing in conven- prevents colonisation by exogenous species)
tional liquid culture (Mah 2012, Koo et al. 2017, Uruen • Downregulating proinammatory host responses to
etal. 2020). For example, concentrations of chlorhexidine benecial species (Devine etal. 2015)
need to be 10- to 50-fold greater than the minimum inhibi- • Regulating gastrointestinal and cardiovascular systems.
tory concentration (MIC) in order to eliminate a biolm Thus it is essential to control oral biolms, and not
eliminate them, to maintain the benecial properties of the oral
of an oral bacterium such as Streptococcus sanguinis. Older microbiota.
biolms are even more tolerant of antimicrobial agents than
younger biolms. Generally, this is a phenotypic response,
as these cells display their original sensitivity when resus- • One of the principal functions of a resident microbiome is
pended from the biolm into liquid broth (mechanisms for the ability to prevent colonisation by exogenous (and of-
this are listed later), and so the reduced sensitivity should be ten pathogenic) microorganisms. is property, termed
“colonisation resistance”, is due to the resident microbes Gingivitis

being more eective at:
 • attaching to host receptors Dental biolm-induced gingivitis is a nonspecic, reversible
 • competing for endogenous nutrients inammatory response to an increased accumulation of bio-
 • creating unfavourable growth conditions to discour- lm around the gingival margin due to poor oral hygiene.
age attachment and multiplication of invading organ- Gingivitis is usually eradicated if eective oral hygiene is
isms, and restored, and the tissues become clinically normal again. e
 • producing antagonistic substances (hydrogen perox- consensus is that there are no specic pathogens associated
ide, bacteriocins, etc.). with gingivitis (Marsh etal. 2016). e increase in biomass
• Attempts to boost colonisation resistance using replace- provides a more suitable environment for the growth of fas-
ment therapy (in which resident organisms are deliber- tidious species including obligate anaerobes, many of which
ately reimplanted), for example, after periodontal ther- have inammatory molecules on their cell surface resulting
apy or by using probiotics or prebiotics (molecules that in the biolm having a raised inammatory potential. Not
boost the growth of benecial resident microbes), are be- all sites with gingivitis progress to more advanced forms of
ing explored (Devine & Marsh 2009). periodontal diseases, but it is accepted that gingivitis does
• ɨe biological mechanisms are being identiëed that precede periodontitis. Gingival diseases can also be modi-
permit a constructive coexistence between the host and ed by systemic factors.
the resident microbiome. e host is actively engaged
in cross-talk with its resident microbiome in order to Periodontitis
maintain a symbiotic relationship. e host has evolved
systems to enable it to tolerate resident microorganisms Numerous cross-sectional microbiological culture studies
without initiating a damaging inammatory response, on periodontal pockets from dierent patient groups from
while also being able to mount an ecient defence various geographical regions have recovered highly diverse
against pathogens (Devine etal. 2015). microbial communities, with increased proportions of pro-
• ɨe resident oral bacteria play an important role in teolytic and obligately anaerobic bacteria, many of which
maintaining many important aspects of the gastrointes- are Gram negative. ese bacteria are dicult to recover,
tinal and cardiovascular systems via the metabolism of grow and identify in the laboratory, and there is often con-
dietary nitrate. Approximately 25% of ingested nitrate icting evidence as to which organisms might be playing an
is secreted in saliva where facultatively anaerobic oral active role in disease (Diaz etal. 2016, Marsh etal. 2016).
resident bacteria reduce nitrate to nitrite. Nitrite aects Some of the bacteria that have been implicated are listed in
a number of key physiological processes including the Table 1.5.1.
regulation of blood ow, blood pressure, gastric integrity Despite the enormous diversity of bacterial species iso-
and tissue protection against ischaemic injury. Nitrite lated from these studies, certain trends and microbial asso-
can be further converted to nitric oxide in the acidied ciations began to be discerned. Socransky and colleagues
stomach, and this has antimicrobial properties and con- (Socransky etal.1998, Socransky & Haajee 2002, 2005)
tributes to defence against enteropathogens; nitric oxide analysed and compared the microbiota from over 13,000
also regulates gastric mucosal blood ow and promotes samples from patients with and without periodontitis,
mucus formation (Koch etal. 2017, Rosier etal. 2020). using an early culture-independent approach (checker-
board DNA–DNA hybridization technique with probes
against 40 preselected subgingival species). ey found
Microbial Composition of Dental Biofilms that certain combinations or “complexes” of bacteria were
in Periodontal Diseases associated with dierent states of periodontal health or
disease. e strongest association with advanced periodon-
Numerous studies with dierent designs and a variety of titis was with three bacterial species (Porphyromonas gin-
populations and sites have consistently shown that the givalis, Treponema denticola and Tannerella forsythia), and
microbiota from periodontal pockets is markedly dierent these were designated the “red complex”. eir presence
from that found at healthy sites, even in the same mouth was often preceded by other consortia which included
(Diaz etal. 2016). e conclusion from these studies is that, various Prevotella species, Fusobacterium nucleatum, Cam-
unlike some medical infections, there is a not a single patho- pylobacter species and Eubacterium nodatum (designated
gen responsible for periodontal disease but that inamma- the “orange complex”). Other bacterial groupings were
tion is a consequence of an increased biomass with higher associated with periodontal health (“purple”, “yellow” and
numbers and proportions of obligate anaerobes, many of “green” complexes) (Socransky etal. 1998). ese studies
which are Gram-negative bacteria expressing a proinam- helped to shift the focus away from trying to identify a
matory phenotype and with a proteolytic metabolism. single pathogen and supported concepts in which complex
Some of the microbiological features of distinct forms consortia of microorganisms were responsible for disease
of periodontal diseases are described in the following (Lamont etal. 2018, Curtis etal. 2020, Hajishengallis &
sections. Lamont 2021).
TABLE Identied species that have been with accurately naming the members of these communi-
1.5.1 implicated with periodontitis ties, whereas it could be more instructive in the future
if the “function” or “role” of each organism within the
Species implicated with periodontitis
consortium was determined (Takahashi 2015, Espinoza
Bacteroidales species Prevotella spp. etal. 2018), as it is probable that bacteria with dierent
Porphyromonas Alloprevotella tannerae “names” could be performing identical “functions” within
endodontalis a community. Hence, we might see a greater consensus
Porphyromonas gingivalis Johnsonella spp.
across studies looking at diseased sites if we reported by
microbial function rather than by bacterial name. Most
Mogibacterium timidium Dialister pneumosintes tissue destruction in periodontitis is a result of the exag-
Peptostreptococcus Dialister invisus gerated inammatory response to the developing subgin-
stomatis gival biolm (see later).
Filifactor alocis Campylobacter rectus Some younger patients can present with a more aggres-
sive form of periodontitis despite only low amounts of
biolm present at aected sites; these patients may have
Selenomonas spp. Johnsonella spp. functional abnormalities associated with their neutro-
Fretibacterium fastidiosum Eubacterium spp. phils. Aected sites can have high numbers of Aggrega-
tibacter (formerly Actinobacillus) actinomycetemcomitans.
Desulfobulbus spp. Leptotrichia spp.
is bacterium produces a powerful leukotoxin, enzymes
Bidobacterium dentium Parvimonas micros capable of degrading collagen and cell-surface-associated
material that can cause bone resorption (Belibasakis etal.
2019, Norskov-Lauritsen et al. 2019). A virulent clone
TM7 Treponema spp.
(JP2) of A. actinomycetemcomitans has been identied that
spp. SR1 taxon overproduces the leukotoxin and is found endemically in
Northwest Africa; the presence of this clone signicantly
The presence or detection of these microorganisms does not neces-
increases the risk of adolescents suering from aggressive
of disease. periodontitis (Belibasakis et al. 2019, Norskov-Lauritsen
(Perez-Chaparro etal. 2014, Diaz etal. 2016)
etal. 2019).
Necrotizing Periodontal Diseases
Necrotizing ulcerative gingivitis (NUG)
NUG, also described as Vincent’s disease, trench mouth or
In recognition of the diversity of the subgingival acute necrotizing gingivitis, is a severe form of necrotizing
microbiota and the fact that perhaps less than 50% can inammation of the interdental papillae, accompanied by
be cultured, most contemporary studies are using open- spontaneous gingival bleeding and intense pain. In smears
ended, culture-independent metagenomic approaches, of the aected tissues, microorganisms (resembling spiro-
which do not have the limitation of detecting only a pre- chaetes and fusiform bacteria – the characteristic fuso-spi-
determined set of species, as occurred with checkerboard rochaetal complex) can be seen invading the host gingival
DNA–DNA hybridization techniques. Such studies have tissues. Culture-independent approaches have conrmed
further emphasised the complexity of the microbiota asso- the predominance of a diverse range of Treponema spe-
ciated with disease and have discovered the presence of cies (spirochaetes) in lesions, many of which cannot be
a large number of novel bacteria (Table 1.5.1), some of cultivated, but showed that the “fusiform” bacteria could
which have no or few cultivable examples, and several belong to a broader range of genera including Leptotrichia,
are currently unnamed. Most studies attempting to cor- Capnocytophaga and Tannerella in addition to Fusobacte-
relate the bacterial composition of subgingival biolms rium spp. (Dewhirst etal. 2000, Paster etal. 2002, Gmur
with periodontal health or disease are, of necessity, cross- etal. 2004). Culture-based studies also recovered Prevotella
sectional in design. A major challenge in such studies is intermedia. Metronidazole is eective in eliminating the
to determine which bacteria are playing an active role fuso-spirochaetal complex from infected sites, and this is
in disease, which are present as a result of disease and associated with rapid clinical improvement.
which are merely bystander organisms. e lack of con-
sistency in microbial composition of subgingival biolms Necrotizing ulcerative periodontitis
isolated from diseased sites when the data from dierent Necrotizing ulcerative periodontitis is a painful condition
studies are compared might be a result of the technical that aects a small proportion of HIV-positive subjects.
methods used to sample, process and analyze the samples, Molecular approaches detected a wide range of bacteria
but it could also indicate that consortia with a dierent including Bulleida extructa, Dialister, Fusobacterium, Sele-
composition can produce the same clinical signs (Perez- nomonas, Veillonella spp., members of the TM7 phylum and
Chaparro etal. 2014). To date, the eld has been obsessed anaerobic streptococci (Paster etal. 2002).
KEY POINT 9 of those listed in Table 1.5.1. Several of the species that were
enriched were present in such low numbers that they were
Periodontal diseases are a result of a perturbation in the local
environment that enables previously minor bacterial members below the level of detection in the original biolm samples.
of the biolm to be more competitive and therefore become At these low levels, these bacteria would have no or minimal
more numerically dominant, within the subgingival microbiota. clinical impact.
Effective disease control needs to identify and resolve the In disease, the host mounts an inammatory response
factors driving the selection of these pathogens and causing
when plaque biolm accumulates beyond levels that are
the disruption of the benecial relationship between biolm and
the host. compatible with health, and this leads to substantial changes
in the subgingival environment. ere is an increase in the
ow of GCF which introduces components of the host
defences into the crevice. However, GCF also contains an
Contemporary Perspectives on the array of complex host molecules, including transferrin, hae-
Aetiology of Periodontal Diseases moglobin, etc., that can be exploited as primary nutrient
sources by the proteolytic Gram-negative anaerobes which
It is now accepted that disease is a consequence of a who- also have the potential to act as periodontal pathogens (see
lescale shift in the balance and composition of the entire previous discussion) (Naginyte etal. 2019). Also, organisms
subgingival microbial community, with the emergence and such as Prevotella intermedia and Porphyromonas gingivalis
increased abundance of many species that are apparently have an absolute requirement for haemin for growth and
absent in health or present as only minor constituents of the derive this cofactor from the catabolism of host glycopro-
normal subgingival microbiome (Diaz etal. 2016, Lamont teins, such as haemoglobin, using proteases such as inter-
etal. 2018). An intriguing question, therefore, is the origin pain and gingipains, respectively. An increase in haemin
of these potential pathogens. Previous theories have sug- availability can dramatically alter the phenotype of bacteria;
gested that disease-associated microbial species could be P. gingivalis displays increased protease activity, changes in
(a) acquired exogenously, (b) translocated from reservoir the structure of its lipopolysaccharide and is more virulent
sites such as the buccal mucosa or tongue, or (c) present when grown in a surplus of haemin. A further consequence
at healthy sites but in numbers too low to be detected. e of this proteolytic metabolism is an increase in local pH
application of sensitive molecular techniques has detected and a fall in the redox potential, which also promotes the
several of the putative pathogens (e.g. P. gingivalis, A. acti- upregulation of some of the virulence factors associated
nomycetemcomitans) at noninamed, healthy sites but, with these putative pathogens and favours their growth at
whichever theory applies to the origins of these putative the expense of the species associated with gingival health
periodontopathogens, a dramatic change to the environ- (i.e. these environmental changes increase the competitive-
ment of the habitat would be necessary for the balance of ness of the potential pathogens).
the microbiota to be shifted to the extent seen in disease Combinations of bacteria in these dysbiotic microbial
in which these species are able to out-compete the resident communities display “pathogenic synergism” in that weakly
benecial bacteria. In other ecosystems, such dramatic shifts pathogenic species combine forces to overcome the host
in microbiota are associated with a major alteration to the defences and drive inammation and tissue damage. Micro-
habitat, such as to the nutrient status (e.g. the overgrowth bial proteolytic activity in the pocket can also target and
of algae in rivers after the wash-o of nitrogenous fertilizers degrade host defence molecules which can result in a dereg-
from neighbouring farm land), pH (e.g., the disruption of ulated and ultimately exaggerated inammatory response,
aquatic life in lakes by “acid rain”) or immune status (e.g. causing bystander damage to the subgingival tissues (Curtis
reactivation of dormant Mycobacterium tuberculosis in the et al. 2020, Hajishengallis et al. 2020). is uncontrolled
lungs of HIV-infected patients). response provides an even broader range of host molecules
Support for the concept that a change in environment for the increasingly metabolically versatile microbial com-
can drive the enrichment of generally minor but poten- munity. Most of the tissue damage is due to this excessive
tially pathogenic components of the microbiota has come and subverted host response. If sustained, the combined
from a biolm model system that attempted to replicate selective pressures of changed nutrient supply, elevated pH
some of the environmental changes associated with inam- and lower redox potential together with an impaired inam-
mation, particularly those that aect the availability of matory response will lead to a substantial rearrangement of
nutrients suitable for proteolytic bacteria. Biolm samples community structure and subsequent damage to the peri-
were taken from healthy oral sites in adult human volun- odontal tissues.
teers (tongue, supragingival plaque) and grown in human us a cyclical situation develops in which, if the host
saliva; this medium was then supplemented with serum fails to control the initial microbial insult, the nature of
as a surrogate for the increased ow of GCF that occurs its response to the subgingival biolm inadvertently pro-
during the inammatory response, and after just 3 weeks vides conditions that will further select for the pathogens
metagenomic analyses could detect most of the pathogens, that will subsequently continue to drive the inammatory
including unculturable species, that are now implicated response. is concept was encapsulated initially in the
with periodontitis (Naginyte etal. 2019), including many “ecological plaque hypothesis” (Marsh 2003) (Figure 1.5.4),
Gingival
Health
Low plaque No / little Low GCF Gram positive
[Health Inflammation flow bacteria
Compatible]
Effective oral hygiene
Environmental Ecological
Stress Disease
change Shift
Host risk factors
Periodontitis
Gingivitis/
Gram negative
Increased High GCF bacteria;
Increased
flow, bleeding, Anaerobic;
Plaque Inflammation.
Proteolytic;
Levels Subverted host raised pH &
Inflammophilic
response temperature
• Figure 1.5.4 The “ecological plaque hypothesis” and periodontal diseases. Biolm accumulation induces
an inammatory host response which causes a change in local environmental conditions that favours the
growth of proteolytic and anaerobic Gram-negative bacteria. Diseases could be prevented by not only tar-
geting the putative pathogens, but also by interfering with the factors driving their selection. Effective oral
hygiene will favour healthy interactions between the host and the biolm (symbiosis), while host risk factors
(e.g. smoking, neutrophil defects) may increase the likelihood of disease (dysbiosis).
in which there is recognition of a direct link between local and inammatory microorganisms which accentuates dys-
environmental conditions in the host and the activity and biosis and perpetuates the inammatory response (Rosier
composition of the biolm community. Any change to the etal. 2018, Curtis etal. 2020, Hajishengallis etal. 2020,
host environment will induce a response in the microbiota Hajishengallis & Lamont 2021) (Figure 1.5.5). Approaches
and vice versa. Implicit in this hypothesis is that although to break this cycle can be via traditional treatments, such as
disease can be treated by targeting the putative pathogens mechanical periodontal therapy (e.g. root surface debride-
directly (e.g. with antimicrobial agents), long-term preven- ment) augmented by improved oral hygiene practices, and
tion will only be achieved by interfering with the underly- lifestyle changes (e.g. elimination of risk factors such as
ing changes in host environment that drive the deleterious smoking), but newer adjunctive strategies are being devel-
shifts in the microbiota (Marsh 2003). With increasing oped that could modulate an excessive and exaggerated host
knowledge, this theory has been further rened with greater response to reduce these detrimental aspects of inamma-
emphasis on the damage caused by the deregulated inam- tion and promote resolution and tissue healing (Curtis etal.
matory response (the polymicrobial synergy and dysbiosis 2020, Hajishengallis etal. 2020, Van Dyke etal. 2020).
model) while reinforcing the concept that the change in
the subgingival environment will drive dysbiosis (Lamont KEY POINT 10
& Hajishengallis 2015). Also, it is recognised that some Periodontal diseases are a result of a perturbation in the local
organisms such as P. gingivalis may play a role in disease environment that enables previously minor components of
that is disproportionately more signicant than their num- the biolm to become more competitive, and therefore more
numerically dominant, within the subgingival microbiota.
bers within the subgingival microbial community, and for These microorganisms are able to subvert and disrupt the
this reason they have been termed “keystone pathogens” inammatory response, leading to tissue damage and further
(Hajishengallis et al. 2012). e presence of the keystone inammation; this process is termed dysbiosis. Effective disease
pathogen may be dependent on the activity of neighbouring control needs to identify and resolve the factors driving the
species, for example, in terms of provision of nutrients or selection of these pathogens and causing the disruption of the
normally benecial relationship between biolm and the host.
inactivation of the host defences, and these are described as
“accessory pathogens”. e keystone pathogens, supported
by accessory pathogens, combine to subvert host immunity Concluding Remarks
and cause the emergence of a detrimental and dysbiotic
microbiota which drives the exaggerated and deregulated e mouth supports the growth of diverse communities of
inammatory response resulting in further tissue destruc- microorganisms that grow as structurally and functionally
tion (Curtis etal. 2020, Hajishengallis etal. 2020, Hajish- organised biolms. ese communities, and those present
engallis & Lamont 2021). A bidirectional and cyclical at other habitats in the body, play an active and critical role
(positive feedback loop) process develops in which the in the normal development of the host and in the mainte-
inammatory response further enriches for inammophilic nance of health. Clinicians need to be aware of the benecial
• Figure 1.5.5 The bidirectional relationship between the subgingival microbiome and the inammatory
and immune response (Curtis etal. 2020). The subgingival symbiotic microbiota in health is dominated
by health-associated species (green) but species linked with gingivitis (orange) and periodontitis (red) are
present in low abundance. Core species are found in both health and disease. Gingivitis is characterised by
an increased biomass (green and orange arrows) comprising both green and particularly orange species
and an associated increase in inammation. In periodontitis, biomass increases further (green, orange and
red arrows), and the red species become increasingly dominant in the dysbiotic microbiota. Furthermore,
the gene expression proles (transcriptome) of the green and orange species are modied with increased
expression of virulence determinants. This is accompanied by the development of a deregulated inam-
matory response and tissue destruction. Interventions which are able to resolve the inammatory response
may also be important in the reversal of the dysbiotic microbiota. Reprinted from Periodontology 2000,
83(1):12, Curtis. et al. (2020), with permission from John Wiley & Sons.
functions of the resident oral microbiota, so that treatment factors that are driving the “dysbiosis”, otherwise the delete-
strategies are focused on the control rather than the elimi- rious changes to the microbiota will reoccur, risking further
nation of these natural biolms. Oral care should attempt episodes of disease.
to maintain plaque biolm at levels compatible with health Multiple choice questions on the contents of this chapter
in order to retain the benecial properties of the resident are available online at Elsevier eBooks+
oral microbiota while preventing microbial overload that
increases the risk of dental disease. References
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1.6
PERIODONTAL RISK
 MODIFYING AND
PREDISPOSING FACTORS
IA I N C H A P P L E A N D M I K E M I LWA R D
CHAPTER OUTLINE
Introduction Diabetes and Obesity
Risk Factors, Markers and Predictors Stress
Poor Oral Hygiene
Complex Diseases and Causal Theory
Periodontal Risk Assessment
Risk Assessment and the “At Risk” Patient Risk Assessment – The Third Dimension
Classication of Risk Factors Risk Assessment Technologies
True or Putative Local Risk (Predisposing) Factors
Modifying or Predisposing Factors Iatrogenic
Modiöable or Non-Modiöable Anatomical
Risk Factors in Periodontitis Progression Root Caries
Tooth Position
Systemic Risk (Modifying) Factors
False/True Pockets
Genetics High Frenal Attachment
Age Calculus
Nutrition Oral Dryness
Smoking
Acknowledgement

This chapter conceptualises periodontitis as a complex non-communicable disease (NCD) and explains how such diseases exhibit not just a single
cause but multiple component causes or risk factors. It describes and denes risk factors, risk predictors and risk indicators for periodontitis. It
reviews both modifying (formerly “systemic”) and predisposing (formally “local”) factors for periodontitis in line with the 2017 World Workshop
Classication (WWC) system and their mechanisms of action. It then details digital risk assessment programmes and online risk assessment tools.
By the end of the chapter the reader should be able to: • Introduce digital risk assessment programmes and online
• Understand causality in the context of complex diseases and risk assessment tools to their practice.
how that relates to risk factors is chapter covers the following topics:
• Describe and deöne risk factors, risk predictors and risk • Introduction
indicators • Risk factors, markers and predictors
• List the critical stages in the development of periodontal • Complex diseases and causal theory
tissue destruction and how these relate to risk factors that • Risk assessment and the “at risk” patient
patients possess or have been exposed to • Classiöcation of risk factors
• Identify the key risk factors for periodontitis and the • Risk factors in periodontitis progression
evidence base for each • Modifying (systemic risk) factors
• Deöne basic terminology and discuss the diòerent types of risk • Predisposing (local risk) factors
factors for periodontitis, including their mechanisms of action • Mechanisms of common risk factors
• Enable the clinician to assess risk at the patient level as a • Periodontal risk assessment
vital part of Step 1 of periodontal therapy in the S3-level • The role of risk assessment and risk factor control in
periodontal treatment guideline (2020–2021) behaviour change as part of Steps 1–4 of the international
S3-level treatment guideline.
56
CHAPTER 1.6 Periodontal Risk – Modifying and Predisposing Factors 57

Risk markers or predictors are not causally related to a
Inammatory periodontal diseases are complex NCDs. disease, but their presence is more a consequence of the
ey are one of the most prevalent chronic diseases of disease being present.
humans, aecting 7.4–11.2% of adults globally (Kasse-
baum 2014, 2017). e incidence of severe periodontitis
globally was 6 million in 2015, resulting in 3.5 million Complex Diseases and Causal Theory
disability-associated life years (DALYs) compared with 1.89
million DALYs for untreated caries in deciduous and adult e majority of NCDs are complex diseases, meaning they
teeth (Kassebaum 2014). Patients vary greatly in their risk do not have a single cause but multiple component causes or
for developing disease because of the interaction between true “risk factors”, which aggregate towards a critical thresh-
microbial, genetic, environmental and lifestyle factors. Risk old, above which the disease is triggered. In periodontitis,
assessment, as a means of attempting to identify the level plaque accumulation is not the cause of periodontitis, oth-
of risk faced by individual patients for the development of erwise 100% of the population would exhibit the disease,
periodontitis over their lifespan, has become a fundamental yet the Sri-Lankan Tea Worker study by Lӧe and colleagues
part of modern preventive practice. (1986) demonstrated natural resistance to the disease in a
By assessing patients’ level of risk, the practitioner can small proportion of individuals (11%), and a high suscepti-
implement individual patient-centred (rather than generic) bility (8%) in a similarly small number, with the remainder
plans for managing an individual patient’s periodontitis and exhibiting a spectrum of medium risk of disease progression
can also help determine an appropriate supportive care recall (81%).
frequency, based upon risk status. is will therefore allow
limited healthcare resources to be targeted at patients with KEY POINT 3
greater risk of developing disease. Rosling and colleagues The majority of NCDs are complex diseases, meaning they do
demonstrated in a 12-year supportive care (SPT) study not have a single cause but multiple component causes or true
that planning SPT interval frequency and length accord- “risk factors”, which aggregate towards a critical threshold,
above which the disease is triggered.
ing to individual patient risk virtually eliminated tooth loss
due to periodontitis in “normal susceptibility” patients and
led to an average loss of two teeth to periodontitis during Rothman (2002) described what is today still regarded as
the 12-year SPT period for “high susceptibility” patients the most plausible theory for causality of complex diseases,
(Rosling etal. 2001). the “causal pie” hypothesis (Figure 1.6.1). For a disease to
manifest in an individual there must be a “sucient cause”,
Risk Factors, Markers and Predictors made up of multiple “component causes” or risk factors.
In the gure each pie represents a patient with disease; the
Risk factors for a disease have been dened as certain char- disease only arises when the pie is full of slices. Slice “A”
acteristics of a person or their environment which, when is common to each patient and is a necessary component
present, directly result in an increased likelihood of that cause, but insucient on its own to cause the disease: for
person getting the disease, and when absent directly result periodontitis this would be the plaque biolm. Slice D may
in a decreased likelihood (Beck etal. 1995). ey are caus- be tobacco smoking, slice G may be glycaemia or hyper-
ally associated with a disease. Examples for periodontitis glycaemia in a diabetes patient and slice I may represent
are genetics, smoking, stress and sub-optimally controlled stress without coping strategies. Key to this concept is that
diabetes. component causes dier between individuals, providing
heterogeneity of disease expression, and importantly, that
KEY POINT 1 eliminating one risk factor may stabilise the disease as the
Risk factors are characteristics of a person or their
pie is no longer full.
environment which, when present, directly result in an
increased likelihood of that person getting the disease, and KEY POINT 4
when absent directly result in a decreased likelihood. For a complex disease to manifest in an individual there must
be a “sufcient cause”, made up of multiple “component
Risk markers or predictors are not causally related to causes” or risk factors.
a disease, but their presence is more a consequence of the
disease being present. Examples in periodontitis are bleed- Risk Assessment and the “At Risk” Patient
ing on probing, suppuration, tooth mobility, interproxi-
mal recession and evidence of past disease. Risk markers An “at risk” patient is someone who has a higher-than-
imply the presence of disease and are often used to detect average probability of developing a specic disease
early stages of disease, before overt clinical signs become over a specic period of time; they either possess or
apparent. have been exposed to risk factors for that disease. us
Sufficient versus necessary cause theory for complex diseases

Sufficient cause I Sufficient cause II Sufficient cause III
D A G A I A
C X1 F E H X1
B X2 X2
Causal pies. Each combination is sufficient for the disease to develop. “A” is a
necessary cause because it is present in every pie. The rest (X1, X2, C, etc.) are
component causes that could belong to different sufficient causes or appear as a
joint element (e.g. sufficient cause III).
• Figure 1.6.1 Rothman’s “causal pie” model for complex diseases. “A” is a necessary cause but insuf-
cient on its own to cause the disease. A sufcient cause is needed for disease to manifest and consists
of aggregated component causes or risk factors, forming a full pie.
a 20-cigarette-per-day smoker with poor oral hygiene is improves. One example might be plaque biolm levels
potentially at high risk for periodontitis and/or necrotising around the teeth. Note that true risk factors do not imply
gingivitis (NG). absolute cause and eect (Rothman 2002), simply that they
One of the strongest predictors of future disease activity increase the likelihood of disease if present. In the case of
is the amount of disease the patient presents with at the rst the oral plaque biolm, high biolm levels do not cause
consultation, taking their age into account. For example, periodontitis in all patients, only those who have some peri-
a 25-year-old with 40% generalised horizontal bone loss is odontal susceptibility.
at far greater risk of tooth loss due to periodontitis than a Putative risk factors for a disease are those factors that are
70-year-old with the same amount of bone loss. is con- associated with the occurrence of a disease, as observed in
cept underpins the “grading” of periodontitis within the cross-sectional studies. Such factors do not satisfy the crite-
2017 WWC (Papapanou etal. 2018). ria for true risk factors because there is a lack of evidence
To help understand the role of systemic risk factors in the from longitudinal studies (which may not have been per-
pathogenesis of periodontitis, the “critical pathway model formed) that removal of the risk factor will improve the dis-
of pathogenesis” was described by Salvi etal. (1997). is ease state. Examples might be stress or nutritional factors.
pathway (updated in Figure 1.6.2) identies nine criti-
cal stages that must be present for disease to develop and Modifying or Predisposing Factors
progress. As discussed in Chapters 1.2 and 1.4, it has been
estimated that merely 20% of the tissue destruction in peri- Modifying factors (systemic risk factors) for periodontitis
odontitis is explained directly by bacterial action (Grossi are those characteristics present in an individual which
etal. 1994); the remainder being attributable to a dysregu- negatively inuence the immune-inammatory response
lated host immune-inammatory response. to a given dental plaque biolm burden, resulting in exag-
gerated or “hyper” inammation (Chapple et al. 2018).
KEY POINT 5 Examples include those aecting the host response either
Approximately 20% of the tissue damage seen in periodontitis directly or indirectly. ey may be environmental factors
is due to direct bacterial action; the remainder is due to a (e.g. stress), lifestyle factors (e.g. nutrition or smoking)
dysregulated host immune-inammatory response. or those relating to general health (e.g. diabetes status,
immunodeciency or other conditions such as leucocyte
Classification of Risk Factors adhesion defects).
Predisposing factors (formerly local risk factors) for peri-
Risk factors can be described in a variety of ways: odontitis are those that encourage plaque accumulation at
• True or putative a specic site by either inhibiting its removal during daily
• Modifying or predisposing oral hygiene practices and/or creating a biological niche that
• Modiëable or non-modiëable. encourages increased plaque accumulation and consequent
inammation (Chapple etal. 2018). ey include biolm
True or Putative retention factors, which may be anatomical in nature (e.g.
root grooves, enamel pearls) or relate to poor restoration
True risk factors for a disease have a causal association, that margins, imbricated teeth or dental appliances that are close
is, when present, they increase the likelihood of the dis- to the gingival margin and oral dryness due to some medica-
ease developing, but when they are removed the disease tions or autoimmune disease.
1
Non-pathogenic flora
endogenous bacteria
Poor oral hygiene
2
Pathogenic flora
low microbial mass
9 3
Pocket formation and Innate defence mechanisms Success Gingivitis and
bone loss and PMNL clearance limited periodontitis
Limited/no success
8 4
Microbial mass increases
Tissue destruction
± tissue penetration
7 5 Acquired immune response Success

Massive infiltration of PMNLs
lymphocytes and monocytes
No success
6 Release of cytokines, Success
lymphokines, chemokines
• Figure 1.6.2 The “critical pathway model” (Salvi etal. 1997) updated to recognise the interplay between
gingival inammation, dysbiosis and periodontal tissue damage.
Modifiable or Non-Modifiable WWC (Dukka etal. 2021). e BSPi grades in the same
manner as the 2017 WWC but employs a dierent thresh-
Modiable risk factors for a disease are those that can be inu- old for dening grade B disease and does not modify the
enced by the patient or the clinician. ese may be systemic grade by risk factors but lists those risk factors present
or environmental in nature and include smoking cessation, without assigning a weight to them, as part of a “diagnostic
improving diabetes control, improved diet and reducing bio- statement”.
lm levels through improved oral hygiene, or correction of Modifying and predisposing factors have an important
local risk factors such as restorations with subgingival ledges. part to play in the progression of periodontal breakdown,
Non-modiable risk factors for a disease are those that and control can only be achieved if a proper assessment
cannot be inuenced by the patient and essentially relate to is made of the factors involved. Figure 1.6.4 shows how
genetic traits or characteristics. In the future, gene therapy systemic (subject-based) and local (site-based) risk factors
may change this. underpin the disease process.
Risk Factors in Periodontitis Progression Systemic Risk (Modifying) Factors

Periodontitis risk can be described as part of a spectrum If applying the strict denition of the term “true risk factors”,
with resistance at the left and the highest risk states at the there is only one true risk factor that has been unequivo-
right (Figure 1.6.3). In the 2017 WWC, periodontitis is cally demonstrated for periodontitis, which is dental plaque.
graded to embrace risk, the grade representing the patient’s Plaque biolm accumulation has been shown to cause gin-
lifetime experience of periodontitis in relation to their age. givitis, but strictly speaking this cannot be extrapolated to
Baseline grading is determined by dividing percentage bone include periodontitis, other than by inference. However,
loss at the worst aected site by the patient’s age. Grade C although there is abundant evidence that biolm reduction
represents rapid progression, grade B, a moderate rate of improves periodontal outcomes, the amount of reduction
progression and grade A, a slow rate. If a patient is a current required varies from patient to patient. Table 1.6.1 shows
smoker or has poorly controlled diabetes, this increased the principal risk factors for periodontitis and our current
the grade from the baseline grade allocated (Tonetti etal. understanding of the evidence for their risk status.
2018). e British Society of Periodontology and Implant
Dentistry (BSP) created a simpler implementation (BSPi) Genetics
of the staging and grading system (Dietrich et al. 2019),
which has been shown to predict tooth loss due to peri- Studies of monozygous twins indicate that genet-
odontitis as well, and indeed slightly better than the 2017 ics may explain about 50% of periodontitis prevalence
No “host Small “host Moderate “host Large “host

susceptibility” susceptibility” susceptibility” susceptibility”
component component component component
Plaque-
Pristine Non-plaque
induced Grade A Grade B Grade C
health -induced gingivitis
gingivitis
Periodontitis Influence of Periodontal susceptibility

Periodontitis resistance
susceptibility in smoking and tissue destruction
presence of local inconsistent with
risk factors local risk factors
• Figure 1.6.3 Risk factors in relation to a spectrum of periodontal susceptibility.
Host factors Parasite factors
Inflammatory Immunological Bacterial Bacterial

response response load composition
Modulators of the above Virulence factors, toxins,

(e.g. drugs, diabetes, smoking) cell-signalling molecules
– +
or Subject-based Site-based
+ risk factors risk factors
Modulation by
e.g. PMNL function e.g. plaque
retention factors
Periodontal tissue
destruction
• Figure 1.6.4 How systemic (subject-based) modifying and local (site-based) predisposing risk factors
underpin the periodontitis process.
TABLE
1.6.1 Levels of evidence for the common risk factors in periodontitis
Good evidence, Some evidence, Some evidence, true Good evidence, true
putative risk factor putative risk factor risk factor risk factor
Genetics ✓
Age ✓
Nutrition ✓
Smoking ✓
Diabetes ✓
Stress ✓
Poor oral hygiene ✓
(Michalowicz etal. 2000). Evidence is stronger for grade employing gene therapies have not been performed to
C forms of periodontitis, where the attachment loss is assess their ecacy in improving periodontal outcomes.
inconsistent with local risk factors (formerly called aggres- Periodontitis is a complex disease and, just as it is regarded as
sive periodontitis). However, genetics cannot be described being polymicrobial and poly immune-inammatory in nature,
as a “true” risk factor because intervention studies it can also be regarded as being polygenetic and epigenetic.
Polymorphisms (dierent forms) of specic genes of the studies is emerging that demonstrates marginal improve-
immune-inammatory responses have also been associ- ments in periodontal outcomes demonstrated following
ated with periodontitis and include those aecting single adjunctive use of micronutrients, either as phytonutrients
nucleotides. ese are referred to as single nucleotide poly- in capsules of dried fruit and vegetable concentrates (Chap-
morphisms (SNPs) and occur when one base pair may be ple et al. 2012), or through non-adjunctive twice daily
dierent. is can result in a dierence in the gene product consumption of vitamin C and associated micronutrients
(e.g. a cytokine or cell surface receptor). An example is the within kiwi fruit in the absence of periodontal instrumen-
SNP for the neutrophil receptor that binds antibody, the tation (Graziani etal. 2018). e role of poor nutrition as
FcγR11a receptor. is may confer high or low avidity to a risk factor for periodontitis remains under-researched at
the receptor’s ability to bind antibody. A compound geno- present but could represent a “component cause” in certain
type of interleukin 1β (IL-1β) is also reported which codes patients.
for excess IL-1β cytokine production.
In addition, epigenetic inuences are becoming impor- Smoking
tant in the study of periodontitis. ese are the eects of
agents such as enzymes produced by bacteria, micronutri- Smoking is as close as any risk indicator can get to being a
ents or oxygen radicals which are able to modify genes by true risk factor. It has been estimated that 42% of periodon-
processes such as methylation, reducing their expression and titis may be attributable to smoking (Tomar & Asma 2000).
preventing the gene from being expressed correctly. Smoking has both topical and systemic eects which
place patients at greater risk of periodontitis progression.
Age • Local eêects:
 • Reduced tissue vascularity
Age was not previously regarded as a risk factor for peri-  • Impaired polymorphonuclear leukocyte (PMNL)
odontitis, more that as we get older our lifetime exposure chemotaxis and function (phagocytosis)
to risk factors increases and therefore more periodontitis is • Systemic eêects:
seen in older patients – approximately 60% of over 60-year-  • Decreased salivary IgA
olds in the UK have some periodontitis, and older patients  • Decreased serum IgG
have more severe disease (14% versus 8% respectively)  • Decreased helper T cells
(White etal. 2012). Smokers have been shown to have more pockets, deeper
Age is a dicult risk factor to evaluate because it is not pockets (especially palatally), more recession, more bone
possible to make patients younger; therefore interventions loss and increased tooth loss in comparison to non-smok-
that aim to test the true nature of age as a risk factor are not ers (Fig. 1.6.5). Smokers may also experience more bone
possible. However, as people age their immune system starts loss in upper anterior regions than non-smokers (Baha-
to weaken – a phenomenon called “immune senescence”, rin et al. 2006). Smokers have also been shown to have
reducing our ability to kill pathogens and increasing the less marginal bleeding that can have the eect of masking
collateral tissue damage caused. For this reason, evidence early critical signs (bleeding gums) of periodontitis. e
is accumulating to suggest that age may indeed emerge as a evidence associating smoking with periodontitis is thus
true modifying factor for periodontitis. robust. However, there remains limited evidence from sub-
It is also important to recognise that the population of stantial and suciently powered intervention studies that
the developed world is ageing and patients expect to keep demonstrate improved periodontal outcomes after smok-
their teeth longer. e World Health Organization has set ing cessation.
a target to dene successful dentistry as the retention of 20 Odds ratios (ORs) for periodontitis in smokers vary
teeth at 80 years of age. Periodontitis will therefore become between a three- and seven-fold increased relative risk for
more prevalent in older patients. disease. A dose response exists between smoking and peri-
odontal risk – 10 cigarettes/day increasing risk by 5% and
Nutrition 20 per day increasing risk by 10%. Moreover, serum lev-
els of the stable nicotine metabolite cotinine correlate with
ere is considerable interest in nutrients as both agonists attachment loss, probing pocket depth and alveolar crest
and antagonists of inammatory processes (Chapple 2009). height.
Evidence demonstrates that rened carbohydrate intake e healing response to non-surgical and surgical peri-
drives systemic or “meal-induced” inammation (Monnier odontal therapy is poorer in smokers, and maintenance
etal. 2006). patients who smoke are twice as likely to lose teeth as
Several association studies demonstrate that blood levels non-smokers.
of certain antioxidant micronutrients are inversely related to Based upon the moderate success of smoking cessa-
periodontitis prevalence; for instance, low vitamin C is esti- tion counselling demonstrated by Ramseier et al. (2020),
mated to account for 4% of attachment loss seen in certain the S3-level treatment guideline 1.6 strongly recommends
populations (Chapple & Matthews 2007). Blood total anti- smoking cessation counselling in the management of peri-
oxidants show similar results. Evidence from intervention odontitis (Sanz etal. 2020, West etal. 2021).
• Figure 1.6.5 Generalised periodontitis in a heavy smoker. • Figure 1.6.6 Poor oral hygiene and gingivitis around subgingival
crown margins.
Diabetes and Obesity
ere is reportedly a “bi-directional relationship” between It has also been demonstrated that patients under nancial
diabetes mellitus and periodontitis (Taylor 2001), whereby stress and strain had greater levels of periodontitis, but those
the presence of one condition adversely aects the other. who had good coping strategies had no more disease than
Severe periodontitis adversely aects glycaemic control in unstressed controls.
diabetes and glycaemia in non-diabetes patients, and there Stress triggers neuroendocrine responses via the hypotha-
is a direct and dose-dependent relationship between peri- lamic–pituitary–adrenal (HPA) axis. is in turn triggers
odontitis severity and diabetes complications. Emerging the activation of complement and the release of proinam-
evidence supports an increased risk for diabetes onset in matory cytokines.
patients with severe periodontitis and mechanisms appear ere is also evidence that certain periodontal pathogens
to involve elevated systemic inammation (acute-phase are able to utilise stress hormones like noradrenaline and
and oxidative stress biomarkers) resulting from the entry of adrenaline to acquire iron for growth and virulence (Roberts
periodontal organisms and their virulence factors into the etal. 2005). Additionally, they appear to produce an auto-
circulation (Chapple & Genco 2013). Whereas the 2020 to inducer of their own growth in response to the same stress
2021 S3-level guidelines returned an open recommendation hormones (Roberts etal. 2002), indicating that certain peri-
(recommendation 1.10) for interventions aimed at weight odontal bacteria can take advantage of a stressed host.
loss through lifestyle modication, indicating insucient
evidence currently, there was a strong recommendation (rec- Poor Oral Hygiene
ommendation 4.19) for the promotion of diabetes control
interventions in periodontitis patients during maintenance e evidence for the oral biolm as a true risk factor for gin-
therapy (Sanz etal. 2020, West etal. 2021). In support of givitis is strong (see Figure 1.6.6), based upon the original
this a consensus report and guidelines produced jointly by experimental gingivitis study of Löe et al. (1965). In this
the EFP and International Diabetes Federation in 2018 study, volunteers were prevented from tooth brushing for
strongly advise joint care pathways for physicians and dental 21 days to allow plaque accumulation. Gingivitis developed,
professionals in managing diabetes for periodontal benet and when the biolm was removed the gingivitis resolved.
(Sanz etal. 2018), and in the UK an NHS commissioning A study in 2009, however, challenged the simplicity of
standard was published in 2020 requiring the same joined- this paradigm (Baumgartner et al. 2009). Ten volunteers
up approach (NHSE 2019). placed on a diet free from simple rened sugars were pre-
vented from brushing for 4 weeks, and while oral biolm
KEY POINT 6 accumulated signicantly, bleeding scores signicantly
Control of periodontitis can only be achieved if systemic and reduced. us the bacterial biolm is a “component cause”
local risk factors are properly assessed and managed. of gingivitis, but there appear to be other factors, equally as
powerful, such as simple rened sugar intake, which con-
tribute towards disease by driving inammation.
Stress Biolm accumulation is essential for periodontitis to
develop but, as it does not cause periodontitis in all patients,
e evidence for stress per se as a risk factor for periodontitis it is regarded as the trigger for disease initiation but not the
is weak; however, there is evidence that poor coping strategies sole cause. e amount of biolm necessary to induce peri-
may negatively aect periodontitis (Wimmer etal. 2002). odontitis, or cause periodontitis progression, varies between
patients and, in any individual, the biolm needs to reach mapped to the steps of care under the S3-level treatment
a “threshold” level for disease to occur. Some patients will guidelines (West etal. 2021).
never develop periodontitis (Lӧe et al. 1986) even if they At the start of treatment, analysis is at the patient level
never brush their teeth, because they are inherently resistant but, as treatment progresses, increasing levels of detail can
to disease development. be employed.
Using the experimental gingivitis model, Bamashmous
et al. (2021) demonstrated three unique clinical inam- Risk Assessment – The Third Dimension
matory phenotypes, which they termed “high”, “low” and
“slow”, in relation to the development of gingival inam- Risk assessment should help clinicians to formulate an eec-
mation. ey mapped various host mediators and micro- tive management plan for a periodontitis patient and to
bial species in the three groups and demonstrated that key establish the frequency of recall intervals for supportive care.
inammatory mediators were not associated with clinical Traditionally, periodontitis management and treatment
gingival inammation in the slow group, where higher lev- planning have been based on a detailed patient history
els of Gram-positive commensal organisms were evident. and examination, but including risk assessment as a third
e low clinical response group exhibited low host media- dimension will tailor a more appropriate treatment plan for
tors compared with the high responder group, despite a an individual patient (Figure 1.6.8).
similar microbial prole in plaque. Interestingly, neutrophil
and bone activation modulators were down-regulated in Risk Assessment Technologies
all response groups, indicating protective tissue and bone
responses during the development of experimental gin- Risk assessment should form a fundamental part of any pre-
givitis. Similar work by Scott and colleagues enabled the ventative practice.
mapping of the clinical and biological phenotypes of experi- Risk assessment tools are already a component of com-
mental gingivitis patients (Scott etal. 2012). prehensive dental and periodontal evaluations as well as part
of all periodic dental and periodontal examinations in many
Periodontal Risk Assessment practices (Busby etal. 2013).
ere are dierent ways of assessing risk, including
Periodontal risk is multifactorial and risk assessment for online tools that oer consistent and accurate scoring and
patients dictates that dierent analytical levels of risk should visual biofeedback to patients. is reduces the need for
be employed at dierent stages of treatment. us multi- complex therapy, in turn leading to an improvement in oral
level risk assessment is necessary (Figure 1.6.7) and can be health with reduced healthcare costs for the patient. One
Patient-level/subject-based risk factors
Mouth-level Tooth-level risk factors

risk
Number of diseased sites
Site-level risk factors
Initial Education PMPR: Scaling of Reinforce step-1 & Post-advanced Maintenance

presentation phase- teeth crowns, subgingival PMPR therapy: phase
post-OHI correct plaque (root surface Tx/RSD) surgical/drug
retention factors delivery
Step 1 therapy Step 2 Step 3 Step 4
Increasing cost & decreasing effectiveness
• Figure 1.6.7 Multilevel risk assessment, taking the treatment stage into account.
Increased risk
More aggressive
treatment
Decreased risk
Less aggressive
Symptoms
treatment
High risk
Low risk History

• Figure 1.6.8 Risk assessment as a third dimension in patient • Figure 1.6.9 Biolm retention around an orthodontic appliance is act-
management. ing as a local risk factor.
study investigating the use of a periodontal risk calcula- KEY POINT 8

tor (PRC) concluded that risk scores determined using a Local risk factors act by allowing plaque retention in localised
PRC predict future periodontal status with a high degree of areas.
accuracy and validity (Page etal. 2003). e 11th European
Workshop in Periodontology assessed risk assessment tools Local risk factors include:
via systematic reviews and in their consensus stated that • Iatrogenic (restorations, appliances, crown and bridge)
the PRC and another system called the PRA (periodontal • Anatomical (e.g. root groove)
risk assessment) could improve clinicians’ ability to iden- • Root caries
tify, communicate and manage periodontitis patients (Lang • Tooth malalignment
et al. 2015). Perhaps more importantly, Asimakopoulou • False/true pockets
and colleagues (2015) demonstrated in a randomised con- • High frenal attachment
trolled trial (RCT) in primary care dental practice that using • Calculus
a risk assessment tool (PRC/PreViser) to provide person- • Oral dryness.
alised biofeedback as an intervention for behaviour change
signicantly improved psychological outcomes, compared
Iatrogenic
with a routine consultation. Patients took their disease
more seriously, understood their susceptibility and experi- ese are factors introduced by poor design or execution of
enced higher self-ecacy (Asimakopoulou etal. 2015). In a dental procedures, examples of which include defective resto-
subsequent RCT, the same group demonstrated that using ration margins or crowns, poorly designed dentures, bridges
the same electronic system for biofeedback and motivation or appliances with excessive gingival coverage (Figure 1.6.9).
signicantly improved gingival bleeding, plaque levels and Common examples of local iatrogenic risk factors
interdental cleaning habits at 3 months (Asimakopoulou include:
et al. 2019). is was the rst time a behaviour change 1. Removable partial denture design
intervention alone had been demonstrated to improve clini- In terms of the periodontal tissues, the key features
cal periodontal outcomes. important in designing a removable partial denture are:
• ɨe appliance must be kept free of gingival margins (no
KEY POINT 7 colleting)
Risk assessment forms a fundamental part of a modern • Tooth supported
preventive dental practice. • Minimal soft tissue coverage
• Cobalt chrome framework if possible
Local Risk (Predisposing) Factors 2. Crown/bridge design
e key features that are important in designing a crown
Local risk factors may have an important role in the ini- are:
tiation and propagation of periodontal diseases and act by • Ideally supragingival crown margins
allowing retention of biolm at the gingival margin leading • Point contact with neighbouring teeth
to an inammatory response. • No overhangs
A wide range of local factors exists and management • Adequate embrasure space
involves removal or modication of the factor along with • No occlusal trauma
detailed home care instruction on subsequent biolm dis- • No excess cement
ruption by the patient. • Instructions to patient in cleaning
• Figure 1.6.10 Root caries, subgingival restoration margins and calcu- • Figure 1.6.11 Signicant supragingival calculus formation impeding
lus acting as local risk factors for periodontitis. adequate biolm control.
Calculus
3. Bridge pontic design e presence of calculus deposits may result in biolm accu-
e key features that are important in designing a bridge mulation (Figure 1.6.11).
pontic are:
• Ideally supragingival margins Oral Dryness
• No overhangs
• Adequate embrasure space e 2017 WWC identied oral dryness as a key predis-
• Adequate support of abutment teeth posing factor for periodontal disease. A lack of salivary
• Hygienic pontic design. ow, availability or alterations in saliva rheology can cause
reduced cleansing of tooth surfaces and enhanced biolm
accumulation. Mouth breathing or an incompetent lip seal
Anatomical have similar eects (Mizutani etal. 2015).
Anatomical factors may result in biolm retention due to
anatomical anomalies of the dental hard tissues; examples Acknowledgement
include furcation involvement, root grooves and enamel
projections. is chapter is based on a session within e-Den which Pro-
fessor Chapple and Professor Milward produced in 2011.
Root Caries Acknowledgement is given to the Faculty of Dental Surgery
of the Royal College of Surgeons of England for giving per-
e presence of caries on the root surface can result in local mission for material from the e-Den session to be used in
biolm accumulation adjacent to the gingival tissues (Figure this chapter.
1.6.10). Multiple choice questions on the contents of this chapter
are available online at Elsevier eBooks+
Tooth Position
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SECTION 2
Periodontal Diagnosis and Prognosis
69
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2.1
Classiöcation and
Diagnosis of Periodontal
Diseases
PH I L I P OW E R
CHAPTER OUTLINE
Introduction The 2017 Classiöcation System
Classiöcation Is Not the Same as Diagnosis Staging and Grading in the 2017 Classiöcation System
Previous Classiöcation Systems Implementation of the 2017 Classiöcation System in Clinical
The 1999 Classiöcation System Practice
I. Gingival diseases The BSP Implementation of the 2017 Classiöcation System in
II. Chronic periodontitis General Practice
III. Aggressive periodontitis Establishing the Periodontal Diagnosis
IV. Periodontitis as a manifestation of systemic disease Summary
V. Necrotising periodontal diseases
VI. Periodontal abscesses
VII. Developmental or acquired deformities or conditions

This chapter will describe the various systems that have been devised to classify periodontal diseases, the objective of disease classication
being to help clinicians develop the most appropriate therapeutic approaches for patients with these conditions, although the important
distinction between classication and diagnosis will be discussed. Numerous classication systems have been devised in the past, and
inevitably the increase in knowledge about the pathogenesis of periodontal diseases over the years has necessitated the revision of
classication systems. The only systems that will be described in any detail in this chapter are those that are in current usage, namely those
that arose from World Workshop proceedings in 1999 (Armitage 1999) and 2017 (Tonetti etal. 2018). The British Society of Periodontology
and Implant Dentistry (BSP) modication of the 2017 World Workshop classication system will be explained in detail, as this is the most
appropriate system to be used in a general practice setting.
This chapter covers the following topics: • Staging and grading in the 2017 classiöcation system
• Background • Implementation of the 2017 classiöcation system in clinical
• Classiöcation is not the same as diagnosis practice
• Previous classiöcation systems • The BSP implementation of the 2017 classiöcation system in
• The 1999 classiöcation system general practice
• The 2017 classiöcation system • Establishing the periodontal diagnosis
• Summary
Introduction present as a wide range of conditions aecting the tooth-

supporting tissues, classication is, and has been, most com-
Classication of any disease is important in terms of helping monly dened in terms of pathological loss of tooth support
to determine the most accurate diagnosis and thus the most and presenting symptoms. Many classication systems for
appropriate care for a patient, as well as forming the basis periodontal diseases have existed in the past, but as ongo-
for research into disease pathology, aetiology and epidemiol- ing research has contributed to the knowledge of these dis-
ogy. Diseases may be classied in terms of cause, pathogen- eases, so classication systems have had to adapt to this new
esis or symptoms. In the case of periodontal diseases, which knowledge.
71
72 SECTION 2 Periodontal Diagnosis and Prognosis
Classification Is Not the Same as Diagnosis 1999. e 1999 World Workshop in Periodontics Classi-
cation System (Armitage 1999) was in widespread use up
A common misconception of classication is that the name until 2017 when a new World Workshop on the Classica-
given to a disease forms the diagnosis and that, in turn, a tion of Periodontal and Peri-implant Diseases and Condi-
specic treatment approach is then indicated. However, the tions was held, co-sponsored by the AAP and the European
name given to a disease is just that, a label, and this is not Federation of Periodontology (EFP), with the proceedings
the same as a comprehensive diagnosis, which should take of this workshop being published in 2018. e 1999 and
into account a variety of other factors. Classication is thus 2017 classication systems are the main systems in current
historical and tells the clinician little or nothing about the use globally, although it is anticipated that the latest system
patient’s current disease status. For example describing a will gradually become the predominant system used to clas-
patient as having chronic periodontitis (using the older classify periodontal and peri-implant diseases. e 1999 sys-
sication system) doesn’t tell the clinician anything about tem will be described briey, and the 2017 system will be
whether the disease is stable or progressive, mild, moder- described in more detail in this chapter.
ate or advanced, how the disease is distributed or what led
the patient to develop the condition in the rst place. us KEY POINT 2
treating a patient on this basis alone would not necessar- The most common classication systems in current use for
ily manage their condition appropriately. A proper diagno- periodontal diseases are the 1999 and 2018 systems, but the
sis on the other hand includes the classication term but latter will become predominant.
should also include information about the patient’s current
disease status and the risk prole of the patient. It is only
The 1999 Classification System
by arriving at this detailed diagnosis that the most appro-
priate treatment plan can be formulated for the patient. In e 1999 World Workshop in Periodontics proposed a clas-
this example the patient may be classied as having chronic sication system (Armitage 1999) which was in use for 19
periodontitis, but a full diagnosis may be generalised moder years. e main dierence between this system and numer-
ate chronic periodontitis, widespread pocketing and bleeding ous predecessors was that it dispensed with age as a criterion.
on probing with smoking and uncontrolled diabetes as risk fac Previous classication systems had related more aggressive
tors. It is only the full diagnosis that can help the clinician forms of periodontitis to age, but the 1999 system sought to
to formulate the most appropriate treatment plan for that identify this type of disease, which was often seen in younger
individual patient. In recent years the failure to diagnose patients, based on clinical, radiographic and historical nd-
periodontal diseases has become one of the most common ings alone. In addition, refractory periodontitis (that is,
reasons for dental litigation in the UK (Briggs 2014). periodontitis not responding to therapy) was no longer rec-
ognised. is emphasised evidence at the time that indicated
KEY POINT 1 that it should be possible to identify why a patient did not
Classication is not the same as diagnosis; diagnosis includes respond to treatment as expected. Periodontitis was classied
the classication term but should also include information as chronic (generalised and localised), aggressive (generalised
about the patient’s current disease status and the risk prole of
and localised), necrotising and as a manifestation of systemic
the patient.
disease. e full 1999 classication system was as follows:
I. Gingival diseases
Previous Classification Systems  • Dental plaque-induced gingival diseases
 • Non-plaque-induced gingival lesions
e rst attempt to classify diseases of the periodontium II. Chronic periodontitis
was made by Pierre Fauchard in 1728. Since then many  • Localised
classication systems have been devised to reect develop-  • Generalised
ing understanding of the causes and eects of these com- III. Aggressive periodontitis
mon conditions. e term pyorrhoea (from the Greek,  • Localised
meaning “discharge of matter”) was rst used in the early  • Generalised
20th century, and this is still a term that clinicians may hear IV. Periodontitis as a manifestation of systemic diseases
used by some older patients today. In 1977 the American  • Associated with haematological disorders
Academy of Periodontology (AAP) Classication system  • Associated with genetic disorders
(Ranney 1977) identied a more aggressive form of peri-  • Not otherwise speciëed
odontitis seen in younger patients with low levels of plaque,  V. Necrotising periodontal diseases
often aecting rst molars and incisors. e term juvenile  • Necrotising ulcerative gingivitis
periodontitis was used to describe this particular group of  • Necrotising ulcerative periodontitis
patients, distinguishing this condition from the more com- VI. Abscesses of the periodontium
mon form, adult periodontitis. is distinction was further  • Gingival abscess
developed in subsequent classication systems in 1989  • Periodontal abscess
(American Academy of Periodontology 1989), 1993 and  • Pericoronal abscess
CHAPTER 2.1 Classication and Diagnosis of Periodontal Diseases 73
 • Periodontitis associated with endodontic lesions V. Necrotising Periodontal Diseases

 • Combined periodontic-endodontic lesions • Necrotising ulcerative gingivitis presenting as interdental
VII. Developmental or acquired deformities and conditions ulcers (giving a “punched-out” appearance) but with no
 • Localised tooth-related factors that modify or bone loss, often in younger patients with smoking, stress
predispose to plaque-induced gingival diseases/ and poor diet as common factors.
periodontitis • Necrotising ulcerative periodontitis as above but with the
 • Mucogingival deformities and conditions around addition of bone loss.
teeth
 • Mucogingival deformities and conditions on eden VI. Abscesses Arising from the Periodontium
tulous ridges Abscess formation aecting the gingiva only, or both the
 • Occlusal trauma gingival and periodontal tissues, and requiring specic treat-
ment strategies.
KEY POINT 3
1999 Classication system – major groups:
VII. Developmental or Acquired Deformities and
I. Gingival diseases
Conditions
II. Chronic periodontitis
III. Aggressive periodontitis • Tooth-related factors that modify the risk of plaque-
IV. Periodontitis as a manifestation of systemic disease related gingival and/or periodontal disease such as
V. Necrotising periodontal diseases enamel pearls and diverticulated roots.
VI. Periodontal abscesses • Mucogingival deformities and conditions around teeth
VII. Developmental or acquired deformities or conditions that modify the risk of plaque-related gingival and/or
periodontal disease, such as recession defects.
e principal clinical and radiographic signs and symp- • Mucogingival deformities and conditions on edentulous
toms of the categories in the 1999 classication system were ridges.
as follows. • Occlusal trauma modiëes the response of the gingival
and periodontal tissues to plaque.
I. Gingival Diseases
• Mostly plaque-induced, chronic gingivitis being the The 2017 Classification System
most common.
• Characterised by gingival inìammation (redness, With advances in knowledge from both clinical and labora-
oedema, bleeding) but with no loss of attachment (LOA) tory research over the last two decades the time was right
or radiographic bone loss. for the introduction of a new classication system, both
for periodontal diseases and also for those aecting the
II. Chronic Periodontitis peri-implant tissues. e international workshop that took
• Inìammation of the gingivae as above but with evidence place in 2017 comprised four main working groups, which
of LOA and radiographic bone loss. considered:
• Mild (LOA 1–2 mm), moderate (LOA 3–4 mm) or • Periodontal health, gingival diseases and conditions
severe (LOA over 5 mm). • Periodontitis
• Radiographic evidence of bone loss, typically horizontal. • Other conditions aêecting the periodontium
• Generalised (more than 30% of sites aêected) or local- • Peri-implant diseases and conditions.
ised (less than 30% of sites aêected). Table 2.1.1 shows the four working groups and their
subject areas. e full consensus reports of the four work-
III. Aggressive Periodontitis ing groups are freely available online at https://onlinelibra
• Rapid LOA (more than 2 mm per year) and bone loss. ry.wiley.com/toc/1600051x/2018/45/S20, and a summary
• Bone loss usually vertical. of the dierences between the 1999 and 2017 classica-
• Often familial aggregation. tion systems was published by the AAP in 2018 (Caton
• Localised if no more than two teeth apart from ërst et al. 2018). e recommendations of Working Group 4
molars and incisors aected (that is all eight incisors and (peri-implant diseases and conditions) will be considered
all four rst molars as well as two other teeth), otherwise in Chapter 7.3.
generalised (Higheld 2009). e main dierences between the 2017 classication sys-
• Tissue destruction greater than would be expected given tem and the 1999 system are as follows:
plaque and calculus levels. • For the ërst time in any classiëcation system, periodontal
health was clearly dened.
IV. Periodontitis as a Manifestation of Systemic • Chronic and aggressive periodontitis were replaced with
Diseases a model based on stages and grades.
Periodontitis that may be associated with systemic disor- • A personalised medicine approach was adopted.
ders; see Chapter 2.4. • Peri-implant diseases and conditions were included.
TABLE World Workshop on the Classication of Periodontal and Per-implant Diseases and Conditions
2.1.1 07 – Working Groups
Classification of periodontal and peri-implant diseases and conditions 2017
Periodontal diseases and conditions
Periodontal health, gingival diseases Periodontitis Other conditions affecting the periodontium
and conditions Papapanou, Sanz et al. 2018 consensus Rept link
Chapple, Mealey, et al. 2018 consensus Rept link Jepsen, Caton et al. 2018 consensus Rept link
Jepsen, Caton et al. 2018 consensus Rept link
Trombelli et al. 2018 case definitions link Papapanou, Sanz et al. 2018 consensus Rept link
Tonetti, Greenwell, Kornman. 2018 case definitions link
Systemic
Periodontal
disease or
Gingival Abscesses Tooth and
Periodontal Gingivitis: Necrotizing Periodontitis as a conditions Mucogingival Traumatic
diseases: and prosthesis
health and Dental periodontal Periodontitis manifestation of affecting the deformities occlusal
Non-dental Endodontic- related
gingival health biofilm-induced diseases systemic disease periodontal and conditions forces
biofilm-induced Periodontal factors
supporting
lesions
tissues
Peri-implant diseases and conditions

Berglundh, Armitage et al. 2018 consensus Rept link
Peri-implant soft and

Peri-implant health Peri-implant mucositis Peri-implantitis
hard tissue deficiencies
Reprinted from Journal of Clinical Periodontology 45(S20):8, Maurizio S Tonetti et al. (2018), with permission from John Wiley & Sons.
KEY POINT 4 periodontal destruction (attachment and bone loss) being

an irreversible process.
Main changes in the 2018 classication system:
• Periodontal health clearly dened.
• Aggressive periodontitis not recognised as a separate KEY POINT 5
condition. Staging describes the severity of disease in a patient.
• Periodontitis classied in terms of stages and grades. Grading describes the level of that individual’s susceptibility
• Peri-implant diseases and conditions included. to disease.
Perhaps the most radical of these principal dierences Staging involves assessment of the following:
was the replacement of the long-recognised distinction • site of greatest attachment loss
between chronic and aggressive periodontitis with a univer- • bone loss (single worst site)
sal system that sought to capture the severity, extent and rate • tooth loss (due to periodontitis)
of progression of a patient’s disease, based on the lack of sci- • other factors (maximum pocket depth, pattern of bone
entic evidence that these were distinct conditions. In other loss, furcation involvement, ridge defects, occlusal
words, although chronic and aggressive periodontitis were trauma, restorative needs).
in the past regarded as separate conditions, they are now rec- Grading involves assessment of the following:
ognised as variations on the same spectrum of disease. How- • bone and attachment loss over a 5-year period
ever, it was also considered that there was a specic clinical • the ratio of percentage bone loss to age
phenotype of extreme periodontal destruction aecting the • the relationship between bioëlm volume and level of
molars and incisors of young patients, previously referred periodontal destruction
to as localised juvenile periodontitis, that was now being • levels of smoking
described as a molar/incisor pattern (MIP) of disease. • blood glucose status.
is detailed system of periodontal classication has been
Staging and Grading in the 2017 Classification summarised in a downloadable practice resource from the
System AAP that can be found at https://www.perio.org/2017wwdc.
e original staging and grading guidance from Tonetti etal.
e 2017 classication system uses a staging and grading (2018) is reproduced in Appendix 1. However, it should be
system (similar to that used in cancer diagnoses) in which appreciated that the staging and grading of a periodontal
staging describes the severity of disease in an individual patient only reects that patient’s historical disease experi-
patient (based on the worst-aected site in the mouth) and ence and that staging and grading alone does not inform the
grading describes the level of that individual’s susceptibility clinician about the patient’s current disease status, which is
to disease. An important underlying principle of staging is indicated principally by probing pocket depths (PPD) and
that it is carried out at initial assessment and that patients bleeding on probing (BoP). Not taking these commonly mea
cannot subsequently reduce their stage, a consequence of sured clinical features into account as part of the diagnosis
risks misdiagnosing the periodontal patient; for example, the classication system, an infographic was produced to show
treatment needs of an untreated periodontal patient with how the workow between BPE screening and a full peri-
pocketing and bleeding will be very dierent from those of odontal diagnosis could be achieved. is infographic can be
a treated periodontal patient with little pocketing or bleed- downloaded from the BSP website at www.bsperio.org.uk
ing, even though their staging and grading may be identi- and is reprinted in Appendix 2. A summary of the algorithm
cal. In addition it should be remembered that a periodontal used to prepare the infographic is shown in Figure 2.1.1.
patient is a periodontal patient for life, and even apparently e BPE system is designed to distinguish between gingival
stable patients can experience recurrent episodes of periodon- and periodontal health, and gingivitis and periodontitis, and
tal destruction if their personal and professional periodontal to indicate when further investigation of periodontal con-
maintenance slips or if their risk factor prole changes. Stag- ditions needs to be carried out. Periodontal patients (BPE
ing and grading of periodontitis therefore has its limitations code 3 and 4) will require a detailed medical and dental
and should not be used as a diagnostic tool in isolation. history, more detailed oral examination and further investi-
gations such as special tests and radiographs that will allow
Implementation of the 2017 Classification dierentiation between dierent types of disease (gingivitis,
System in Clinical Practice periodontitis, periodontitis associated with systemic disease,
necrotising periodontal disease and so on) and, when appro-
ere is no doubt that the 2017 classication system is priate, a full periodontal diagnosis will then need to be per-
a more detailed and scientically robust diagnostic tool formed, as shown in Fig 2.1.1.
than previous systems. Such a system should result in more e BSP implementation of the 2017 classication sys-
appropriate therapeutic strategies and more personalised tem accepts the four stages of severity (I – mild, II – mod-
treatment plans for periodontal patients. However, whereas erate, III – severe, IV – very severe) and the three grades
the 2017 system lends itself to research and specialist prac- of progression (A – slow, B – moderate, C – rapid), but
tice, after publication of the World Workshop proceedings the attribution of stage/grade to an individual patient has
in 2018 some doubts were raised about the practicalities been simplied to enable clinicians to do so quickly and
of adopting such a complex system in general dental prac- consistently. Recognising that clinicians in general prac-
tice. Guidance on the implementation of the new system tice already routinely assess periodontal disease severity by
in clinical practice and education was published in 2019 means of pocket depths (not attachment levels, which are
(Tonetti & Sanz 2019), but concerns remained that the rarely used in a practice setting) and bone levels, and that the
system, as recommended by the World Workshop, was still bone level is the most useful and objective determinant for
too complex to be used in a general practice setting. In severity, the BSP implementation plan proposed bone level
2018 the British Society of Periodontology and Implant (at the worst aected site) as the sole determinant for sever-
Dentistry (BSP) formed a working group to consider these ity, depending on whether the bone loss was less than 15%
diculties, and in 2019 the BSP published an adaptation or was within the coronal, middle, apical third of the root
of the 2017 classication that would allow dentists and (see Table 2.1.2). is method of stage assessment requires
hygienists to adopt a more practical approach to imple- radiographs, but these are highly likely to be in existence in
ment the new system in such settings (Dietrich et al. any event as a result of routine patient examinations (which
2019). Following publication, this modied implemen- periodically require the taking of bitewing radiographs) and
tation scheme has received widespread acceptance in the the BPE because the BSP’s BPE Guidelines (British Society
profession, not only in the UK but also globally. of Periodontology 2016) require the existence of suitable
radiographs for all BPE code 3 and 4 sextants (see Chapter
KEY POINT 6 2.2). It was also recognised, in the BSP modication pro-
The British Society of Periodontology and Implant Dentistry posals, that the radiograph was a crucial component of grad-
has modied the 2017 World Workshop classication system ing in the World Workshop system, specically the extent
for use in general dental practice. of bone loss in relation to the age of the patient, a ratio that
most clinicians would be assessing instinctively; for example
The BSP Implementation of the 2017 20% bone loss in an 80- or 90-year-old patient would not
cause the clinician any great alarm, unlike the same amount
Classification System in General Practice
of loss in a 20- or 30-year-old. e comparison of succes-
One of the objectives of the BSP implementation of the sive radiographs (as proposed in the World Workshop) is
2017 World Workshop classication system was to describe often impractical in the general practice setting and such
how the BSP’s Basic Periodontal Examination (BPE) Guide- information adds little useful information to that obtained
lines (British Society of Periodontology 2016), which have from the percentage bone loss/age ratio alone. Similarly,
been widely used by UK clinicians as a means of screen- the inclusion of specic risk factors (biolm volume, smok-
ing all patients for periodontal status for many years, could ing and diabetes) in grade determination, as proposed in
be integrated into the new system. e BPE guidelines the World Workshop, also provides little additional infor-
are described in more detail in Chapter 2.2, but as part of mation because the percentage bone loss/age ratio shows
the BSP’s implementation recommendations for the new a patient’s lifelong exposure to such risk factors, although
History
Extraoral examination
lntraoral examination
Evidence of periodontitis?
(interdental recession)
No Yes
BPE
Yes Take and/or assess Take and/or assess

BPE code 3 or 4? appropriate appropriate
radiographs radiographs
No
Yes
No
<10% BoP? BPE code 4?
Yes No (code 3)
Initial periodontal
Yes treatment
>30% BoP?
No Full periodontal assessment

(incl. detailed pocket chart)*
MIP?
No
Yes
<30% of
teeth?
No
Yes
Periodontal Localised Generalised Periodontitis Localised Generalised

health gingivitis gingivitis molar/incisor pattern periodontitis periodontitis
• Staging/grading
Risk factor assessment • Risk factor assessment
• Assessment of current disease status**
• Currently stable
• Currently in remission
• Currently unstable
Definitive diagnosis / treatment planning
• Figure 2.1.1 Algorithm for screening and assessment of periodontal status. BPE, Basic periodontal
examination; BoP, bleeding on probing; MIP, molar incisor pattern. *A diagnosis of periodontitis requires
radiographic bone loss at two non-adjacent teeth that cannot be attributed to causes other than periodon-
titis. **See Table 2.1.4. (Reprinted by permission from Springer Nature: Br. Dent. J. Periodontal diagnosis
in the context of the 2017 classication system of periodontal diseases and conditions - implementation in
clinical practice, Dietrich, T., Ower, P., etal., copyright 2019.)
TABLE
2.1.2 Staging of periodontitis (BSP modication 09)
Stage I Stage II Stage III Stage IV

(early/mild) (moderate) (severe) (very severe)
Maximum %
<15% or <2 mm** Coronal third Mid third Apical third
interproximal bone loss
Describe as:
• Localized (up to 30% of teeth)
Extent
• Generalised (more than 30% of teeth)
• Molar/incisor pattern
** Measurement in mm from cemento-enamel junction if only bitewing radiograph available (bone loss) or if no radiographs clinically justied (clinical attachment level)
(
conditions - implementation in clinical practice, Dietrich, T., Ower, P., etal., copyright 2019. )
TABLE
2.1.3 Grading of periodontitis (BSP modication 09)
Grade A Grade B Grade C

(slow) (moderate) (rapid)
Maximum % bone loss/age <0.5 0.5–1.0 >1.0
(Reprinted by permission from Springer Nature: Br. Dent. J. Periodontal diagnosis in the context of the 2017 classication system of periodontal diseases and
conditions - implementation in clinical practice, Dietrich, T., Ower, P., etal., copyright 2019. )
assessment of these risk factors will inevitably form part of describes stable, unstable and “in remission” periodontal
the diagnosis, if not the classication of disease. e BSP patients, further adapting cancer diagnosis principles. Fur-
therefore recommended that the ratio of percentage bone thermore, unlike the World Workshop assessment of cur-
loss to age was the main determinant for grade, or rate of rent status, which depends on measurement of attachment
progression of periodontal destruction (see Table 2.1.3). levels, the BSP recommended determination of current
However the ranges of the percentage bone loss/age ratios status by PPD and BoP measurements, parameters that
for grade assessment suggested by the World Workshop, have always been routinely used in the general practice set-
which were estimates, did not seem to be of practical use in ting. e criteria for determining current status are shown
a general practice setting, and the BSP modication of the in Table 2.1.4, although it should be noted that the BSP
grading ratios is slightly dierent. e reasoning behind this also recognised that periodontal patients in long-term sup-
departure from the World Workshop recommendation is portive care may have pockets of 5 or 6 mm with no BoP,
complex and is fully explained by Dietrich etal. (2019), to and such patients may well be considered stable, empha-
which readers are referred. In practical terms, using the BSP sizing the importance of clinical discretion when estimat
modication of the classication system means that grade ing current status.
can be quickly determined as follows: Risk factor prole is a crucial part of establishing a
working periodontal diagnosis because such factors will
• Grade A If the maximum percentage bone loss is less than need to be addressed in the earliest stages of treatment plan-
half the patient’s age in years (e.g. <30% in a 60-year-old) ning if successful outcomes are to be achieved. Both sys-
• Grade B All other situations temic and local risk factors (such as tooth position, poor
• Grade C If the maximum percentage bone loss is greater restorations, calculus deposits) need to be considered. Chief
than the patient’s age in years (e.g. >30% in a 29-year-old) among systemic risk factors are diabetic status and smoking
habits, probably the most important factors that need to be
Establishing the Periodontal Diagnosis assessed, and for which the strongest evidence base in the
pathogenesis of periodontitis exists but other, less strongly
Staging and grading therefore establishes the severity of dis- evidence-based factors are also likely be involved and should
ease and the level of patient susceptibility, but in order for a be commented upon. Such putative systemic risk factors
full diagnosis to be made, and for an appropriate and person- include diet, genetics, obesity and stress (see Chapter 1.6).
alised treatment approach to be selected, the current status Full and proper periodontal diagnosis, which includes a
and the risk factor prole of the patient needs to be assessed. stage/grade classication, informs and indeed dictates the
Current status was described by the World Work- appropriate management of the periodontitis patient; a full
shop in terms of a stable patient, an unstable patient or a periodontal diagnosis should therefore contain the follow-
patient with residual inammation. e BSP modication ing elements:
TABLE Determining the current status of a • Distribution generalised, localised or molar/incisor
2.1.4 periodontitis patient (BSP modication pattern
09) • Classiëcation stage/grade
• Current status stable, in remission or unstable
In • Risk factor proële
Stable Remission Unstable
BoP <10% >10% >10%
PPD <4mm <4mm >5mm KEY POINT 7
Diagnosis should include:
4mm sites no BoP no BoP BoP • Distribution
with • Classication
• Current status
BoP: bleeding on probing; PPD: probing pocket depths.
• Risk factor prole
• Figure 2.1.2 Male patient, aged 42, former heavy smoker but with no other risk factors, widespread
pockets of 4–6 mm, most of which display BoP.
An example patient is shown at Figure 2.1.2; this patient British Society of periodontology and Implant Dentistry. e Basic
is male, age 42, a former heavy smoker but with no other Periodontal Examination; 2016. http://www.bsperio.org.uk/publi
risk factors, with widespread pockets of 4–6 mm, most of cations.
which displayed BoP. e full diagnosis for this patient BriggsL. Probing deeper into periodontics claims. DDU Journal;2014:9-21.
https://www.theddu.com/guidance-and-advice/journals/march-
would be:
2014/probing-deeper-into-periodontics-claims.
Distribution – most teeth have some bone loss, so the dis- Caton JG, Armitage G, Berglundh T, et al. A new classication
tribution is generalised. scheme for periodontal and peri-implant diseases and conditions
Classication – the worst aêected site is UR7, where there - introduction and key changes from the 1999 classication. J Peri
is about 50% bone loss in the middle third of the root, odontol. 2018;89(suppl 1):S1S8.
Chapple ILC, Mealey BL, etal. Periodontal health and gingival dis-
making the stage/grade III/C.
eases and conditions on an intact and a reduced periodontium:
Current status – there is pocketing over 4 mm with BoP so consensus report of workgroup 1 of the 2017 World Workshop on
status is unstable. the Classication of Periodontal and Peri‐Implant Diseases and
Risk factor prole – the patient is a former smoker, and Conditions. J Clin Periodontol. 2018;45(Suppl 20):S68–S77.
this should be recorded in the diagnosis because former Dietrich T, Ower P, Tank M, et al. Periodontal diagnosis in the
smokers often take up the habit again. context of the 2017 classication system of periodontal diseases
and conditions - implementation in clinical practice. Br Dent J.
In this case the diagnosis that would be recorded in the 2019;226(1):1622.
patient’s records would be: generalised periodontitis stage Fauchard P. Le chirurgien dentiste, ou traite des dents. Ou l’on ensei
III/grade C, currently unstable, former smoker. gne les moyens de les entretenir propres & faines, de les embellir, d’en
For further examples of periodontal diagnosis using the réparer la pette & de remedier à celles des gencives & aux accidens
2017 classication system (BSP modication), the reader is qui peuvent furvenir aux autres parties voilines des dents. Paris: Jean
referred to the online content of this book. Mariette; 1728.
Higheld J. Diagnosis and classication of periodontal disease. Aust
Dent J. 2009;54(suppl 1):S11–S26.
Summary Jepsen S, Caton JG, etal. Periodontal manifestations of systemic dis-
e classication of periodontal (and peri-implant) diseases eases and developmental and acquired conditions: consen‐ sus
report of workgroup 3 of the 2017 World Workshop on the Clas-
represents a crucial rst step in the management of patients
sication of Periodontal and Peri‐Implant Diseases and Condi-
with periodontal problems, but used alone the classication tions. J Clin Periodontol. 2018;45(Suppl 20):S219–S229.
of periodontal diseases does not provide a thorough enough Papapanou PN, Sanz M, et al. Periodontitis: Consensus report of
framework for subsequent treatment planning. It is important workgroup 2 of the 2017 World Workshop on the Classication
when planning the most appropriate therapeutic approach to of Periodontal and Peri‐Implant Diseases and Conditions. J Clin
take other factors into account, namely current status and Periodontol. 2018;45(Suppl 20):S162–S170.
risk factor prole, in order to arrive at an accurate diagnosis Proceedings of the World Workshop on the Classication of Peri-
which will then inform the treatment-planning process. odontal and Peri-implant Diseases and Conditions. J Clin Peri
Multiple choice questions on the contents of this chapter odontol. 45(Suppl 20):S1S291.
are available online at Elsevier eBooks+. Ranney RR. 1977. Pathogenesis of periodontal disease. In: Proceed
A series of videos demonstrating how to assess the peri- ings of the International Conference on Research in the Biology of
Periodontal Disease. 1977:223–265.
odontium are also available online.
Tonetti MS, Greenwell H, Kornman KS. Staging and grading of
periodontitis: framework and proposal of a new classica-
References tion and case denition. J Clin Periodontol. 2018;45(suppl
20):3S149S161.
American Academy of Periodontology, 1989. In: Proceedings of the Tonetti MS, Greenwell H, Kornman KS. Staging and grading of peri‐
World Workshop in Clinical Periodontics, American Academy of Peri odontitis: Framework and proposal of a new classication and case
odontology, Chicago. 1989:1/23–1/24. denition. J Clin Periodontol. 2018;45(Suppl 20):S149–S161.
Armitage GC. Development of a classication system for periodontal Tonetti MS, Sanz M. Implementation of the new classication of
diseases and conditions. Ann Periodontol. 1999;4:1–6. periodontal diseases: decision-making algorithms for clinical prac-
Berglundh T, Armitage G, etal. Peri‐implant diseases and conditions: tice and education. J Clin Periodontol. 2019;46:398405.
Consensus report of workgroup 4 of the 2017 World Workshop Trombelli L, Farina R, Silva CO, Tatakis DN. Plaque‐induced gin-
on the Classication of Periodontal and Peri‐Implant Diseases and givitis: Case denition and diagnostic considerations. J Clin Peri
Conditions. J Clin Periodontol. 2018;45(Suppl 20):S286–S291. odontol. 2018;45(Suppl 20):S44–S66.
2.2
Periodontal Assessment
and Monitoring
PH I L I P OW E R A N D L E O B R I G G S
CHAPTER OUTLINE
Introduction The Simplied Gingival Index (Ainamo & Bay 1975)
What should be Assessed? Advantages and Disadvantages of the Simplied Gingival
Index
The Basic Periodontal Examination
Assessment of Calculus
How to Record BPE
BPE Scores Assessment of Periodontal Pockets
Advantages and Disadvantages of BPE Probing Pocket Depths
When to Record BPE Inter- and Intra-Operator Variability in Probing
Assessment of Disease Activity Measurements
Other Probing Errors
Marginal Bleeding and Bleeding on Probing
Assessment of Attachment Loss
Assessment of Plaque (BIOFILM)
The Dierence between Probing Pocket Depth and Loss of
Plaque Index (Silness & Löe 1964)
Attachment
Advantages and Disadvantages of the Plaque Index
Simplied Plaque Index (Ainamo & Bay 1975) Assessment of Bleeding on Probing
Advantages and Disadvantages of the Simplied Plaque Assessment of Tooth Mobility
Index Assessment of Furcation Involvement
Quigley Hein Index (Modied by
Probing
Turesky etal. 1970)
Radiographic Assessment
Advantages and Disadvantages of the Quigley Hein Index
Clinical Assessment
Plaque Control Record (O’Leary etal. 1972)
Advantages and Disadvantages of the Plaque Control Assessment of Suppuration
Record Assessment of Bone Support
Assessment of the Gingivae Radiographs in Periodontal Assessment
Appearance Interpretation of Radiographs
Assessment of Gingival Inammation Viewing and Reporting on Radiographs
Gingival Indices New Radiographic Techniques
The Gingival Index (Löe & Silness 1963)
Monitoring a Periodontal Patient
Advantages and Disadvantages of the Gingival Index
80
CHAPTER 2.2 Periodontal Assessment and Monitoring 81

This chapter details commonly used clinical assessment techniques for new patients, recalled patients and patients on longer-term monitoring.
By the end of the chapter the reader should: • Assessment of disease activity
• Be able to describe how to carry out a full assessment of a • Assessment of plaque (bioölm)
periodontal patient • Assessment of the gingivae
• Be aware of the use and limitations of the basic periodontal • Assessment of periodontal pockets
examination (BPE) • Assessment of loss of attachment
• Be able to assess and monitor a periodontal patient. • Assessment of tooth mobility
• Assessment of furcation involvement
The chapter covers the following topics: • Assessment of suppuration
• Introduction • Assessment of bone support
• What should be assessed? • Radiographs in periodontal assessment
• The Basic Periodontal Examination (BPE) • Monitoring a periodontal patient.
Introduction •Calculus and other plaque-retentive factors

•Periodontal pockets
Over the years, various methods have been described for assess- •Recession
ing the condition of the periodontal tissues of a patient. Each •Marginal bleeding
clinician needs to decide which methods they will use to assess •Bleeding on probing
a patient and ensure that their assessment is as consistent as pos- •Mobility of teeth
sible. An understanding of the advantages and disadvantages of •Presence of suppuration (pus)
the various assessment methods is vital and detailed records •Level of alveolar bone support
about the methods used should always be kept. It is fundamen- •Furcation involvements.
tal that there is an understanding of the dierences between ese factors must be considered in the broader context
health and disease. Past disease activity should be distinguished of the patient’s medical and social histories and the other
from current (active) disease. Patients who have been success- oral structures.
fully treated can achieve periodontal health although they may To do this for every patient would be very time consum-
have reduced bone support as well as loss of attachment, which ing and unnecessary. For this reason, the Basic Periodontal
is often seen clinically as recession, residual pocketing and Examination (BPE) was developed as a screening tool for
tooth mobility. e 2017 World Workshop on Classication use in general practice in the UK. Similar systems operate
(Chapple et al. 2018) described periodontal health on both in other countries.
an intact (no past periodontitis) and reduced (past periodon-
titis, treated and stable) periodontium, whilst recognising that The Basic Periodontal Examination
the latter group of patients are at increased risk of recurrent
periodontitis and should be closely monitored throughout life. ɨe BPE was developed by the British Society of Periodontology
Periodontal assessment is therefore a vitally important aspect and Implant Dentistry (BSP) from the Community Periodontal
of periodontal management, both at the start of disease control Index of Treatment Needs (CPITN) (Ainamo etal. 1982). e
and throughout the life of the periodontal patient. CPITN was created to help with workforce planning by assess-
ing treatment need of a population. ɨe BPE was designed as
KEY POINT 1 a fast and simple general practice screening system to identify
Full periodontal assessment should include: patients with periodontal diseases. ɨe purpose of the BPE is
• Plaque to screen for the presence or absence of periodontal diseases.
• Gingival inammation It should not be used for the full assessment of patients with
• Calculus periodontal diseases or for the monitoring of patients who have
• Probing pocket depths (PPD)
been treated for periodontal diseases. It is a hierarchical scor-
• Recession
• Marginal bleeding (MB) ing system which means that the higher the score, the greater
• Bleeding on probing (BoP) the level of disease. Appendix 2, which describes how the 2017
• Mobility classication system can be used to arrive at a diagnosis, also
• Suppuration describes how BPE is mapped to the new classiëcation system.
What should be Assessed? How to Record BPE

e ideal periodontal assessment of a patient should take 1. e dentition is divided into six sextants: e upper right
into consideration all of the following: posterior sextant (UR7–UR4); the upper anterior sex
• Plaque tant (UR3–UL3); the upper left posterior sextant (UL4–
• Gingival inìammation UL7).ɨe lower right posterior sextant (LR7–LR4); the
lower anterior sextant (LR3–LL3); the lower left poste 5.5 mm in the sextant and at least one tooth with a furca-
rior sextant (LL4–LL7). tion involvement.
2. All teeth in each sextant are examined except for third
molars. Advantages and Disadvantages of BPE
3. For a sextant to qualify for recording, it must contain at
least two teeth. If only one tooth is present in a sextant, ɨe BPE is a quick and simple method of establishing a provi-
the score for that tooth is included in the recording for sional diagnosis of periodontal health, gingivitis or periodon-
the adjoining sextant. titis in patients with or without overt signs of periodontal
4. A WHO (World Health Organization) probe is used. diseases. In addition, because sextants are scored, it helps to
is has a “ball end” 0.5 mm in diameter and a black produce a simple map of the healthy and diseased areas of
band from 3.5 to 5.5 mm. A probing force of 20–25 the mouth. However, the hierarchical scoring assumes that a
grams should be used. A picture of this probe is shown higher score is worse than a lower score. is is not always the
earlier in this book (see Figure 1.3.1). case. For example, a patient may have a 6 mm pocket with no
5. e probe should be “walked around” the sulcus or pock- recession, which would give a score of 4. However, this pocket
ets in each sextant, and the highest score recorded. As soon may be easily accessible to oral hygiene and debridement so
as a code 4 is identiëed in a sextant, the clinician can then should be relatively simple to treat compared to a tooth which
move directly on to the next sextant, though it may be has large calculus deposits in a more inaccessible site in the
better to continue to examine all sites in the sextant. is mouth but with a pocket of 5 mm and 3 mm of recession,
will help to gain a fuller understanding of the periodontal which would give a score of 3. Code 2 may also be mislead-
condition and will make sure that furcation involvements ing; it is possible for calculus, or other plaque retention fac-
are not missed. If a code 4 is not detected, then all sites tors, such as restoration overhangs, to be present at sites with
should be examined to ensure that the highest score in the no gingivitis or attachment loss. In addition, BPE is of little
sextant is recorded before moving on to the next sextant. or no value in established periodontitis patients because BPE
6. e scores are recorded in a grid (see Figure 1.3.2). is based on bleeding on probing (BoP) and PPD, rather than
A video showing how the BPE is performed can be recording attachment and bone loss. Such patients require
viewed in the online section of this book. It should be noted regular and full periodontal assessment.
that while the WHO probe used to record BPE has the
black band marking from 3.5 mm to 5.5 mm, clinicians When to Record BPE
and researchers often refer to 4 mm and 6 mm pockets as
being thresholds for clinical decision-making. is is not as ɨe BSP has produced guidelines on the use of the BPE
anomalous as it may seem at ërst sight; if the black band that are updated regularly. ese may be viewed at: https:
starts to enter a pocket, then that pocket is at least 4 mm in //www.bsperio.org.uk/assets/downloads/BSP_BPE_Guideli
depth and if the black band just disappears into a pocket, nes_2019.pdf.
then that pocket is at least 6 mm in depth. Readers are advised to visit the website to check for the
latest updates to BPE guidelines.
KEY POINT 2 e guidelines state that:
Basic periodontal examination (BPE) codes: • All new patients should have the BPE recorded.
0 Health, pockets less than 3.5 mm • For patients with codes 0, 1 or 2, the BPE should be
1 Pockets less than 3.5 mm, bleeding on probing recorded at least annually.
2 Pockets less than 3.5 mm, calculus or other plaque- • For patients with BPE codes of 3 or 4, more detailed
retentive factor is present
3 Pocket depth between 3.5 and 5.5 mm
periodontal charting is required:
4 Pocket deeper than 5.5 mm  • Code 3: initial therapy including self-care advice (oral
* Furcation involvement. hygiene and risk factor control), then post–initial ther-
apy, record a 6-point pocket chart in that sextant only
BPE scores  • Code 4: if there is a code 4 in any sextant, then record
full probing depths (six sites per tooth) throughout
0 = Health, pockets less than 3.5 mm the entire dentition.
1 = Pockets less than 3.5 mm, bleeding on probing • ɨe BPE cannot be used to assess the response to peri-
2 = Pockets less than 3.5 mm, calculus or another plaque- odontal therapy because it does not provide information
retentive factor is present about how sites within a sextant change after treatment.
3 = Pocket depth between 3.5 and 5.5 mm To assess the response to treatment, probing depths should
4 = Pocket deeper than 5.5 mm be recorded at six sites per tooth pre- and post-treatment.
* = Furcation involvement. • For patients who have undergone initial therapy for
periodontitis (i.e., who had pre-treatment BPE scores of
If an * is recorded, both the number and the * should be 3 or 4), and who are now in the maintenance phase of
recorded for that sextant; for example, 4* would indicate care, full probing depths throughout the entire dentition
that there is at least one tooth with pocketing deeper than should be recorded at least annually.
In addition the guidelines state that: Assessment of Disease Activity

• BPE should not be used around implants (4- or 6-point
pocket charting should be used) Disease activity is dened as current loss of connective tis-
• Radiographs should be available for all code 3 and code sue attachment with apical migration of the junctional epi-
4 sextants. ɨe type of radiograph used is a matter of thelium and loss of alveolar bone. ere are no validated
clinical judgement but crestal bone levels should be vis- methods for determining disease activity. It is a common
ible. Many clinicians would regard periapical views as misconception that BoP is an indicator of disease activity.
essential for code 4 sextants to allow assessment of bone However, inìammation and deviation from health can be
loss as a percentage of root length and visualisation of the detected using surrogate markers of disease activity, such as
periapical tissues. PPD and BoP. In order to assess a patient fully, it is impor
• When a 6-point pocket chart is indicated it is only neces tant to take into consideration the amount of plaque that is
sary to record sites of 4 mm and above (although six sites present, the condition of the gingivae, the presence of cal-
per tooth should be measured). culus and other plaque-retentive factors, the depth of peri
• BoP should always be recorded in conjunction with a odontal pockets and any gingival recession or overgrowth.
6-point pocket chart. In addition, bleeding from the gingival margin, bleeding
A C
B D
• Figure 2.2.1 (A) Diagram showing bleeding from the gingival margin. (B) Bleeding from the gingival mar-
gin after shallow probing as shown in (A). (C) Diagram showing bleeding from the base of a pocket. (D)
Bleeding from the base of a pocket.
In the Simpliëed Plaque Index, there are two scores, 0 or 1.

on probing, any mobility of teeth, the presence of suppura-
tion (pus), the level of alveolar bone support and any furca- Score 0 – no plaque detected.
tion involvements should be noted. Score 1 – visible plaque detected.
Advantages and Disadvantages of the Simplified

Marginal Bleeding and Bleeding on Probing Plaque Index
Marginal bleeding (MB) and BoP are not the same; MB is ɨe main advantage of the Simpliëed Plaque Index (Ain-
bleeding from the gingival margin when the gingivae have amo & Bay 1975) is that the criteria are easy to interpret
been gently touched. MB is thus a reliable indicator of the (visible plaque is either present or absent) so repeatability is
eêectiveness or otherwise of self-performed plaque control. better. e main disadvantage is that no attempt has been
BoP is bleeding from the base of a pocket following probing made to quantify the amount of plaque present.
to the full pocket depth (Figure 2.2.1). is system can be used to produce a percentage score
Absence of BoP indicates the likelihood of periodontal for sites with plaque present. ɨis system for recording
stability. Although BoP indicates the presence of inìam- plaque has been incorporated into many dental software
mation, it does not necessarily indicate that a periodontitis packages.
site is active (that there is progressive loss of attachment). A
shallow pocket is more likely to remain stable than a deep Quigley Hein Index (modified by
pocket because it is more accessible for a patient, but a deep
Turesky etal. 1970)
pocket will not inevitably deteriorate.
ɨis plaque index (modiëed by Turesky etal. 1970) assigns a
Assessment of Plaque (BIOFILM) score of 0 to 5 to each buccal/labial and lingual/palatal non-
restored surface of all the teeth except third molars, as follows:
Plaque (bioëlm) is assessed by determining a plaque score.
ɨere are a number of diêerent systems for scoring plaque. 0 – no plaque.
Some examples are: 1 – separate ìecks of plaque at the cervical margin of the tooth.
2 – a thin continuous band of plaque up to 1 mm at the
• ɨe Plaque Index (Silness & Löe 1964) cervical margin of the tooth.
• ɨe Simpliëed Plaque Index (Ainamo and Bay 1975) 3 – a band of plaque wider than 1 mm but covering less
• ɨe Quigley Hein Index (modiëed by Turesky etal. 1970) than one-third of the crown of the tooth.
• ɨe Plaque Control Record (O’Leary 1972). 4 – plaque covering at least one-third but less than two-
thirds of the crown of the tooth.
5 – plaque covering two-thirds or more of the crown of the
Plaque Index (Silness & Löe 1964) tooth.
ɨe Plaque Index (Silness & Löe 1964) has scores of 0, 1, A score for the entire mouth is determined by dividing
2 or 3. the total score by the number of surfaces (a maximum of
Score 0 – absence of plaque deposits. 2 × 2 × 14 = 56 surfaces) examined.
Score 1 – a ëlm of plaque adhering to the free gingival margin
Advantages and Disadvantages of the Quigley
and adjacent area of the tooth. ɨe plaque may only be
Hein Index
recognised by running a probe across the tooth surface.
Score 2 – moderate accumulations of soft deposits within the ɨe main advantage of this plaque index (modiëed by Turesky
gingival pocket, and on the gingival margin and/or adja- etal. 1970) is that it quantiëes the amount of plaque present.
cent tooth surface, which can be seen by the naked eye. e criteria are well-dened, enabling more accurate repeat-
Score 3 – abundance of soft matter within the gingival pocket ability of measurements. e main disadvantages are:
and/or on the gingival margin and adjacent tooth surface.
• interpretation of the diêerent scores may vary between
Advantages and Disadvantages of the operators leading to inconsistent scoring
Plaque Index • only non-restored surfaces are scored
ɨe main advantage is the attempt to quantify the amount • no measurement of plaque on the interdental surfaces is
of plaque present. ɨe main disadvantage is the interpreta- recorded.
tion of the dierent scores. e criteria are subjective, which
can lead to errors in repeatability of measurements. Plaque Control Record (O’Leary etal. 1972)
ɨe Plaque Control Record (O’Leary etal. 1972) was devel-
Simplified Plaque Index (Ainamo & Bay 1975) oped to give a simple method of recording the presence of
the plaque on individual tooth surfaces. ɨese surfaces are:
Ainamo & Bay (1975) introduced a simplied version of
the Plaque Index. ɨis is probably one of the most com- • Mesial
monly used and reliable methods of assessing plaque. • Distal
• Figure 2.2.2 Disclosed dentition. • Figure 2.2.3 Healthy gingivae.
• Buccal the recorded plaque score with the presence of gingival inìam
• Lingual. mation. Because of this, marginal bleeding (see later) may be a
A suitable disclosing solution, such as Bismarck Brown more reliable indicator of the patient’s ability to remove acces-
or a proprietary brand, is painted on all exposed tooth sur- sible plaque and so control marginal inìammation.
faces (Figure 2.2.2). After the patient has rinsed, the opera- Remember that the presence of plaque does not inevita
tor, using the tip of a probe, examines each stained surface bly lead to gingivitis or periodontitis at that site.
for soft accumulations at the dento-gingival junction. When
found, deposits are recorded as present. e surfaces which KEY POINT 3
do not have soft accumulations at the dento-gingival junc- Plaque scoring is one of the least reliable indices. Marginal
tion are not recorded. After all teeth are examined and bleeding is a more reliable indicator of a patient’s plaque
scored, the index is calculated by dividing the number of removal ability.
plaque-containing surfaces by the total number of available
surfaces. It is expressed as a percentage.
Assessment of the Gingivae
Advantages and Disadvantages of the Plaque
Control Record e two most common features of the gingivae to assess are
the appearance and levels of inìammation.
ɨe main advantages of this plaque index (O’Leary et al.
1972) are:
Appearance
• plaque is disclosed to enable easy detection
• criteria are well-deëned, which enables more accurate Colour, contour and consistency are assessed.
repeatability of measurements.
e main disadvantages are: • Colour – describe the colour of the gingivae. Remember
• soft deposits are stained, which can lead to over-record that healthy gingivae (Figure 2.2.3) will be paler in
ing of plaque if other debris (such as food) is present colour than inìamed gingivae. It is important to take
• stain needs to be removed. into account normal pigmentation of the gingivae when
deciding whether or not they are inìamed. Smoking
ɨere is no universally accepted plaque score. However, might mask some outward signs of inìammation.
the Simpliëed Plaque Index (presence or absence of visible • Contour – healthy gingivae should have a scalloped
plaque) is one of the most useful systems to use in clinical shape with a knife-edge margin.
practice due to the ease with which it can be used as well as • Consistency – gingivae can be inìamed (Figure 2.2.4),
the clarity of interpreting the dierent scores. in which case they tend to lose the knife-edge margin
It should be appreciated that plaque scoring is one of the least with the tissues appearing slightly thicker and slightly
reproducible indices; this is because many patients will improve “spongy”.
their usual oral hygiene immediately before a dental appoint-
ment so there may be an unusually low score when they visit a Some people can have hypertrophic or hyperplastic
dental professional. On the other hand a patient who normally gingivae which will also appear enlarged, but the gingival
cleans to a high standard may attend having not been able to colour may be pale due a lack inìammation. Fibrotic gingi
brush before the visit and would then record an abnormally vae will tend to be larger than normal and appear paler and
high plaque score. ɨis can give rise to diïculties in relating thicker, as is commonly seen in smokers (Figure 2.2.5).
interpretation of the diêerent scores; criteria are subjective,

potentially leading to errors in repeatability of measurements.
The Simplified Gingival Index (Ainamo &

Bay 1975)
Ainamo & Bay (1975) developed the Simpliëed Gingival
Index. It has two scores, 0 or 1.
Score 0 – no bleeding from the gingival margin detected after
a periodontal probe is brieìy run along the gingival margin.
Score 1 – bleeding from the gingival margin detected after a
periodontal probe is brieìy run along the gingival margin.
• Figure 2.2.4 Inamed gingivae.
Advantages and Disadvantages of the Simplified
Gingival Index
ɨe main advantage of the Simpliëed Gingival Index is that
the criteria are easy to interpret (bleeding is either present
or absent), so repeatability is better. e main disadvantage
is that no attempt has been made to quantify the amount of
inìammation present.
is is one of the most widely used systems for assessing
gingival inìammation in practice. It is simple and reliable.
It can also be expressed as a percentage score. Many of the
commercially available dental computer software packages
allow this index to be recorded on a computer.
Assessment of Calculus
A number of systems for assessing calculus have been pro-
posed. e main disadvantage of many of these is the dif-
• Figure 2.2.5 Fibrotic gingivae in a smoker. culty in interpretation of the criteria set down. A simple
visual assessment should be made of the presence or absence
of both supragingival and subgingival calculus.
Assessment of Gingival Inflammation
Gingival indices are used to assess gingival inìammation by Assessment of Periodontal Pockets
identifying marginal bleeding.
Periodontal pockets are assessed by measuring the pocket
depth with a periodontal probe. Charts will often be recorded
Gingival Indices as 4-point pocket charts (mesial and distal measurements on
both the buccal/labial and lingual/palatal surfaces), or 6-point
A number of gingival indices have been proposed.
pocket charts (measuring a mid-buccal/labial and mid-lin-
gual/palatal point as well as the four “corners” of the tooth
The Gingival Index (Löe & Silness 1963)
measured in a 4-point pocket chart). Although the measure
ɨe Gingival index (Löe & Silness 1963) has scores of 0, ment of PPD is an important indicator of past periodontal
1, 2 or 3. disease, it is important to appreciate that PPD is not an indi-
cator of current disease activity and PPD does not correlate
0 – normal gingiva. with future disease progression – a deeper pocket may stay
1 – mild inìammation – slight change in colour, slight oe stable, and a shallow pocket can progress (Lindhe etal. 1983).
dema. No bleeding on probing.
2 – moderate inìammation – redness, oedema and glazing.
Bleeding on probing.
Probing Pocket Depths
3 – severe inìammation – marked redness and oedema. Ul e probing pocket depth is the distance from the gingival
ceration. Tendency to spontaneous bleeding. margin to the location of the tip of a periodontal probe, ide-
ally located at the base of the pocket. e probe should be
Advantages and Disadvantages of the Gingival inserted in the pocket with a light probing force of 20–25 g.
Index e type of probe used aects the measurement. Narrow
ɨe main advantage is the attempt to quantify the amount probes tend to give higher values than wider probes. e
of inìammation present. ɨe main disadvantage is the force used also aects the measurement.
• Figure 2.2.6 Manual probe (University of North Carolina [UNC] 15).
• Figure 2.2.8 Computerised probe.
Other Probing Errors

It is important to try to angle the probe correctly so that it is
kept as parallel as possible to the long axis of the tooth. is
is not always straightforward because of crown or root mor-
phology. ere can also be obstructions, such as subgingival
calculus, which prevent an accurate pocket depth reading.
e position of the probe will also aect the measurement
because pocket bases have complex shapes due to the highly
variable pattern of destruction that is usually seen. As a
• Figure 2.2.7 Constant pressure probe.
result, the true pocket depth may be diïcult to measure.
ere are many dierent types of probes available. Clini-
cians should become procient with using one type of probe
Measurements can be aêected by the use of diêerent so that their measurements are as reproducible as possible.
probes; it is therefore critical to use the same type of probe In addition, the same type of probe should always be used
whenever a pocket is measured. Clinicians should try always (and the type noted in the records) when repeated measure-
to use the same probing force whenever measuring a pocket. ments are taken.
ɨis can sometimes be more diïcult than it sounds. If tis
sues are inìamed, probing can be very uncomfortable for KEY POINT 4
a patient, which leads to a tendency to use lighter pressure Sources of probing error:
and so under-record the true pocket depth. In addition, • Pressure
when tissues are inìamed, if the correct probing force is • Position
• Angulation
used there can be a tendency for the probe to penetrate the • Obstacles
base of the pocket, which results in over-recording the true • Probe shape
pocket depth (and further pain for the patient). • Probe tip diameter
ere are three generations of periodontal probes. e • Inammatory status.
rst generation are manual probes, the second are manual
constant pressure probes and the third are computerised Assessment of Attachment Loss
probes (Figures 2.2.6, 2.2.7 and 2.2.8).
Constant pressure and computerised probes can help reduce e clinical attachment level is the distance from a xed
inappropriate probing force as a possible source of error. point on a tooth, usually the cemento-enamel junction, to
the tip of the probe when the probe is inserted into the full
Inter- and Intra-Operator Variability in Probing depth of the sulcus or pocket.
Measurements
The Difference between Probing Pocket Depth
ere can be considerable variation in the reproducibility of
and Loss of Attachment
probing depth measurements; repeat examinations by the
same examiner will assess intra-operator variability. Dupli- e probing pocket depth is the distance from the gingival
cate examinations by two or more examiners will assess margin to the depth of the pocket. Loss of attachment (LOA)
inter-operator variability. An experienced operator should measures the distance from a xed point on the tooth to the
be able to reliably record a pocket depth to ± 1 mm when depth of the pocket (Figure 2.2.9). Measuring any recession
using a manual probe. and adding it to the pocket depth will record LOA.
Enamel
CEJ
Recession
GM
Loss of
Pocket
attachment
JE
Key
CEJ Cemento-enamel junction
GM Gingival margin
JE Junctional epithelium
• Figure 2.2.9 Diagram showing the difference between pocket depth and loss of attachment.
ɨe LOA measurement is sometimes referred to as the KEY POINT 5

clinical attachment level. If a patient has active periodontal The assessment of BoP is the most important measure
destruction which involves progressive recession, measuring of periodontal disease status. It is the only measure that
pocket depths alone may fail to record this, which is why it evaluates the inammatory status of the periodontal tissues.
is useful to note recession as well as pocket depths.
Identifying the cemento-enamel junction can often be Assessment of Tooth Mobility
diïcult; sometimes it has been worn down by tooth surface
loss, and if there is gingival enlargement it may be subgingi- Most systems for assessing tooth mobility have developed crite
val. As a result, full mouth 6-point clinical attachment level ria to dene mild, moderate or severe tooth mobility. e most
measurements are rarely taken in general practice. commonly used system to record tooth mobility is that devised
by Miller (1950), which identiëes 4 degrees of movement.
Assessment of Bleeding on Probing Degree 0 – “physiological” mobility; the tooth can be moved
0.1–0.2 mm in a horizontal direction.
ɨe assessment of BoP is the most important measure of
Degree 1 – the tooth can be moved between 0.2 and 1
periodontal disease status. It is the only measure that evalu-
mm in a horizontal plane (bucco-lingual or mesio-distal
ates the inìammatory status of the periodontal tissues. ɨere
direction).
have been various BoP indices developed over the years. As
Degree 2 – the tooth can be moved 1–2 mm in a horizontal
with the plaque indices, some have tried to quantify the
plane but there is no mobility in a vertical plane (occlu-
amount of bleeding. ɨe most widely used BoP measure is
so-apical direction).
the simple presence or absence of bleeding following prob-
Degree 3 – the tooth can be moved in excess of 2 mm in a
ing to the base of the pocket. As noted above MB is not
horizontal plane and/or in a vertical direction.
the same as BoP, and it is sometimes diïcult to distinguish
between the two. One way around this, however, is to delay
BoP measurements until initial therapy (which includes oral Assessment of Furcation Involvement
hygiene instruction) has reduced marginal inìammation
and MB readings. It is then more likely that any bleeding ere are three basic ways to assess a furcation involvement:
recorded is coming from pocket depths rather than the mar- probing, radiographic assessment and clinical appearance.
ginal gingival tissues.
When interpreting a BoP score, it is important to Probing
remember that bleeding on probing indicates the presence
of inìammation; it does not necessarily indicate that there Furcations are diïcult to probe, particularly the distal fur
is active periodontitis. cation of an upper molar. e Nabers probe is a curved
• Figure 2.2.10 Nabers probe.
• Figure 2.2.12 Clinically visible furcation involvement at the upper rst

molar.
Degree III – a “through-and-through” furcation defect.

A similar system devised by Hamp etal. (1975) uses the
width of the tooth as the measure of furcation involvement
and is more commonly used:
Degree 1 – loss of horizontal periodontal support not ex
ceeding one-third of the width of the tooth.
Degree 2 – loss of horizontal periodontal support exceeding
one-third of the width of the tooth but not encompass-
ing the total width of the furcation.
Degree 3 – a “through-and-through” furcation defect.
Assessment of Suppuration
• Figure 2.2.11 Radiograph showing a furcation involvement at the
upper rst molar. Suppuration is assessed by noting the presence or absence of
suppuration (pus). Pus can sometimes be mixed with blood
probe that has been designed to overcome these diïculties
and can be under-recorded.
(Figure 2.2.10).
Assessment of Bone Support
Radiographic Assessment
e only practical way of assessing bone levels is by radiog-
Furcation involvements should be visible on radiographs. How
raphy. Choice of radiographic technique should be made
ever, it is not always possible to interpret accurately the amount
after a thorough clinical examination. e overall dental
of bone loss in the furcation area. Upper molars are usually the
needs of the patient, not just the periodontal needs, should
most diïcult teeth to assess on radiographs (Figure 2.2.11).
be considered. For further guidance, see the Faculty of Gen
eral Dental Practice (UK) Selection Criteria for Dental Radi-
Clinical Assessment ography, 3rd edition (2013, updated 2018).
If a patient has uniform loss of attachment less than 6 mm,
ɨe diïculty with relying on the visible appearance of a
horizontal bitewing radiographs of the posterior teeth should
furcation is that there needs to have been enough recession
capture the bone levels of the posterior teeth (Figure 2.2.13).
for the furcation to be visible (Figure 2.2.12).
If a patient has loss of attachment of 6 mm or more, con-
In common with the classication systems for tooth
sider taking vertical bitewing radiographs rather than hori-
mobility, most systems for the assessment of furcation
zontal bitewing radiographs. However, vertical bitewings
involvement have developed criteria to dene mild, mod-
are rarely used in general practice and most clinicians would
erate or severe furcation involvements. One example is
prefer periapical views, using a paralleling technique (Figure
the system described by Lindhe & Nyman (1975) using a
2.2.14), which have a number of advantages:
Nabers probe graduated at 3 mm:
Degree I – horizontal penetration into furcation <3 mm. • ɨe periapical tissues can be assessed for pathological change.
Degree II – horizontal penetration into furcation >3 mm • ɨe entire root system can be assessed for other pathology.
but not encompassing the total width of the furcation area. • Bone loss can be assessed in percentage terms.
If detailed clinical measurements have been recorded KEY POINT 6

and previous radiographs are available, consider care-
Advantages of periapical radiographs:
fully whether new radiographs are required or not. • The periapical tissues can be assessed for pathological
ere should always be clinical justication for taking change.
radiographs. • The entire root system can be assessed for other
If there are concurrent problems for which radiography pathology.
• Bone loss can be assessed in percentage terms.
is indicated, for example, symptomatic third molars or orth-
odontic considerations, or if intra-oral lms cannot be tol-
erated, a panoramic radiograph of optimal quality may be Radiographs in Periodontal Assessment
an appropriate alternative to consider. However, in general,
periapical radiographs have better diagnostic value than Interpretation of Radiographs
panoramic radiographs.
Radiographs tend to underestimate the level of bone loss. In
addition, changes in the settings of an X-ray machine, such
as voltage and exposure time, will aect the image seen as
will changes in the angulation of the lm and/or the X-ray
beam. Particular care needs to be taken when interpreting
panoramic radiographs because if teeth or parts of teeth fall
outside the focal trough, the appearance will be distorted.
is sometimes happens because of the angulation of the
roots of anterior teeth. e roots can appear shorter and
blunter than they actually are. Also, panoramic radiographs
can magnify some areas of the jaw, leading to a distortion in
the appearance of the bone levels.
Viewing and Reporting on Radiographs

Whenever a radiograph is taken, all the information that can
be obtained from the radiograph should be reported in the
patient records. For example, if radiographs were taken pri
marily for assessment of the bone levels, remember to report
• Figure 2.2.13 Bitewing radiograph showing bone loss. Not all of on any other abnormalities or pathology seen. It can be easy
the bone margins are visible on this bitewing radiograph. This is an
example of which it might have been better to take vertical bitewing
to forget to note a carious lesion when the primary reason
radiographs. for taking the radiograph was for a periodontal assessment.
A B
• Figure 2.2.14 Periapical radiographs of anterior teeth with bone loss.
• Figure 2.2.15 CBCT image, including periodontal defects.
When assessing the periodontium on a radiograph, always paper record charts. It does not matter which system is
note the amount of bone present as a percentage of the total used as long as the information is recorded accurately and
that should be present. Take into account the age of the can be retrieved at a later date so that any record can
patient. Always compare older radiographs with recently be compared with previous records to monitor patient
taken ones. It is then possible to monitor the amount of progress.
bone loss that has occurred since the last radiographs were
taken. It might be possible to obtain copies of older radio- KEY POINT 7
graphs from a colleague so consider asking for these before To assess and monitor the periodontal condition of an
deciding whether or not new radiographs need to be taken. individual patient:
• Take a complete set of measurements.
• Compare with previous sets of measurements.
New Radiographic Techniques • Decide if any radiographs are required.
• Interpret all the information gathered.
Cone beam computerised tomography (CBCT) is starting • Draw up an appropriate treatment plan which should
to gain wider acceptance. It has the advantage of providing include how frequently to reassess the patient.
a very detailed image of the site under investigation. It is • Monitor the patient by repeated reassessments to check
possible to view the full three-dimensional appearance of the condition of the patient.
a periodontal bony defect (Figure 2.2.15). e main dis-
advantage of CBCT is the amount of radiation required to Multiple choice questions on the contents of this chapter
obtain the image. If a CBCT image is taken, as with any are available online at Elsevier eBooks+
radiographic image, it is vital that everything detected on A series of videos demonstrating how to assess the peri-
the image is fully reported. It may therefore be necessary to odontium are also available online.
obtain a report from a colleague who has additional training
in this form of dental radiography. References
Monitoring a Periodontal Patient Ainamo J, Bay I. Problems and proposals for recording gingivitis and
plaque. Int Dent J. 1975;25:229–235.
Once a patient has been assessed, a diagnosis can be reached Ainamo J, Barmes D, Beagrie G, Cutress T, Martin J, Sardo-Inri J.
and a treatment plan can be formulated. Following treat Development of the World Health Organisation (WHO) Com
ment, it is essential that the patient is reassessed to see if munity Periodontal Index of Treatment Needs (CPITN). Int Dent
the treatment has been successful or not. Once periodontal J. 1982;32:281–291.
stability has been achieved, it is important to monitor the Chapple ILC, Mealey BL, etal. Periodontal health and gingival dis-
eases and conditions on an intact and a reduced periodontium:
patient to ensure there is no recurrence of disease.
consensus report of workgroup 1 of the 2017 World Workshop
Monitoring for life will be important to check that the on the Classication of Periodontal and Peri-Implant Diseases and
patient remains stable. Conditions. J Clin Periodontol. 2018;45(suppl 20):S68–S77.
All assessments and reassessments should be accurately Hamp SE, Nyman S, Lindhe J. Periodontal treatment of multi-
recorded in the dental records. ere are a number of rooted teeth. Results after 5 years. J Clin Periodontol. 1975;2:126–
computerised record management systems and various 135.
Lindhe J, Nyman S. ɨe eêect of plaque control and surgical pocket Miller SC. Textbook of Periodontia. 3rd ed. Philadelphia: ɨe Blakeston
elimination on the establishment and maintenance of periodon- Co; 1950.
tal health. A longitudinal study of periodontal therapy in cases of O’Leary TJ, Drake RB, Naylor JE. ɨe plaque control record. J Peri-
advanced disease. J Clin Periodontol. 1975;2:67–79. odontol. 1972;43:38.
Lindhe J, Haêajee AD, Socransky SS. Progression of periodontal dis- Silness J, Löe H. Periodontal disease in pregnancy. II. Correlation
ease in adult subjects in the absence of periodontal therapy. J Clin between oral hygiene and periodontal condition. Acta Odontol
Periodontol. 1983;10:433–442. Scand. 1964;22:121–135.
Löe H, Silness J. Periodontal disease in pregnancy. Prevalence and Turesky S, Gilmore ND, Glickman I. Reduced plaque formation by the
severity. Acta Odontol Scand. 1963;21:533–551. chloromethyl analogue of vitamine C. J Periodontol. 1970;41:41–43.
2.3
Gingival Enlargement
AL A N WO O D M A N
CHAPTER OUTLINE
Introduction Management of DIGE
The Aetiology of Gingival Enlargement Non-Surgical Management of DIGE
Surgical Management of DIGE
The Mechanisms of Gingival Enlargement Changing Medication for DIGE
Common Causes of Gingival Enlargement Hormonal Gingival Enlargement
Drug-Induced Gingival Enlargement (DIGE) Managing Hormonal Gingival Enlargement
Distribution of DIGE Diabetes
Risk Factors for DIGE Other Causes of Gingival Enlargement
Age Hereditary Gingivo-Fibromatosis
Gender Individual Fibromas
Drug Variables Mouth Breathing
Periodontal Status at Onset of Medication Down’s Syndrome
Incidence of DIGE Neoplasms
Conclusion – Reaching a Diagnosis

This chapter explains the varied aetiology, descriptive terminology, clinical signicance and practical management of gingival enlargement.
By the end of the chapter the reader should:
• Appreciate the practical dióculties which gingival The chapter covers the following topics:
enlargement presents in periodontal treatment • Introduction
• Understand the varied origins of gingival enlargement • The aetiology of gingival enlargement
• Recognize the potential interactions with associated • The mechanisms of gingival enlargement
medications • Common causes of gingival enlargement
• Understand the options for reduction of gingival • Drug-induced gingival enlargement
enlargement • Hormonal gingival enlargement
• Be able to discuss with patients the implications of gingival • Other causes of gingival enlargement
enlargement. • Conclusion (reaching a diagnosis)
Introduction in the description of this condition. However, without his-

tological examination of the aected tissues these terms
Gingival enlargement may, in very rare circumstances, be are unsuitable and are best avoided unless a rm histo-
associated with serious disease such as leukaemia but, in the pathological diagnosis is made. us the use of the term
vast majority of cases, the condition has a less sinister ori- “gingival enlargement” is considered more appropriate, as
gin and causes problems of a more practical nature. From recommended by the 2017 World Workshop on Classi-
the patient’s perspective, gingival enlargement may reach cation in Periodontology, than the formerly used “gin-
disguring proportions and be a cause of cosmetic dis- gival overgrowth”, to which historical references will be
tress, whereas the clinician’s cause for concern lies with the frequently found (Caton etal. 2018).
obstruction of good oral hygiene practice and its probable
consequences: the development of gingivitis or periodonti- The Aetiology of Gingival Enlargement
tis and dental caries.
In the past, the terms “gingival hyperplasia” and “gin- ere are many causes of enlargement of the gingival tis-
gival hypertrophy” have been used, often inappropriately, sues, the most common and obvious being the presence of
93
A B
C
• Figure 2.3.1 Examples of inammatory, oedematous, plaque-induced gingival enlargements: (A) poor
plaque control in the presence of a desquamative gingivitis; (B) poorly designed crowns prohibiting effec-
tive oral hygiene; (C) a pyogenic granuloma.
inammatory oedema associated with gingivitis (Figure • myoblasts.

2.3.1). However, the term “gingival enlargement” is generally Histologically, the cell type that is aected will have a
regarded as being related to an altered production of the cellu- normal appearance in all aspects except for the fact that it is
lar components of the tissue, in particular gingival broblasts. abnormally large.
is chapter concentrates on the non-inammatory com- Hyperplasia means that the tissue contains an abnormal
ponents of the process, although inammation of the disor- number of or “too many” cells.
dered tissue may well accompany the cellular irregularities. Deënition: “An abnormal increase in the number of cells
To achieve such changes in cell activity, a stimulus is in an organ or a tissue with consequent enlargement”.
required, which may be in the form of: Any cell type can become hyperplastic:
• Drugs • epithelium
• Hormones • ëbroblasts
• Developmental aberrations • myoblasts.
• Genetic inìuences Histologically, the cell type that is aected will have a
• Neoplasms. normal appearance but there is simply an excessive number
Types of tissue enlargement may be determined histo- of cells.
logically as:
• Hypertrophic The Mechanisms of Gingival Enlargement
• Hyperplastic.
However, the clinical appearance of enlarged tissues Although extensively studied, the actual mechanism for the
alone cannot distinguish between these descriptors. over-production of gingival tissues remains unproven. e
Hypertrophy means that the tissue is enlarged due to the most common cell involved in the development of gingival
presence of enlarged cells. enlargement appears to be the broblast, but the develop-
Deënition: “A non-tumorous enlargement of an organ or ment is only rarely found without some inuence of plaque
a tissue as a result of an increase in the size rather than the biolm (Seymour etal. 1996).
number of constituent cells”. Studies of drug-induced gingival enlargement (DIGE)
Any cell type can become hypertrophic: have implicated the broblast in three possible ways (Sey-
• epithelium mour etal. 1996).
• ëbroblasts • An over-production of cells (hyperplasia)
CHAPTER 2.3 Gingival Enlargement 95
• An over-production of collagenous matrix, associated

with the actions of known inammatory mediators such
as matrix metalloproteinases (MMPs) and tissue inhibi-
tors of MMPs (TIMPs)
• An over-production of non-collagenous matrix (glycos
aminoglycans and proteoglycans), as shown by in vitro
studies
• An alteration in connective tissue metabolism, resulting
in reduced degradation of collagen.
In drug-induced enlargement, which has been most
extensively studied, it is proposed that the broblasts in
those subjects who show gingival enlargement are more
susceptible to the presenting stimuli, especially medica-
tion, having been shown to exhibit increased protein syn-
thesis (of collagen). However, there is no evidence of such
brotic change in other parts of the body, thus allow- • Figure 2.3.2 DIGE associated with phenytoin.
ing for speculation that the local presence of the dental
plaque biolm and the attendant inammatory patho-
genic pathways and subsequent inammatory mediators
conspire to produce an enhanced response to the plaque
(Seymour etal. 1996).
A common ënding of many histochemical studies of such
tissues is that there is a shift in the normal calcium/sodium
ux within the broblasts, irrespective of the particular drug
used, which may provide the common link between the dif-
ferent groups of drugs associated with gingival enlargement
(Seymour etal. 1996).
More recently it has been proposed that, under the
inuence of certain medications, decreased cation inux of
folic acid active transport within gingival broblasts leads
to decreased cellular folate uptake, which in turn leads to
changes in matrix metalloproteinase metabolism and the
failure to activate collagenase. Decreased availability of acti • Figure 2.3.3 DIGE associated with amlodipine.
vated collagenase results in decreased degradation of accu-
mulated connective tissue, which presents as DIGE (Brown widespread “at risk” population and such enlargement is
& Arany 2014, Ramirez-Ramiz etal. 2017). presenting in the dental surgery more frequently as a result
As gingival enlargement develops, the epithelial layer (Figure 2.3.3). Fortunately such eects are now more widely
deepens and the rete pegs become more pronounced into recognized within the specialty of cardiology in particular,
the connective tissue layer, where the majority of the changes and the need for an inter-disciplinary approach to patient
take place. e increasing density of collagen gives the tissue management is clear (Bajkovec etal. 2021).
a pitted or ssured appearance and increased surface kerati-
nization is common (American Academy of Periodontology
[AAP] 2004). KEY POINT 1
Check the patient’s medical history for drugs such as:
• Anticonvulsants
Common Causes of Gingival Enlargement • Immunosuppressants (calcineurin inhibitors)
• Calcium channel blockers.
Drug-Induced Gingival Enlargement (DIGE)
For many years, the drug most commonly encountered Commonly used drugs that can cause gingival enlarge-
in patients presenting with gingival enlargement was that ment include:
associated with anti-epileptic therapy, phenytoin (brand • Phenytoin (Dilantin, Epanutin)
names Dilantin, Epanutin) (Figure 2.3.2). However, with  • for treatment of epileptic conditions
the development of medical techniques for organ transplan-  • use has declined in recent years, as other medication has
tation, several “anti-rejection” drugs have also been associ- been introduced (e.g. phenobarbitone and carbamaze-
ated with DIGE. In more recent years, the increasing use pine), but when used in combination with these other
of “calcium channel blocking” medication in the control of anti-convulsants the overgrowth is likely to be greater
hypertension, a very common complaint in the middle aged  • also used prophylactically in the prevention of post-
and elderly, has led to the development of a much more neurosurgical seizures.
• Cyclosporin
 • immunosuppressant used in anti-rejection treatment
for transplant patients that
may also be used in the treatment of:
 • diabetes
 • Bechet’s syndrome
 • multiple sclerosis
 • systemic lupus erythematosus
 • erosive lichen planus.
• Calcium channel blockers (e.g. nifedipine, amlodipine,
diltiazem) used as
 • blood pressure regulators and as vasodilators in angina
and hypertension.
Several other drugs have reportedly been associated with
gingival enlargement, but there is insucient evidence to
prove their involvement: • Figure 2.3.4 Gingival enlargement and delayed maturation in a
• Tacrolimus: a relatively new anti-rejection drug; however, 13-year-old affected by heroin in utero.
it may be that patients who are changed from cyclosporin
to tacrolimus have a residual eect from the cyclosporin
• Sodium valproate and erythromycin, but these are both of enlargement, whereas transplant patients also receiving
case reports only. prednisolone and azathioprine show reduced severity (King
etal. 1993, Wilson etal. 1998, Montebugnoli etal. 2000).
Distribution of DIGE Drug abuse may have an eêect on the development of the
gingival tissues in utero, producing “thick” tissues obstruc-
Findings from various studies, mainly based on patients tive to normal eruption (Figure 2.3.4).
seen in referral centres, show that:
• DIGE is more prevalent in the anterior labial gingiva Periodontal Status at Onset of Medication
• the interdental areas predominate It is logical to assume that poor plaque control plays a major
• the enlargement is dense, ërm and characteristically role in predisposing the tissues in the susceptible patient;
lobulated however, it is uncertain whether the plaque initiates the
• there is a minimal tendency to bleed, unless plaque levels enlargement or accumulates subsequently. It is agreed that
are high the re-growth of tissue can be reduced by meticulous plaque
• gingival changes usually occur within 3 months of start control (Seymour etal. 2000).
ing medication
• growth is most rapid in the ërst year Incidence of DIGE
• histologically, enlargement shows an increase in the con
nective tissue component of the gingiva, rather than a e incidence of clinically signicant gingival enlargement
cellular hyperplasia in patients receiving the three main drugs has been esti-
• thus ëbroblasts are the cells usually deemed responsible mated as (omason etal. 1993):
for the over-reaction or proliferation. • Phenytoin 50%
• Cyclosporin 27%
Risk Factors for DIGE
• Nifedipine 20%
Age • Cyclosporin and nifedipine 48%.
Children and teenagers are more susceptible; this may be a
hormonal factor as androgens stimulate broblast activity. Management of DIGE
Gender Mavrogiannis et al. (2006) have suggested that the man-
Males are more susceptible than females. However, there agement of the enlargement will depend upon the under-
have been more males in the relevant studies, and the stud- lying cause and the clinical signicance, considering the
ies may have been inuenced by related periodontal, genetic following:
or hormonal factors. • How obstructive or disëguring are the tissues?
• Is there restriction of normal function by gross
Drug Variables enlargement?
Drug dosage does not appear to be related to severity or • Is a change in medication realistic or possible?
prevalence. • Could a simple change to oral hygiene activity control
Drugs used in combination, e.g. cyclosporin with nifedip the plaque component?
ine or amlodipine, may increase the severity and prevalence • Would the patient accept a surgical approach?
• Figure 2.3.6The same patient on long-term nifedipine; note the gin-

• Figure 2.3.5 Patient on long-term nifedipine, managed by good gival enlargement is not unsightly, nor a problem for function.
plaque control alone and regular dental hygienist supportive care.
erefore, three approaches may be taken, either singly

or in combination.
• Conventional, non-surgical periodontal therapy
 • With meticulous personal and professional plaque
control
• Surgical reduction of the enlargement
 • Accompanied by meticulous personal and profes
sional plaque control
• Change in medication
• With meticulous personal and professional plaque
control.
Non-Surgical Management of DIGE

e main aim is to reduce the inammatory component in • Figure 2.3.7Gingivectomy approach using radiowave frequency sur-
gery to the upper and lower gingiva for the child in Figure 2.3.4 at age
the tissues (Seymour etal. 1996, Montebugnoli etal. 2000,
13, recurrence of the enlargement having taken place.
AAP 2004).
Case reports show that the conventional non-surgical
management and subsequent plaque control can result Surgical Management of DIGE
in complete resolution of DIGE, especially from calcium
Surgical management of DIGE also applies to other causes
channel blockers (omason et al. 1993, Montebugnoli
of gingival enlargement. e objective is to remove the excess
etal. 2000) (Figures 2.3.5 and 2.3.6).
tissue for improvement in plaque control and aesthetics.
All patients at risk will beneët from a course of non-
is can be done as a gingivectomy, using:
surgical periodontal treatment and extensive follow up.
ey should ideally receive such treatment before they start • Incisional surgery
medication, but this is often impractical especially for organ • Electrosurgery (diathermy) or
transplant patients. • Radiowave frequency surgery (Figure 2.3.7).
Antiseptic mouthwash, such as chlorhexidine gluconate, • ɨese approaches leave a painful raw surface, and a protec
may be used as an adjunct to the non-surgical management tive periodontal dressing may be required for 7–10 days.
and, in animal studies, it has been shown that chlorhexidine e nal shape of the healed tissue may prove unpredict-
alone can reduce the cyclosporin DIGE. able, especially if the medication remains unchanged.
Systemic antibiotics have also been studied and it is postu- • Alternatively an inverse bevel (“ëlleting”) ìap procedure
lated that antibiotics reduce the bacterial infection and hence may be used. is leaves a less exposed, more comfort-
inammation and also reduce the activity of the broblasts. able surface and more control can be exercised over the
Phenytoin is known to inhibit folic acid metabolism, so nal shape (Figure 2.3.8) but
a folic acid mouthwash may be of use in patients who are • the technique is more diïcult to carry out, especially on
low in folate. grossly enlarged, brous tissues.
• Figure 2.3.9Healing 10 months after the radiowave frequency sur-

• Figure 2.3.8 Flap approach to the lower gingiva for the same child gery shown in 2.3.7. Note the tissues are again showing a tendency
at age 16. for enlargement to recur.
Whichever approach is undertaken, it is essential that the

patient’s personal and professional plaque control is meticu-
lous to avoid recurrence of the enlargement, especially if their
medication does not change
Should the patient’s medication not change they must be
warned that re-growth of the tissues may still occur despite
the preventive approaches described previously (Figure 2.3.9).
Studies have reported as many as 34% of patients requiring
repeated surgical intervention (Mavrogiannis etal. 2006).
KEY POINT 2
Regular dental hygiene supportive care is an integral part of
the management process, usually at 3 to 4 monthly intervals.
• Figure 2.3.10 A pregnancy “epulis”.
Changing Medication for DIGE to the plaque – “pregnancy gingivitis” (Carrillo-de-

Albornoz etal. 2012).
is is the ideal long-term solution but, while it may seem • Speciëc localized gingival enlargement, in combination
appealing to the dentist simply to ask the patient’s medi- with plaque-induced inammatory processes:
cal practitioner to change the medication, this is not always  • Pregnancy epulis (tumour) (Figures 2.3.10 and
practical. e underlying health reasons for the continuing 2.3.11).
prescription of these important drugs will carry more weight • Generalized plaque-related enlargement and similar gin
than the dental complications. It may be that alternative gival fragility can be associated with:
medications have already been tried and found less eective,  • Puberty
but patients should always be made aware that either they  • Oral contraception (OC)
or their dentist should approach the medical practitioner to  • Hormone replacement therapy (HRT)
explore their options. e major diculty lies in convinc-  • Any situation where disturbed levels of progesterone/
ing the treating physician that reducing the eects on their oestrogen is found, such as ovarian disease.
patient’s “gums” will be worthwhile. Usually, the gingiva returns to normal when plaque con-
trol is achieved and the hormone levels are stable but, in
Hormonal Gingival Enlargement some cases, brotic scarring may remain and distort the gin-
gival contour.
is is plaque related, and the female hormones during
pregnancy, oestrogen in particular, can be responsible for Managing Hormonal Gingival Enlargement
inducing:
• An altered microcirculation (from increased progester A pregnancy epulis may need surgical resection (in the same
one) and an altered sub-gingival microora from the manner as DIGE) (see Figure 2.3.11) if it becomes unsightly
second to eighth months of pregnancy, allowing gingival or obstructive to oral hygiene or occlusal function. Lesser
fragility, increased bleeding and an enhanced reaction lesions usually resolve with the end of pregnancy.
• Figure 2.3.12 A 26-year-old woman after 8 years with poor diabetic

• Figure 2.3.11 Pregnancy “epulis” removed with electrosurgery. control.
In the majority of cases, when the pregnancy ends, any

fragility of the gingival tissue will resolve with good oral
hygiene and suitable dental hygiene support.
Varying the type or dosage of OC or HRT medication
may reduce the problem. Many patients receive HRT
without having a true titre of their oestrogen or proges-
terone levels taken. us the oestrogen level achieved by
the medication may be too high or too low and a degree
of trial and error is often required to nd the acceptable
level to cope with the symptoms and eects of meno-
pause. It is during this period that any gingival eects are
most likely.
Good personal oral hygiene and continued regular pro-
fessional hygiene support are the most important factors to
minimize the risk of continuing gingival enlargement, or
re-growth after surgical reduction.
• Figure 2.3.13 The same patient as seen in Figure 2.3.12, 3 months
after non-surgical periodontal care and stabilisation of her diabetic
Diabetes control, showing an improvement in the gingival condition.
Periodontal diseases in the presence of unstable diabe-

tes may be associated with an exaggerated response to the
plaque, resulting in an enlargement of inammatory ori-
gin, which is often referred to as “hyperplastic gingivitis”,
as illustrated in Figure 2.3.12. With conventional non-
surgical care, this will resolve and, in many cases (such as
this 26-year-old patient), the reduction in inammatory
mediators may facilitate an improvement in diabetic stabil-
ity (Figure 2.3.13).
Other Causes of Gingival Enlargement
Hereditary Gingivo-Fibromatosis
is is a rare condition of unexplained origin where mul-
tiple enlargements occur within the oral environment.
• ɨese may be obstructive to oral hygiene, or disëguring. • Figure 2.3.14 A localized broma with both aesthetic and hygienic
• Surgical resection may be carried out but there is a strong compromises.
tendency to recur.
removal of the base of the brous tissue, thus minimizing
Individual Fibromas the chance of recurrence (Figure 2.3.15).
Such localized enlargements of the gingival margin are Other unusual conditions that have been associated with
uncommon but, when they do occur (Figure 2.3.14), pro- gingival enlargement include:
vide a cosmetic challenge to the clinician. ese are best • Wegner’s granulomatosis, described as “strawberry
treated with an incisional approach, allowing for maximum gingivae”
Neoplasms
Among the many sites and varieties of neoplastic disease
identied within the oral cavity, tumours of the gingival tis-
sues are fortunately rare, but squamous cell carcinoma may
present as enlargement, with or without ulceration, and
be confused with the other causes of gingival enlargement
discussed previously. us the presentation of unexplained
enlargements should always be considered suspicious, partic-
ularly as leukaemias may present in this way and do not
always follow the characteristic bluish appearance generally
described.
KEY POINT 3
Should excisional surgery be performed for localized lesions
• Figure 2.3.15The same patient as seen in Figure 2.3.14 after broma without a denitive drug- or hormone-related aetiology,
excision to improve tissue contour. histological analysis should always be undertaken to rule out a
neoplasm.
•Neuro-ëbromatosis
•Sarcoidosis • ɨe enlargement in leukaemic patients is associated
•Crohn’s disease with both the dense inltration of white blood cells into
•Scurvy – vitamin C deëciency the tissues and an inability of the aected white blood
•Acromegaly. cells to control the gingival infection associated with
ese may have eects on the development of the gin- plaque. Although the management of neoplasms lies
gival and dental tissues, presenting with delayed eruption outside the scope of this chapter, the reader is strongly
– very thick gingival tissues resulting in failure of matura- recommended to refer to the case report of gingival inl-
tion of the normal gingival margin:crown relationship and tration in acute monoblastic leukaemia in the British
a reduced clinical crown height. Surgical treatment may be Dental Journal (Gallipoli & Leach 2007). is reminds
indicated to achieve an improvement in aesthetics, to remove clinicians that the acute onset of gingival enlargement
the tissues obstructing eruption or to facilitate orthodontic is an unusual physical sign with a narrow dierential
treatment. e previous illustrations in Figures 2.3.4, 2.3.7, diagnosis.
2.3.8 and 2.3.9 provide an example of a 13-year-old girl,
whose mother was a drug abuser throughout pregnancy, at Conclusion – Reaching a Diagnosis
presentation and subsequently following gingival corrective
surgery with an incisional approach and using radiowave Determining the cause of the visible enlargement can usu
frequency surgery. ally be achieved by careful observation and history taking,
without the need for histological analysis, in the case of:
Mouth Breathing • Prescription drugs: always establish the name of the drug
Patients who persistently mouth breathe, with poor lip seal, the patient is prescribed
often show enlargement of the upper labial gingiva in the • Non-prescription drugs: is there a history of admitted
presence of minimal plaque and may present with an estab- abuse?
lished enlargement of inammatory origin. If brous scar- • Hormones: pregnancy is usually admitted or
ring occurs within the gingiva, this condition can be very identiable!
stubborn and may be dicult to suppress unless some pro- • Hormones: OC or HRT should be known as part of the
tection from the drying eect of the mouth breathing can medical history, but has this changed?
be achieved by lubrication or physical protection. Unless the • Hormones: is the patient a diabetic and, if so, stable?
mouth breathing can be addressed, a surgical solution is not • Genetics: a family history may be obvious or admitted.
appropriate. However, the periodic use of botulinum toxin e practitioner should also establish:
to produce some immobilization of the upper lip over the • How long has the enlargement been present?
revealed gingiva may prove benecial. • Are there any systemic or local modifying factors?
• Is there a known medical factor which might be impli
Down’s Syndrome cated, e.g. diabetes?
Patients with Down’s syndrome have characteristically thick • Has the patient recently been hospitalized or received a
and ëbrous gingiva. Although not usually considered as transplant?
“gingival enlargement”, the tissue may be similarly obstruc- • Is a detailed drug history available? (the most com
tive to oral hygiene measures, and, in some extreme circum- mon cause of recent onset gingival enlargement is drug
stances, reshaping of the tissue may be deemed necessary to therapy)
manage periodontal problems. • Are there any other unusual signs or symptoms?
Gallipoli P, Leach M. Gingival inltration in acute monoblastic leu-

KEY POINT 4 kaemia. Br Dent J. 2007;205:507–509.
If the primary care clinician is unable to reach a diagnostic King GN, Fullinfaw R, Higgins TJ, Walker RG, Francis DMA, Wie-
conclusion or if, after initial periodontal treatment there is no
senfeld D. Gingival hyperplasia in renal allograft recipients receiv-
resolution of the enlargement (or inammation), referral to a
ing cyclosporin-A and calcium antagonists. J Clin Periodontol.
specialist in periodontics should be effected without delay.
1993;20:286–293.
Multiple choice questions on the contents of this chapter Mavrogiannis M, Ellis JM, omason JM, Seymour RA. e man-
agement of drug-induced gingival overgrowth. J Clin Periodontol.
are available online at Elsevier eBooks+.
2006;33:434–439.
Montebugnoli L, Servidio D, Bernardi F. e role of time in reduc-
References ing gingival overgrowth in heart-transplanted patients following
cyclosporin therapy. J Clin Periodontol. 2000;27:611–614.
American Academy of Periodontology. Report on drug-associated Ramirez-Ramiz A, Brunet-Llobet L, Lahor-Soler E, Miranda-Ruis J.
gingival enlargement. J Periodontol. 2004;75:1424–1431. On the cellular and molecular mechanism of drug-induced gingi-
Bajkovec L, Mrzljak A, Likic R, Alajbeg I. Drug-induced gin- val overgrowth. Open Dent J. 2017;11:420534.
gival overgrowth in cardiovascular patients. World J Cardiol. Seymour RA, omason JM, Ellis JS. e pathogenesis of drug-
2021;13(4):6875. induced gingival overgrowth. J Clin Periodontol. 1996;23:165–
Brown RS, Arany PR. Mechanism of drug-induced overgrowth revis- 175.
ited: a unifying hypothesis. Oral Diseases. 2014;21(1):5161. Seymour RA, Ellis JS, omason JM. Risk factors for drug-induced
Carrillo-de-Albornoz A, Figuero E, Herrera D, Cuesta P, Bascones- gingival overgrowth. J Clin Periodontol. 2000;27:217–223.
Martínez A. Gingival changes during pregnancy: III. Impact of clin- omason JM, Seymour RA, Rice N. e prevalence and severity of
ical, microbiological, immunological and socio-demographic factors cyclosporin and nifedipine-induced gingival overgrowth. J Clin
on gingival inammation. J Clin Periodontol. 2012;39:272–283. Periodontol. 1993;20:37–40.
Caton JG, Armitage G, Berglundh T, et al. A new classiëcation Wilson RF, Morel A, Smith D, Koman CG, Ogg CS, Rigden SPA,
scheme for periodontal and peri-implant diseases and conditions – Ashley FP. Contribution of individual drugs to gingival over-
Introduction and key changes from the 1999 classication. J Clin growth in adult and juvenile renal transplant patients treated with
Periodontol. 2018;45(suppl 20):S1–S8. multiple therapy. J Clin Periodontol. 1998;25:457–464.
2.4
PERIODONTITIS AND
SYSTEMIC DISEASES
M A R I LO U C I A N TA R A N D K E N N E T H E ATO N
CHAPTER OUTLINE
Introduction Periodontitis and Cardiovascular Diseases
Periodontitis and Systemic Disease Periodontal Treatment and Cardiovascular Diseases
Periodontal Disease and Adverse Pregnancy Outcomes
Potential Mechanisms Linking Oral Disease to Secondary
Periodontal Treatment and Adverse Pregnancy Outcomes
Non-Oral Disease
Periodontitis and Respiratory Diseases
Metastatic Infection (Due to Transient Bacteraemia)
Periodontal Treatment and Respiratory Diseases
Inammation and Inammatory Injury (Due to Innate
Periodontitis and Dementia
Immunity)
Periodontitis and Other Systemic Diseases
Adaptive Immunity
Systemic Conditions Aòecting the Periodontium
Periodontal Diseases Contributing to Systemic Disease
Systemic Medication Aòecting the Periodontium
Susceptibility
Periodontitis and Diabetes Mellitus Summary
Diabetes Mellitus
The Relationship Between Periodontitis and Diabetes Mellitus
Periodontal Treatment in Diabetes Patients

This chapter covers the possible inter-relationship between periodontal and systemic diseases. It will examine how this may occur at a
molecular level with a view to preventing and managing the respective diseases and their potential interactions.
By the end of this chapter the reader should be able to: is chapter will cover the following topics:
• Understand the possible interactions between periodontitis • Periodontitis and diabetes mellitus
and certain systemic diseases • Periodontitis and cardiovascular disease
• View the management of periodontitis in the wider • Periodontitis and adverse pregnancy outcomes
(systemic) context • Periodontitis and respiratory diseases
• Oòer better advice to patients suòering from periodontitis • Periodontitis and dementia
and concurrent systemic diseases which seem to have a • Periodontitis and other systemic diseases, including COVID-19
possible interaction with periodontitis • Systemic conditions aòecting the periodontium
• Consider the importance of liaising with physicians in • Systemic medication aòecting the periodontium.
managing such patients
• Recognise systemic conditions aòecting the periodontium
• Be aware of the eòect of medication on the periodontium.
Introduction whereas the diseases aicting the rest of the body are encom-
passed in medicine often with little interaction taking place
Although the oral cavity is an integral part of the human between the two disciplines. However, the perception that
body, it tends to be perceived, both by the general public an interactive link between oral infections and systemic dis-
and by dentists and doctors, as a separate entity from the eases might exist has long been established (Figure 2.4.1).
rest of the body. is might be because the oral cavity and In the latter part of the last century, there was renewed
diseases associated with it fall within the remit of dentistry, interest in the focal infection concept, especially with respect
102
CHAPTER 2.4 Periodontitis and Systemic Diseases 103
664BC–AD427 17th century 20th century 20th century 20th century
Ancient civilisations Antonie van Miller 1891, Colyer 1902, Offenbacher 1996
Assyrian, Greek, Leewenhoek Hunter 1900 Billings 1911,
Roman, Galloway 1931,
Babylonian (Ring 1985) Williams and
Burkitt 1951
Possible association Role of Mouth as a Focal infection Periodontal
between oral disease organisms source of theory medicine
and systemic disease in health and infection
disease
• Figure 2.4.1 Periodontal–systemic interactions: chronological development.
Dental biofilm at tooth/gingiva junction
Genetic factors
Time Environmental
factors
Gingivitis / periodontitis:
Local features: Possible systemic

interactions with:
Swelling
Diabetes mellitus
Bleeding on probing Long incubation period
Cardiovascular disease
Loss of attachment
Pre-term low birthweight
Bone resorption
Pneumonia
• Figure 2.4.2 Possible link between periodontal diseases and systemic diseases.
to the eld of periodontology. Within dentistry, periodontal (probing depths averaging 5–6 mm per pocket), the total sur-
diseases are a distinct entity in that they are more akin to face area of the pocket epithelium coming into contact with
medicine rather than the rest of dentistry in terms of disease the subgingival bacterial biolm is 25 cm2 (Page 1998). is
aetiology, pathobiology and treatment. is has led to the presents a large, ulcerated surface area in close approximation
development of periodontal medicine (Oenbacher 1996) to the periodontal biolm leading to potential transmigration
– a two-way relationship in which periodontitis may inu- of bacteria or their toxic products into the circulatory system.
ence the individual’s systemic health and systemic disease is, in addition to the severity and chronic nature of peri-
may inuence periodontal health. odontitis, initiates a host-mediated immune response forming
In the last two decades there has been increasing interest a reservoir of cytokines (interleukin-1 or IL-1, tumour necrosis
and research in the topic, and new knowledge of the links factor-α or TNF-α, prostaglandin E2 or PGE2, thromboxane)
between periodontitis and systemic diseases is being uncov- in the periodontium which can induce and perpetuate both
ered. For example in the last 6 years there have been several local and systemic eects (Figure 2.4.2) (Page 1998).
studies which have conrmed a link between periodontitis
and dementia. Most recently, links between the severity of Potential Mechanisms Linking Oral Disease to
COVID-19 and periodontitis have been investigated. Secondary Non-Oral Disease
Periodontitis and Systemic Disease ree mechanisms have been suggested which could poten-
tially link oral and systemic disease (oden van Velzen
A clinical feature of periodontitis is inammation leading to etal. 1984, Van Dyke & Winkelho 2013).
swelling of the gingiva and destruction of the periodontium.
Histologically, this is conrmed not only by alveolar bone Metastatic Infection (Due to Transient
resorption and breakdown of the periodontal ligament but Bacteraemia)
also by extensive ulceration of the pocket epithelium. It is esti- Oral bacteria at the tooth/gingiva interface are capable of
mated that in a patient with generalized moderate periodontitis entering the periodontal tissues and eliciting a transient
bacteraemia, not only in periodontally healthy subjects but • Periodontitis and adverse pregnancy outcomes
more so in periodontitis patients who manifest a large ulcer- • Periodontitis and respiratory diseases
ated subgingival periodontal surface (Saito etal.1981, Page • Periodontitis and dementia
1998). e bacteraemia might be caused by dental pro- • Periodontitis and other systemic diseases, such as
cedures (Kinane et al. 2005) or by daily activities such as COVID-19.
chewing and tooth brushing (Lucas etal. 2008, Fine etal.
2010). e bacteria are usually eliminated within minutes,
Periodontitis and Diabetes Mellitus
but if they encounter favourable conditions, the bacteria Diabetes Mellitus
might settle at a site and, after a time, start to multiply. Diabetes mellitus (DM) is a clinical syndrome characterized
by hyperglycaemia (high blood glucose) due to an absolute
Inflammation and Inflammatory Injury (Due to or relative deciency of insulin (WHO 1999).
Innate Immunity) In the UK, DM complications are the seventh lead-
Bacterial accumulation at the tooth–gingiva interface elicits ing cause of death and in 2019, there were 4.9 million
cellular release of inammatory molecules (or cytokines), e.g. known diabetics, a national prevalence of 7.4% (Diabetes
TNF-α, IL-1 and IL-6 by resident epithelial cells, broblasts UK 2020). However, many other countries have a higher
and phagocytes. Release of such chemical pro-inammatory national prevalence of diabetes, for example 32.8% in Saudi
mediators may have an impact on systemic inammation, Arabia in 2019. Treatment for DM accounts for 5–10% of
e.g. endothelial dysfunction (D’Aiuto etal. 2004). the UK NHS annual expenditure.
Bacterial antigens may enter the blood stream where e classication of DM is based on its aetiology and
they react with host antibodies to produce antigen–anti- is divided into four categories, though the rst two are the
body complexes which may give rise to a variety of acute major types (Table 2.4.1).
and chronic inammatory reactions at sites of deposition Type 1 DM (formerly known as insulin-dependent DM,
(oden van Velzen etal. 1984, Van Dyke etal. 1986). Fur- IDDM or juvenile DM), is caused by cell-medicated auto-
thermore, bacteria are capable of releasing toxins (exotoxin immune (or rarely idiopathic) destruction of the insulin-
from Gram-positive bacteria, endotoxin or lipopolysaccha- producing pancreatic β cells (Atkinson & Maclaren 1994).
ride (LPS) from Gram-negative bacteria) which have potent In all cases, there is complete destruction of the β cells, lead-
pharmacological activity and, once in the circulatory sys- ing to an absolute deciency of insulin. is explains why
tem, can induce vascular pathology (Mattila 1989). all type 1 DM patients need insulin treatment (given by
injection) for survival.
Adaptive Immunity Type 2 DM (formerly known as non-insulin-depen-
Persistence of gingival/periodontal inammation leads to pro- dent DM, NIDDM or maturity-onset DM) results from
cessing of bacterial antigens by the adaptive immune system, the interplay between genetic factors, obesity, increasing
i.e. T-cell and B-cell activation. e B cells release antibodies age and lack of physical exercise (Yki-Jarvinen 1994).
(Ab), a soluble form of immunoglobulin, the aim of which is Although the specic aetiologies of this type of DM are
to eliminate invading bacterial antigens. T cells release a host not known, autoimmune destruction of the β cells does
of cytokines including IL and TNF-α which can contribute not occur. Type 2 DM is characterized by impaired insu-
to periodontal tissue destruction and to other inammatory lin secretion, peripheral resistance to insulin and hepatic
conditions such as diabetes and cardiovascular disease. insulin insensitivity. Impaired insulin secretion is due to
reduced cell mass and altered insulin release (Crawford
Periodontal Diseases Contributing to Systemic & Cotran 1994). us the pulsating release of insulin in
Disease Susceptibility response to a high glucose load seen in non-DM subjects
is lost in type 2 DM patients. e hyperglycaemia seen in
Periodontitis may aect the patient’s susceptibility to disease type 2 DM subjects can be controlled by dietary restric-
in three ways (Page 1998): tion and exercise. If it does not respond to such measures,
1. shared risk factors, e.g. smoking, ageing, stress and eth- additional treatment may include oral hypoglycaemic tab-
nicity are risk factors for both periodontitis and cardio- lets and insulin.
vascular disease
2. subgingival biolm – acts as a reservoir for bacterial toxins Diagnosis
3. a persistently inamed periodontium acts as a reservoir e primary methods used to diagnose and monitor
for inammatory mediators (cytokines). blood glucose levels have traditionally been fasting blood
Recent advances and research into periodontal medicine glucose, a combination of fasting blood glucose and a
have shown that there is a possible relationship (correlation 2-hour post-prandial glucose loading and oral glucose
not causation) between periodontitis and the following sys- tolerance tests (American Diabetes Association 2015;
temic diseases (Van Dyke & van Winkleho 2013, Linden Box 2.4.1). DM may be diagnosed by any one of the
etal. 2013): three methods; whichever method is used, it must be
• Periodontitis and diabetes mellitus conrmed on a subsequent day using one of the three
• Periodontitis and cardiovascular disease methods.
TABLE Classication of diabetes mellitus • BOX 2.4.1 American Diabetes Association (ADA)
2.4.1 (DM) based on the American Diabetes Diagnostic Criteria for Diabetes Mellitus
Association Classication (ADA 0)
Type of DM Aetiology 1. Symptoms of DM plus casual (non-fasting) plasma glucose
of ≥11.1 mmol/L (≥200 mg/dL) Casual: any time of day or
Type 1 DM Autoimmune night without regard to time since last meal Symptoms of
Idiopathic DM: polyuria, polydipsia, polyphagia
Type 2 DM Obese type 2 DM 2. Fasting plasma glucose of ≥7 mmol/L (≥126 mg/dL);
Non-obese type 2 DM fasting: no caloric intake for 8 hours
Maturity onset diabetes of the 3. Two-hour post-prandial glucose ≥11.1 mmol/L (≥200 mg/
young (MODY) dL) after an oral glucose tolerance test (as per WHO, using
a glucose load containing the equivalent of 75 g anhydrous
Gestational DM Pregnancy glucose dissolved in water).
4. Glycated haemoglobin (HbA1c) ≥6.5% (test should be
DM secondary to Genetic defects in β-cell function
performed in a laboratory using an NGSP-certied method
systemic disease Genetic defects in insulin function
and standardized to DCCT assay).
Pancreatic diseases or injury
Infections
DCCT: diabetes control and complications trial; NGSP: national
Drug/chemical induced glycohaemoglobin standardization programme
Endocrinopathies
Other genetic syndromes
associated with DM
American Diabetes Association 2015 patients, recurrent periodontal abscesses might indicate the
possibility of undiagnosed type 1 DM.
For a long time, the association between periodontitis
Pathobiology of diabetes mellitus and DM was considered unidirectional, i.e. DM predispos-
Prolonged hyperglycaemia leads to the formation of irre- ing to periodontitis. Recent research has shown that the
versible proteins known as AGEs (advanced glycation end relationship is most likely to be bi-directional (see Figure
products). e AGEs are widely deposited in cells and tis- 2.4.3 and Chapter 1.6) in that DM predisposes to peri-
sues and are responsible for the pathological features of DM, odontitis while periodontitis might exacerbate DM com-
namely ophthalmic, neurological, cardiovascular, renal and plications in a dose-dependent manner and is associated
vascular dysfunction and damage (WHO 1999). e altered with an increased risk of developing type 2 diabetes (Taylor
vascular function and permeability, the altered cellular func- 2001, Mealey 2006, Lalla & Papapanou 2011, Lakschevitz
tion (including migration and phagocytic activity of mono- etal. 2011, Borgnakke etal. 2013).
nuclear and polymorphonuclear cells) and higher cytokine e cytokine reservoir produced as a result of periodonti-
production increase the patient’s susceptibility to infection, tis not only leads to periodontal destruction, but it also inter-
including periodontitis (Figure 2.4.3). feres with glucose metabolism leading to hyperglycaemia,
therefore exacerbating the pathology associated with diabe-
The Relationship Between Periodontitis and tes. Chronic hyperglycaemia undermines macrophage and
Diabetes Mellitus neutrophil function, reducing their antibacterial activity,
and alters vascular function, increasing the patient’s suscep-
e relationship between DM and periodontitis has long tibility to periodontitis. e inammatory cell phenotype
been established (Seiert 1962). DM per se does not cause consequent to hyperglycaemia leads to a burst of inam-
periodontitis. However, it is known to be a risk factor for peri- matory cytokines (TNF-α, IL-1, IL-6) which contribute to
odontal breakdown (Taylor 2001). DM patients manifest an periodontal destruction and interfere with wound healing.
increased susceptibility in terms of periodontitis prevalence, In addition, alterations in gingival crevicular uid, collagen
severity and progression (Cianciola et al. 1992, Löe 1993, metabolism and altered subgingival microora (McNamara
Collin et al. 1998), particularly in those with poorly con- etal. 1982, Ciantar 2002) contribute to periodontitis.
trolled DM (Ainamo etal. 1990, Seppälä & Ainamo 1994)
and DM of long duration (Firatli 1997). Periodontitis has Periodontal Treatment in Diabetes Patients
been implicated as the sixth complication of DM (Löe 1993). Eective antimicrobial (plaque control) therapy is the
e clinical features of periodontitis in DM subjects mainstay of periodontal treatment. In DM–periodontitis
are no dierent to those seen in non-DM subjects. How- subjects, diabetes needs to be controlled in order to achieve
ever, the extent and severity of periodontitis may be more satisfactory outcomes after periodontal treatment. Where
pronounced in patients with undiagnosed or poorly con- diabetes control is established, the periodontal outcome
trolled diabetes. is holds true for both type 1 and type 2 is the same as for non-diabetics (Tervonen & Karjalainen
DM. Patients who manifest advanced periodontitis should 1997). In addition, recent evidence has shown that peri-
be questioned as to the possibility of having undiagnosed odontal treatment seems to improve glucose control in both
DM especially if they have a positive family history; a refer- type 1 and type 2 diabetic subjects (Grossi etal. 1997, Iwa-
ral to the patient’s doctor should be encouraged. In young moto et al. 2001, Engebretson & Kocher 2013, Sgolastra
Periodontitis Diabetes mellitus
Host−bacteria interaction Hyperglycaemia
Immuno-inflammatory response Altered cell phenotype
Altered vascular function

PMNL, monocyte and
macrophage accumulation
Risk of infection
Cytokine release Inflammatory phenotype
TNF-α, IL-1, IL-6
Periodontal destruction Interferes with glucose metabolism
• Figure 2.4.3 Bi-directional relationship between periodontitis and diabetes mellitus.
et al. 2013). e most plausible explanation is that peri- Periodontitis and Cardiovascular Diseases
odontal treatment reduces circulating levels of TNF-α,
increased levels of which suppress insulin action thereby Cardiovascular diseases comprise high blood pressure, coro-
leading to elevated blood glucose (Kanety etal. 1995). us nary heart disease, angina pectoris and myocardial infarc-
control of periodontal inammation is crucial to eliminate tion, peripheral arterial disease and stroke (cerebrovascular
periodontal disease and seems to benet diabetes control. accident). ese diseases are consequent to narrowing of
Robust and consistent evidence showing that severe peri- blood vessels or atherosclerosis. Atherosclerosis can lead to
odontitis undermines glycaemic control in DM subjects and signicant morbidity and mortality; atherosclerosis and the
that it contributes to DM complications in a dose-dependent ensuing cardiovascular complications are the leading cause
manner has led to guidelines being issued highlighting the of death in the Western world. Although the main cause of
importance of periodontal care in such patients (Chapple & atherosclerosis is fat deposition in the arterial wall possibly
Genco 2013). e guidelines provide patient management due to a high fat diet and lack of exercise, increasing evi-
recommendations to dentists, physicians and other healthcare dence suggests that chronic infections may cause atheroscle-
professionals and educational information to DM patients rosis (Syrjanen etal. 1998, Leinonen etal. 2002).
regarding the need for periodontal care. DM patients should Periodontitis, because of its chronic nature, has been
also be made aware of other oral complications of diabetes, implicated as a potential risk factor leading to atheroscle-
e.g. burning mouth, xerostomia, increased risk of infections rosis (Beck & Oenbacher 2001, Desvarieux etal. 2003).
(bacterial and fungal) and delayed wound healing. e hypothesis linking periodontitis and cardiovascular
disease was rst proposed in the late 1980s (Mattila et al.
KEY POINT 1 1989). is research was initiated as the traditional risk factors
• Periodontitis and DM have a bi-directional relationship for cardiovascular disease (hypertension, smoking, diabetes,
• DM does not cause periodontitis high serum cholesterol concentration, low high-density lipo-
• DM is a risk factor for periodontitis protein cholesterol concentration and low socio-economic
• Uncontrolled DM of long duration exacerbates status) could not fully account for the clinical and epidemio-
periodontitis logical features of atherosclerotic cardiovascular disease.
• Treatment of periodontitis seems to lead to some
improvement in diabetes control e original hypothesis implicating periodontitis as a
• Dentists should ask patients about the possibility of contributory factor to atherosclerosis was that periodontal
undiagnosed DM pathogens (such as Porphyromonas gingivalis) were isolated
• For all recently diagnosed type 1 & 2 DM patients, from atheromatous plaques (Haraszthy etal. 2000). Invitro
periodontal examination is recommended as part of their
studies have shown that this organism is capable of invading
diabetes management
• Dentists and physicians should collaborate in the endothelial cells (Deshpande etal. 1998, Dorn etal. 1999,
management of DM patients Kuramitsu etal. 2002). e subsequent abundant release of
• Patients should be made aware of the importance of biochemical mediators consequent to P. gingivalis invasion is
periodontal care especially if they are diagnosed with DM thought to be an important contributor to the development
• Oral health care education should be provided to all DM
of atherosclerosis (Yumoto etal. 2005). Furthermore, oral
patients
bacteria are also capable of inducing platelet aggregation
Periodontitis Cardiovascular disease
Host−bacteria interaction
Immuno-inflammatory response CRP Atherogenesis
PMNL, monocyte and

Cytokine release
TNF-α, IL-1, IL-6 Atherosclerosis and

thromboembolic events
Periodontal destruction
• Figure 2.4.4 Possible mechanisms between periodontitis and cardiovascular disease.
and thrombus formation, thereby contributing to the pro- (Löe etal. 1965, Axelsson & Lindhe 1981) and systemically,
gression of the atherosclerotic lesion (Herzberg etal. 1994). by improving endothelial function (Tonetti etal. 2007) and
However, while oral bacteria might become nested within by reducing systemic cytokine levels (D’Aiuto etal. 2004,
atherosclerotic lesions and contribute to their progression, 2005), all of which might deter atherosclerosis disease ini-
this might not always be the case. tiation and progression.
An indirect plausible hypothesis linking periodontitis to Stroke: A stroke occurs when cerebral blood vessels sup-
atherosclerosis and, therefore, cardiovascular disease is based plying blood to the brain are blocked; it can also occur after
on the systemic increase of inammatory cytokines (TNF- a cerebral aneurysm. Some studies suggest that poor oral
α, CRP, IL-1, IL-6) triggered by bacterial components, such health is more common in patients with cerebrovascular dis-
as lipopolysaccharide, subsequent to periodontitis-induced ease (Syrjanen etal. 1989, Loesche & Lopatin 1998).
bacteraemia and endotoxaemia (Figure 2.4.4). C-reactive pro-
tein (CRP) is an acute phase protein produced by the liver KEY POINT 2
in response to an infection or inammatory process. Most • A direct causal relationship between periodontitis and
importantly, CRP is positively associated with cardiovascular cardiovascular disease is not established.
disease (Danesh etal. 1998). erefore, periodontitis-induced • Periodontitis is a risk factor or risk marker for coronary
heart disease.
systemic bacteraemia, endotoxaemia and cytokine release seem • The two conditions have many common risk factors.
to contribute to the inammatory aetiology of atherosclero- • Periodontitis seems to potentiate systemic elevation of
sis. Other factors, which either singularly or in combination cytokines associated with atherosclerosis.
could contribute to the link between periodontitis and car- • Atherosclerosis seems to have an inammatory aetiology.
diovascular disease, include an exaggerated host hyper-inam- • The host’s inammatory response is a signicant
determining factor.
matory immune response, increased pro-thrombotic state and • Periodontal treatment reduces the oral microbial burden.
increased cholesterol biosynthesis (Schenkein & Loos 2013). • Periodontal treatment reduces systemic inammatory
Some clinical human studies have shown that patients response.
manifesting cardiovascular disease tend to experience higher • Patients should be encouraged to maintain good
levels of periodontitis (Mattila et al. 1989, Paiuno et al. periodontal health especially if they have an increased
risk of atherosclerotic heart disease.
1993, Deliargyris etal. 2004, Dietrich et al. 2013). However, • Dentists, physicians and healthcare workers should
it is important to remember that the two conditions share work together and encourage patients to adopt a
common risk factors. Although there is biological plausibil- healthy lifestyle.
ity linking cardiovascular disease and periodontitis, further
investigations are required (Schenkein & Loos 2013). Periodontal Disease and Adverse Pregnancy
Periodontal Treatment and Cardiovascular Outcomes
Diseases Oral infections seem to increase the risk for, or contribute
ere is currently no evidence to indicate that treatment of to, adverse pregnancy outcomes (Oenbacher etal. 1998).
periodontitis will prevent or treat atherosclerosis (D’Aiuto Adverse pregnancy outcomes include preterm low birth-
et al. 2013). However, conventional periodontal therapy weight (PTLBW), miscarriage or early pregnancy loss and
is eective both locally, by reducing the microbial burden pre-eclampsia (elevated blood pressure in a pregnant mother
Periodontitis Pregnancy
Host−bacteria interaction Maternal exposure to periodontal

pathogens and products
Immuno-inflammatory response
Foetal exposure to periodontal
pathogens and products
PMNL, monocyte and

Cytokine release
TNF-α, IL-1, IL-6, CRP
Periodontal destruction Adverse pregnancy outcome
Bacterial vaginosis
• Figure 2.4.5 Possible mechanisms between periodontitis and adverse pregnancy outcomes.
which can have signicant morbidity and mortality out- predominantly Gram negative during the second trimester
comes for both mother and child). Preterm birth is dened as of pregnancy (Kornman & Loesche 1980). Pregnant females
birth prior to 37 weeks’ gestation; low birthweight is dened manifesting an increased susceptibility to periodontitis have
as birthweight less than 2500 g. Such adverse pregnancy an elevated inammatory response. erefore, the rationale
outcomes lead to signicant infant mortality or morbidity, behind the hypothesis is that the resulting elevated bacter-
which is often associated with lifelong consequences, e.g. aemia, endotoxaemia and increased cytokines (IL-1β, TNF-
neurodevelopmental disturbances (Oenbacher etal. 1996a, α, IL-6, CRP), all of which are potent inducers of labour,
Williams et al. 2000), respiratory disturbances, congenital owing through the maternal circulation could augment
malformations and developmental delays (Hack etal. 1983); the levels of these same cytokines produced physiologically
this has substantial social and public health implications. and collectively. ese can aect the foetal–placental unit,
Known risk factors for PTLBW include: maternal age leading to premature rupture of membranes and there-
(younger than 17 years or older than 34 years), ethnic origin fore premature birth (Figure 2.4.5). Although periodontal
(increased prevalence in Hispanics, African-Americans and those pathogens are important inducers of the maternal inam-
with low socio-economic status), drug, alcohol and tobacco use, matory response, the scale of the response is dependent
maternal stress, inadequate prenatal care, diabetes and genito- on the host’s immuno-inammatory trait. If the maternal
urinary infections. An acute example of the latter is bacterial infection is contained, the foetus is spared; if not, then
vaginosis which is an infection caused by Gram-negative bacte- local foetal cytokine release may lead to premature rupture
ria (similar to periodontitis). e infection can aect the mater- of the membranes and uterine contractions, which could
nal foetal membranes, leading to an increased production of lead to miscarriage or preterm birth (Madianos etal. 2013).
inammatory cytokines which can in turn lead to premature Although there is some evidence to show a modest associa-
rupture of membranes and hence preterm low birthweight. tion between periodontitis and adverse pregnancy outcomes
Childbirth is a normal physiological process which is (Ide & Papapanou 2013), and that periodontitis is more
eected by a steady increase of cytokines (prostaglandin E 2 severe in subjects giving birth to PTLBW infants (Oen-
[PGE2] and TNF-α) until a critical threshold is reached that bacher etal. 1996b, 1998), the results are inconclusive. e
induces delivery of the neonate (Oenbacher etal. 1996b). association between the two conditions might be due to the
Distant sites of infection can contribute to the build-up of patient’s elevated inammatory response making periodon-
these cytokines in the maternal circulation either directly titis a risk marker, rather than a risk factor, for PTLBW.
due to the host response or indirectly due to lipopolysac-
charide (LPS), a known potent inducer of cytokines such as Periodontal Treatment and Adverse Pregnancy
IL-1, IL-6, TNF-α and PGE2 (Darveau etal. 1997). Outcomes
In the mid-1990s, it was hypothesized that oral Gram- A number of studies have investigated the eect of treat-
negative infections such as periodontitis might contribute to ment of periodontitis on adverse pregnancy outcomes.
adverse pregnancy outcomes (Oenbacher etal. 1996a). e e results are conicting, with some studies suggesting
subgingival microora in pregnant females tends to become that periodontitis is a signicant risk factor for PTLBW
(Oenbacher et al. 1996a, 2001, 2006, Goepfert et al. inrm, more so in those in intensive care units or subjects
2004, Lie etal. 2004, Boggess etal. 2006, Bosnjak etal. residing in nursing homes. is has signicant social, medi-
2006), whereas others found no association (Davenport cal and nancial implications.
etal. 2002, Holbrook etal. 2004, Moore etal. 2005, Meur- e lower respiratory tract beneath the oropharynx is usu-
mann etal. 2006). e conicting results could be due to ally sterile. Infection may result from a defect in host defences,
population/ethnic dierences. A common feature of all infection with a particularly virulent organism or aspiration
studies showed that periodontal treatment delivered during of oral/oropharyngeal uids. e crucial factor is colonisation
pregnancy was safe. All pregnant females should be encour- beneath the oropharynx, as this will in turn lead to microbial
aged to maintain good oral health before, during and after colonisation of the lower respiratory tree (Finegold 1991).
pregnancy. Currently, there is no evidence to support the Obligate anaerobes constitute the predominant microora in
notion that non-surgical periodontal therapy improves the oropharynx and in the oral cavity of periodontitis patients.
adverse pregnancy outcomes (Polyzos etal. 2010, Weidlich An increasing number of reports (Terpenning etal. 2001, Scan-
etal. 2013). napieco etal. 2003, Scannapieco 2006) show that pneumonia is
more common in patients with poor oral hygiene, dental caries
KEY POINT 3 and periodontal diseases and especially in those who are prone
• A direct causal relationship between periodontitis and
to aspiration of oral uids (intubated intensive care patients
preterm delivery is not established. and elderly/inrm patients who have trouble swallowing).
• Increased susceptibility to periodontitis seems to result Oral bacteria, such as Aggregatibacter actinomycetemcomitans,
in an increased susceptibility to premature births. Eikenella corrodens, Fusobacterium nucleatum, Porphyromonas
• Periodontitis might increase the cytokine burden, and Prevotella species, have been isolated from lung uid speci-
precipitating adverse pregnancy outcomes.
• The host’s inammatory response is a signicant
mens (Suwanagool etal. 1983, Brook & Frazier 1993, Chen
determining factor. etal. 1995, Verma 2000, Van decandelaere etal. 2012).
• Dentists should work in close collaboration with physicians, Potential mechanisms (Figure 2.4.6) by which oral bac-
obstetricians and midwives to encourage good oral health teria could be implicated in the pathogenesis of respiratory
in pregnant females before, during and after pregnancy. diseases (Scannpieco etal. 1999) are:
• It is safe for pregnant females to undergo periodontal
therapy.
• Bacterial aspiration: poor oral hygiene manifesting as exces-
• Non-surgical periodontal therapy does not reduce the sive dental plaque (biolm) accumulation (whether on
risk of adverse pregnancy outcomes. teeth, mucosal surfaces or dentures), periodontitis and den-
• Elective procedures should be avoided during the rst tal caries can act as a source/reservoir of potential respiratory
trimester due to possible foetal stress; these are preferably pathogens (PRPs) which initially colonise the oral cavity
delayed or carried out during the second trimester.
• Pregnant females should be educated regarding the
and can subsequently be aspirated into the lower respiratory
possible interaction between periodontal disease and tract, leading to pneumonia or COPD (Scannapieco etal.
pregnancy; they should be made aware of possible 1992, 2003, Russel etal. 1999, Terpenning etal. 2001)
physiological periodontal changes occurring during • Periodontitis-induced enzyme modiëcation of the oral
pregnancy such as higher incidence of gingival bleeding mucosa: periodontitis-related bacteria produce enzymes
and gingival enlargement.
which are released into saliva and can enhance adhesion
and colonisation of the oral mucosa with PRPs (Woods
Periodontitis and Respiratory Diseases etal. 1981)
• Periodontitis-induced salivary pellicle destruction:
Pneumonia and chronic obstructive pulmonary disease hydrolytic enzyme activity in saliva is related to peri-
(COPD) are two respiratory conditions which have been odontal and oral hygiene status (Gibbons & Ethereden
associated with periodontitis. 1986). Elevated levels of such enzymes may destroy pro-
Pneumonia is an infection of the lower respiratory tract tective host mechanisms which would otherwise protect
(alveoli) most often caused by bacteria or viruses and, against colonisation with respiratory pathogens
less commonly, by other microorganisms, certain drugs • Periodontitis-induced cytokine alteration of the respira-
and other conditions such as autoimmune diseases. Typi- tory epithelium: cytokines released in response to peri-
cal symptoms include a cough, chest pain, fever and di- odontitis can upregulate the expression of receptors on
culty breathing. Pneumonia can be classied as community the mucosal surfaces, encouraging colonisation with
acquired or hospital acquired (nosocomial). PRPs (Svandborg etal. 1996).
COPD is a condition characterised by chronic obstruction
to airow caused by excessive sputum production resulting Periodontal Treatment and Respiratory Diseases
from chronic bronchitis and/or emphysema. Clinical symp- Although the precise contribution of periodontitis to the
toms include cough, diculty breathing, dyspnoea and fatigue, development of pneumonia is unknown, poor oral health
all of which become more pronounced during a period of exac- has been linked to increased levels of hospital-acquired pneu-
erbation. It is not known what causes an exacerbation, though monia (Mehndiratta et al 2016), and studies have shown
it is thought to be provoked in part by a bacterial infection. that interventions improving oral hygiene can reduce the
Both of these respiratory conditions cause signicant incidence of nosocomial pneumonia quite signicantly –
morbidity and mortality especially in the elderly and the between 40% (Scannapieco etal. 2003, Scannapieco 2006)
Periodontitis Respiratory infections
Host−bacteria interaction Bacterial colonisation (PRP)
Immuno-inflammatory response Salivary enzymes Bacterial aspiration
PMNL, monocyte and

macrophage accumulation Destroy host Favour adhesion and
defences colonisation of PRPs
Cytokine release
Pneumonia/COPD
TNF-α, IL-1, IL-6
Periodontal destruction Alter respiratory epithelium
• Figure 2.4.6 Potential mechanisms by which oral bacteria could be implicated in the pathogenesis of
respiratory diseases. PRP, Potential respiratory pathogens.
and 83% (Azarpazhooh & Leake 2006) – and of pneumo- Periodontitis and Dementia
nia in institutionalised elderly subjects (Yoneyama et al.
2002). ere is increasing evidence that better oral health- At least three systematic reviews published between 2017
care improves the outcome of patients in intensive care units and 2020 have investigated the relationship between peri-
(Rabello etal. 2018) and of those in nursing homes (Terpen- odontitis and Alzheimer’s disease. One review (Leira etal.
ning etal. 2001, Okuda etal. 2005, Terpenning 2005). 2017) concluded that there was “a signicant association
e importance of maintaining the oral hygiene of between periodontitis and Alzheimer’s disease and that fur-
patients on mechanical ventilation has been recognised ther studies should be carried out in order to investigate the
(Wainer 2020). is is becoming more important as patients direction of the association and factors that may confound
are living longer and are undergoing more complex medical it”. Liccardo etal. (2020) concluded that periodontitis and
care, and because they are tending to retain their teeth for Alzheimer’s disease often coexist. Dioguardi et al. (2020)
longer. In some medical intensive care units, it is becoming concluded that bacteria involved in, and inammatory
standard practice to implement oral hygiene care to intu- products arising from, periodontitis can intensify inam-
bated patients on a daily basis. mation in the central nervous system but that as yet there is
no denitive evidence to consider periodontitis a risk factor
KEY POINT 4 for Alzheimer’s disease. Nevertheless, they considered that
• A direct causal relationship between periodontitis and the oral hygiene of older people with dementia should be
pneumonia has not been rmly established. improved and that this should be achieved by educating care
• However, it appears that periodontitis increases the risk assistants to carry out daily oral hygiene of the residents in
of pneumonia in immune-compromised and frail patients. their care homes and regular monitoring of these patients’
• Poor oral hygiene seems to be associated with a higher
oral health by dental professionals (Dioguardi etal. 2020).
incidence of respiratory diseases.
• Dental biolms seem to harbour potential respiratory Research into periodontitis and dementia continues.
pathogens.
• Oral colonisation of such bacteria could contribute to Periodontitis and Other Systemic Diseases
pulmonary infections.
• Some studies have shown reduced risk of pneumonia A number of other systemic diseases have been associated
and COPD with improved oral hygiene. with periodontitis (Box 2.4.2). Apart from COVID-19, the
• The importance of good oral hygiene especially in
evidence to date is tenuous. However, with more studies
subjects who are at high risk of respiratory infections
(intensive care patients and elderly/inrm patients with underway and improved scientic techniques, it is antici-
feeding problems, especially those in nursing homes) pated that clearer and more convincing scientically based
should be emphasized. data will be obtained.
• Dentists, dental hygienists and therapists as well as By August 2021, a number of studies and case reports
physicians and staff working in intensive care units and
which investigated oral health and severity of COVID-19
nursing homes should emphasize the importance of
oral hygiene in these vulnerable patients. complications had been published. One found that after
• Dental and oral hygiene can potentially have cost- adjusting for potential confounders, “Periodontitis was asso-
saving and life-saving implications. ciated with higher risk of ICU admission, need for assisted
ventilation and death and with increased blood levels of bio- Systemic Medication Affecting the
markers linked to worse disease outcomes” (Marouf et al. Periodontium
2021). ere is considerable interest, and further research
into this topic is taking place. Systemic medication may affect the periodontium.
Drug-influenced gingival enlargement is seen in patients
Systemic Conditions Affecting the
Periodontium • BOX 2.4.2 Possible Associations between
Periodontitis and Other Systemic
A number of systemic conditions (acquired or genetic) Conditions
aect the periodontium. e clinical picture will vary
COVID-19
depending on the aetiology; however, in most cases, severe Obesity
periodontitis seems to be a common feature. Although Osteoporosis
these conditions are rare, they should be included in the Rheumatoid arthritis
dierential diagnosis, especially when the severity of peri- Head and neck squamous cell carcinoma
odontitis is not commensurate with the presenting clinical Inammatory bowel disease
Erectile dysfunction
picture (e.g. young child presenting with advanced peri-
odontitis) (Table 2.4.2).
TABLE
2.4.2 Systemic conditions aecting the periodontium
Condition Underlying pathology Clinical features

Haematological conditions
Neutropenia Reduced levels of PMNLs Severe periodontitis leading to premature loss of both
deciduous and permanent dentition
Leukaemia Bone marrow malignancy Oral mucosal ulceration, gingival hyperplasia/hypertrophy,
gingival haemorrhage, gingival pallor, periodontitis
Genetic conditions
Down’s syndrome Defective PMNLs Excessive plaque and calculus accumulation leading to rapid
and severe periodontitis before 30 years of age; noted
also in deciduous dentition
Papillon–Lefèvre Defective PMNLs Severe periodontitis noted in deciduous dentition, may affect
syndrome permanent dentition
Chronic granulomatous Defective PMNLs and macrophages Oral ulceration but may also manifest gingivitis, periodontitis
disease
Chediak–Higashi Defective phagocytes Severe childhood periodontitis
syndrome
Ehlers–Danlos syndrome Defective collagen synthesis Childhood periodontitis
Hypophosphatasia Defective formation/mineralization of Premature loss of deciduous teeth
cementum
Job’s syndrome Excessive IgE and histamine release Painful, bleeding gingivae, aggressive periodontitis
by mast cells and IgE immune
complex formation
Histiocytosis X Proliferation and dissemination of Gingivitis, severe periodontitis
Langerhans cells
Leucocyte adhesion Defective PMN diapedesis Acute inammation, proliferation of gingival tissues, rapid
deciency syndrome bone loss, reduced wound healing
Cohen syndrome Neutropenia Periodontitis
Marfan’s syndrome Connective tissue disorder Severe periodontitis
Diabetes mellitus Increased risk of infection, reduced Recurrent periodontal abscesses, advanced periodontitis
wound healing
Adapted from Chapple & Gilbert 2002. IgE: immunoglobulin E; PMNLs: polymorphonuclear leucocytes.
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2.5
DETERMINING
PERIODONTAL PROGNOSIS
MONICA LEE
CHAPTER OUTLINE
Introduction 5. Tooth Type
What is a Prognosis? 6. Anatomical Defects
7. Mobility
Factors Aecting Prognosis 8. CrowntoRoot Ratio
General Factors 9. Abutment Tooth
1. Patient Adherence 10. Other Pathology
2. Smoking Assigning a Prognosis
3. Diabetes
Good Prognosis
4. Other Systemic Conditions
Questionable Prognosis
5. Interleukin 1 (IL-1) Genotype
Hopeless Prognosis
6. Age
7. Gender When to Determine Prognosis
Local Factors 1. Initial Prognosis (Baseline)
1. Bacterial Biolm 2. Revising Prognosis
2. Bone loss Weighting Prognostic Factors
3. Furcation Involvement Improving the Determination of Prognosis
4. Pocket Probing Depth (PPD)

Sound periodontal health provides a foundation for overall dental health and should be established before any other form of dental treatment,
such as restorative reconstruction or orthodontic realignment, can be considered. However, a patient with periodontitis may be at risk of tooth
loss, and it can be helpful when treatment planning to estimate the life expectancy of individual teeth in order to improve the predictability of any
proposed treatment. This chapter will examine the reliability of trying to determine the likely future of periodontally involved teeth.
By the end of this chapter the reader should: is chapter covers the following topics:
• Understand the principles of prognosis • Introduction
• Recognise which factors aòect prognosis and their • What is a prognosis?
weighting • Factors aòecting prognosis
• Be aware of the diòerent prognostic classiöcation schemes • Assigning a prognosis
• Understand how the determination of prognosis can be • When to determine prognosis
improved. • Weighting prognostic factors
• Improving the determination of prognosis.
Introduction explore what information is required in order to determine

the prognosis of a tooth or teeth for periodontal patients. e
One of the hardest tasks for a dentist is to determine the aim is always to make clinical decisions based on good sound
prognosis of an individual tooth predictably. Sometimes, it scientic research. However, the determination of periodon-
is necessary to try to predict the future without having any tal prognosis is an inexact science. is is because multiple
knowledge of what has happened in the past. is chapter will factors (local, systemic, psychological amongst others) can
116
CHAPTER 2.5 Determining Periodontal Prognosis 117
inuence the prognoses of teeth. Nevertheless, estimating supportive periodontal therapy (SPT) are essential to
prognosis is a useful component of periodontal treatment maintain a stable periodontium and improve prognosis.
planning. It can only be achieved by gathering as much infor- • Several studies have shown that a lack of regular SPT will
mation as possible about the patient and individual teeth. adversely aect prognosis even if the periodontal disease
process has been stabilised (Nyman etal. 1975, Axelsson
What is a Prognosis? & Lindhe 1981, Hujoel etal. 2000, Eickholz etal. 2008,
Rahim-Wöstefeld etal. 2020).
e denition of prognosis is the forecasting of the course • Patients attending for SPT irregularly were shown to
and outcome of a specic disease, and the chances of recov- have nearly three times more tooth loss (17.6%) com-
ery. When a prognosis is suggested, it is an attempt to predict pared with patients attending regularly for SPT (6%)
how a tooth or teeth will respond to treatment in the long over a period of 20 years (Rahim-Wöstefeld etal. 2020),
term, taking into account all the factors which may aect the with similar ndings seen in shorter studies.
outcome. Inammatory periodontal diseases are complex and • Other studies and reviews have demonstrated similar
are among the most prevalent chronic diseases of humans. ndings in teeth with hopeless prognosis, showing teeth
As described in previous chapters of this book, patients vary can be maintained and even improve their prognosis with
greatly in their risk for developing disease as a result of the appropriate treatment and regular SPT (Lindhe & Nyman
interaction of microbial, genetic and environmental factors. 1984, Cortellini etal. 2011, Carvalho etal. 2021).
e factors that determine the initiation and progression of
disease are referred to as risk factors (see Chapter 1.6). Risk KEY POINT 2
factors for a disease have been dened as certain characteris- Poor compliance with oral hygiene and irregular supportive
tics of a person or their environment which, when present, periodontal therapy have a negative effect on the prognosis,
directly result in an increased likelihood of that person getting with greater risk of tooth loss.
the disease and, when absent, directly result in a decreased
likelihood (Beck 1995). ey are causally associated with a 2. Smoking
disease. Examples for periodontal diseases are genetics, smok- • Smoking is a signiëcant risk factor and prognostic factor
ing, stress and some systemic diseases. in periodontal diseases and tooth loss (Fardal etal. 2004,
Eickholz etal. 2008).
KEY POINT 1 • Even in patients undergoing regular SPT, smokers are
Risk factors are characteristics of a person or their environment
almost ve times more susceptible to periodontal tooth
which, when present, directly result in an increased likelihood of loss (Chambrone etal. 2010).
that person getting the disease, and when absent directly result • Smoking is strongly associated with worsening prognosis
in a decreased likelihood. and has been shown to double the likelihood of worsen-
ing prognosis at 5 years (McGuire & Nunn 1996).
Many risk factors are also prognostic factors since they • ɨe eêects of smoking after cessation are dose related,
are characteristics that help the clinician to predict outcome and heavy smokers continue to have a signicant risk of
(tooth survival) once the disease process has been initiated. tooth loss compared with non-smokers for up to 15 years
Such factors include smoking, diabetes and poor oral hygiene. (Dietrich etal. 2015, Ravidà etal. 2020).
Determining the prognosis of individual teeth can be
dicult because of the multiple factors that inuence KEY POINT 3
treatment outcome. In order to evaluate the prognosis of There is a dose-related effect between the number of
a tooth, sucient information is required with regards cigarettes smoked and severity of the disease/response to
treatment, which signicantly affects prognosis.
to patient factors and local factors. is means that in
an individual, each tooth will have a dierent prognosis
because of diering local factors, despite the same patient 3. Diabetes
factors occurring. • Diabetic control is an important factor in periodontal
prognosis, with poor glycaemic control associated with
Factors Affecting Prognosis worse periodontal outcomes (Sanz etal. 2017).
• ɨe bi-directional relationship between diabetes and
Any factor that contributes to the way a disease progresses periodontitis is well established, and an increased risk of
can be dened as a prognostic factor. Both general and local periodontitis and severity of disease is associated with hyper-
factors need to be considered. glycaemia. Poorer periodontal outcomes have been shown
following periodontal treatment in hyperglycaemic patients,
General Factors
therefore aecting prognosis (Mealey & Oates 2006).
1. Patient Adherence
• Bacterial plaque is the major aetiological factor for KEY POINT 4
periodontal diseases. It follows therefore that eective Uncontrolled diabetics have a poorer periodontal prognosis
plaque removal by the patient and adherence to regular than well-controlled diabetics.
4. Other Systemic Conditions Local Factors

Some systemic disorders have been shown to be associated 1. Bacterial Biofilm
with poorer periodontal prognosis; these are beyond the • It is widely accepted that patient compliance is a key ele-
scope of this chapter but conditions include: ment in improving long-term tooth survival rates.
• Neutrophil disorders such as Down’s syndrome, • Good patient oral hygiene and compliance have been
Chediak–Higashi syndrome, Papillon–Lefèvre syndrome major factors in maintaining teeth, even for teeth with
and chronic neutropaenias questionable/hopeless prognoses (Chace & Low 1993,
• Osteoporosis: Increased periodontal attachment loss in McGuire & Nunn 1996, Graetz etal. 2011).
post-menopausal women with osteoporosis has been
shown in a small cohort of patients, and higher levels 2. Bone Loss
of tooth loss are reported (Nicopoulou-Karavianni etal. • Advanced bone loss has been reported to be associated with
2009, Penoni etal. 2017) greater future bone loss and reduced tooth survival rates
when bone loss is over 75% (McGuire & Nunn 1996).
5. Interleukin 1 (IL-1) Genotype e type of bone loss (vertical or horizontal) appears to
• IL-1-positive genotype has been reported to have an have little impact on tooth survival. Baseline interproximal
increased eect on tooth loss with a risk ratio (RR) bone loss is associated with increased risk of tooth loss.
of 2.66 over a period of 5–16 years. ɨe combined However with regular SPT 93% of teeth with 60–80%
eect with heavy smoking increases this eect to RR bone loss at baseline survived 10 years (Pretzl etal. 2008).
7.7 (McGuire & Nunn 1999). A positive IL-1 geno-
type can be detected by genetic testing, but it seems to 3. Furcation Involvement
inuence the severity of disease rather than initiation • Less favourable outcomes in treatment have been shown
of the disease (Kornman et al. 1997). Other studies for furcation-involved teeth; McFall (1982) showed that,
have shown that the presence of the IL-1 polymor- over 15 years, 57% of furcation-involved teeth were lost,
phism has been a signicant factor when assessing whereas Hirshfeld & Wassermann (1978) showed over
tooth loss; however, when including tooth-related 22 years that 19.3% of furcation-involved teeth were
logistic multilevel regression analysis the IL-1 positive lost, even in well-maintained individuals. Higher rates of
genotype failed to show signicance (Eickholz et al. tooth loss in furcation-involved teeth have been shown in
2008, Pretzl etal. 2008). longitudinal studies (Helal etal. 2019).
• More recent studies have shown better outcomes of fur-
6. Age cation-involved teeth, with only 15–30% tooth loss over
• Age has been shown to be associated with greater tooth 15–20 years (Dannewitz et al. 2006, Rahim-Wöstefeld
loss. Age over 60 years has been correlated with the num- etal. 2020).
ber of teeth lost for periodontal reasons with various
odds ratios (OR) between 1.1–7.1 reported (Fardal etal. 4. Pocket Probing Depth (PPD)
2004, Chambrone & Chambrone 2006). When consid- • Higher initial probing depths have been suggested to be
ering tooth loss in the older cohorts >80 years of age, associated with a poorer prognosis than shallower pock-
higher risk of losing ≥3 teeth has been shown with an ets (McGuire & Nunn 1996, Nieri etal. 2002), although
OR of 3.3 (1.6–6.8) compared with younger old catego- other studies have shown no correlation between pocket
ries (Nilsson etal. 2019). depth and further attachment loss, suggesting that PPD
• Prevalence and severity of periodontitis does not seem to may be less helpful to consider as a prognostic factor
be aected by age (Needleman etal. 2018). (Goodson etal.1982, Lindhe etal. 1983).
• Greater exposure over time, rather than increased sus-
ceptibility and altered immune function, may play a role 5. Tooth Type
in the increased tooth loss seen in older patients. Other • Inferior survival rates for molars (78.9%) compared to
factors to consider are access to dental care and ability to premolars (86.2%) or anterior teeth (93.1%) have been
perform eective oral health measures, which will also found (Rahim-Wöstefeld etal. 2020).
aect the prognosis of the teeth. • Similar ëndings have been observed in other studies and
shown maxillary molars to have a worse prognosis than
7. Gender mandibular molars, especially when furcation involve-
• Male gender has been described as a prognostic indica- ment is present (Ramɦord etal. 1980, Graetz etal. 2017).
tor for tooth loss (Fardal et al. 2004), but the gender • Tooth type and location has been found to be a factor
diêerences have been low, with less than 10% diêer- associated with tooth loss in periodontal maintenance
ence in disease prevalence between men and women (Chambrone etal. 2010). Signicant dierences have
(Shiau & Reynolds 2010). Gender has been shown to been shown for retention of single-rooted teeth (91%)
have little signicance in tooth loss rates in many stud- compared with multi-rooted teeth with furcations
ies (Needleman etal. 2018). (76.5%) over 20 years (Rahim-Wöstefeld etal. 2020).
6. Anatomical Defects factors they found they could correctly assign a prognosis
• Cervical enamel projections, enamel pearls and develop- 81% of the time. However, they found that if the teeth
mental grooves in maxillary incisors are all local factors which had been assigned a prognosis of “good” were not
associated with disease progression (Shiloah & Kopczyk included then the predictability level dropped to 50% (i.e.
1979). the same level of predictability as tossing a coin). e fol-
• Maxillary premolars with pronounced root concavities lowing are some other studies that have attempted to devise
or “v”-shaped grooves have a worse prognosis because of a prognosis classication system:
an inability to access the concavities for treatment and • Kwok & Caton (2007) described a system to determine
maintenance (Badersten etal. 1987). prognosis based on future stability rather than an end-
point of tooth loss
7. Mobility • Fardal etal. (2004) studied prognosis and actual outcome
• ɨe relationship between tooth mobility and periodontal and found 75% of teeth lost had been given an initial
prognosis is still unclear. prognosis of questionable or poor, whereas the other 25%
• Some studies have shown a poorer long-term prognosis of teeth lost had been given an initial prognosis of “good”.
for mobile teeth (Miller classiëcation 2/3) with greater us it would seem that the predictive accuracy is poor for
risk of loss of attachment (Wang etal. 1994, McGuire & the “questionable” prognosis teeth and only moderate even for
Nunn 1996, Martinez-Canut 2015). “good” prognosis teeth. is is partly due to the multifactorial
• Other studies have shown reduced mobility following nature of the disease, which makes it dicult to know, in indi-
various modalities of treatment and an improvement in vidual patients, which factors are having the greatest eects and
prognosis (Persson 1980, 1981). Similar results over a which may most inuence future disease progression.
5-year period were shown when good plaque control was • Martinez-Canut & Llobell (2018) designed a compre-
maintained (Nyman etal. 1975). hensive approach to assigning periodontal prognosis.
is involved rst assessing the risk of tooth loss due to
8. CrowntoRoot Ratio periodontal disease and second estimating the survival
• Unsatisfactory crown-to-root ratio has been reported to time of periodontally involved teeth. A long-term out-
worsen periodontal prognosis (McGuire & Nunn 1996, come index was used to assess tooth loss due to peri-
Martinez-Canut 2015). Percentage bone loss-to-root odontitis, and a tooth loss prediction model was used
length also inuences prognosis. to ascertain survival time of the periodontally involved
tooth. e prediction model failed to accurately assign
9. Abutment Tooth survival times in patients with an initial low risk of tooth
• Increased loss of teeth used as abutments has been shown, loss due to periodontal disease. It highlights the dicul-
particularly abutment teeth for removable prosthesis ties such prediction models have in accurately assigning
with three times the rate of tooth loss (18%) compared prognosis. is model considered both patient-related
to non-abutment teeth (6%), and twice the rate on xed factors and tooth-related factors.
abutments (12%) compared with the non-abutment Future prognostic models may try to target the most “at-
group over 10 years (Pretzl etal. 2008). risk” groups of patients, which may be useful in identifying
• Reduced loss of abutment teeth in periodontally com- those patients at risk of higher rates of tooth loss (>3 teeth)
promised patients with cross-arch bridgework has been at an earlier stage.
reported (5%) with regular periodontal maintenance Although there is no universal accepted system for deter-
over 10 years (Lulic etal. 2007). mining prognosis, and it is recognised that a high level of sub-
jective clinical judgement is involved in the determination of
10. Other Pathology prognosis, there are some common terms that are used. is
• Perio-endo lesions – if the correct diagnosis is made allows some comparison in retrospective studies and system-
and appropriate treatment carried out, prognosis is not atic reviews. Some of the criteria that have been used to deter-
aected. mine a good, questionable or hopeless prognosis are described
• Non-vital teeth or pulpal lesions which are undetected below to give the reader an understanding of the terms.
and left untreated will have a negative impact on overall
prognosis. Good Prognosis
Assigning Prognosis • tooth projected to be retained as a functional unit with
little or no treatment
ere have been many attempts to devise prognostic clas- • no evidence of disease
sication schemes and criteria but none has been validated • no signiëcant periodontal risk factors
or widely adopted. Patient prognostic factors:
McGuire & Nunn (1996) devised a prognostic system • no systemic conditions
which took certain factors from the initial clinical data to • no local factors
try to correctly assign a prognosis to each tooth. Using these • good oral hygiene (OH) and good compliance
When to Determine Prognosis

Questionable Prognosis
1. Initial Prognosis (Baseline)
• tooth projected to be retained as a functional unit after
treatment has been completed but may still be lost >2 • Tooth-by-tooth prognosis is common practice when ërst
years following treatment seeing a periodontal patient.
• evidence of disease • ɨis relies on eêective history taking to determine patient
• presence of periodontal risk factors factors such as diabetes and smoking history, sound clini-
Patient prognostic factors: cal examination and relevant special tests (vitality testing/
• Controlled systemic disease radiographs).
• Smoker <20 cigarettes/day • Often no information is available on previous disease
• Moderate OH and variable compliance progression but as mentioned this would be helpful
Individual tooth prognostic factors have also been used when determining initial prognosis.
(McGuire & Nunn 1996):
• Greater than 50% attachment loss KEY POINT 5
• Poor root form/length and poor crown-to-root ratio Initial prognosis is a helpful guide to plan treatment but
• Class 3 or class 2 furcation involvement accessible to usually is altered at the reassessment phase when the
maintenance individual’s healing potential, compliance and susceptibility are
determined.
• Mobility 2 or greater
Hopeless Prognosis 2. Revising Prognosis

• Tooth projected to be extracted during the course of Lifestyle factors, immune status, behaviour and local fac-
treatment tors change with time, and these factors can be expected to
Patient prognostic factors: have some inuence on the prognosis, both overall and on
• Uncontrolled systemic disease individual teeth. Treatment plans and supportive care have
• Smoker >20 cigarettes/day to adapt to these changes over time. Determining prognosis
• Poor OH and poor compliance should therefore be thought of as a “dynamic” process (Kwok
Individual tooth prognostic factors (Becker et al. & Caton 2007) and that prognosis should be re-evaluated
1984): periodically as treatment and maintenance progress.
• 75% bone loss is supports the rationale for regular supportive care,
• Pocket depths 8 mm or more as it allows clinicians to reassess risk and, if appropriate,
• Hypermobility provide intervention at each visit. Supportive care is thus
• Class 2 furcations not easily accessible to maintenance crucial in the maintenance of periodontal health, because
• Poor crown-to-root ratio it allows an assessment of patient compliance to supportive
• Close root proximity care, the monitoring of changes in health (i.e. control of
• Repeated abscesses systemic conditions) and the identication of early signs of
Most clinicians do agree when a tooth is beyond treat- disease recurrence (i.e. bleeding on probing, increasing in
ment, although there is still a “grey area” when some clini- pocket depths and increasing bone loss).
cians categorise a dubious prognosis tooth as “hopeless” and
others as “questionable”. Weighting Prognostic Factors
e reason this grey area exists is many research papers
have shown good responses to treatment even from previ- Certain factors seem to have a greater impact on prognosis –
ously hopeless prognosis teeth, with 88% survival rates of “valuable prognostic factors”. Some have a synergistic eect,
hopeless prognosis teeth over 10 years with regeneration worsening prognosis if present together, e.g. smoking and
(Cortellini etal. 2020). hyperglycaemia are believed to have a greater eect together
Hopeless prognosis teeth have also been retained for than the sum of the individual factors alone.
many years without adversely aêecting the adjacent teeth e diculty is “weighting” the prognostic factors and
(De Core et al. 1988). Questionable or hopeless progno- deciding which factor(s) will have the greatest eect in any
sis teeth which have undergone treatment and long-term given individual.
maintenance have shown only 8% tooth loss over 5 years Worsening prognosis has been associated with:
(Cortellini et al. 2011) and 12% tooth loss over 40 years • Smoking – dose related
(Chace & Low 1993). • Uncontrolled systemic factors, e.g hyperglycaemia
Many clinicians therefore opt to retain teeth, even those • Advanced initial probing depths with increasing attach-
considered questionable or hopeless, until initial periodon- ment loss
tal treatment has been carried out. is will of course also • Advanced initial bone loss with increasing bone loss
depend on the wishes of the patient. • Increasing mobility
BOX 2.5.1 Example Of Criteria Used To Determine KEY POINT 6

Prognosis (Checchi et al. 2002) Determining prognosis is a dynamic process. A good history
and examination are essential to determine prognosis.
Tooth prognosis was determined as follows:
To improve the long-term prognosis it is important to
• hopeless: teeth with bone loss greater than 75% or teeth
ensure:
that had at least two characteristics of “questionable”
• Good patient compliance
category;
• Regular supportive periodontal therapy
• questionable: bone loss between 50% and 75%, or the
• Early smoking cessation to reduce risks to level of a
presence of an angular defect or furcation involvement;
non-smoker
• good: teeth with less than 50% bone loss or not tting one
• Encouragement of better general health and well being
of the two previous categories.
Multiple choice questions on the contents of this chapter

(Reprinted from Journal of Clinical Periodontology, 29(7):7, Trombelli et al.
(2002), with permission from John Wiley & Sons. are available online at Elsevier eBooks+
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SECTION 3
Periodontal Treatment Planning
123
3.1
TREATMENT PLANNING –
GINGIVITIS AND
PERIODONTITIS
PAU L B A K E R
CHAPTER OUTLINE
Introduction Step 3
Management of Simple Step 4
Plaque-Induced Gingivitis Structuring Periodontal Treatment
Achieving the Ideal End Points of Treatment
Acute Gingival Conditions and Their Management
Periodontal Reassessment
Periodontal Abscess
Necrotising Gingivitis Management of Furcations
Acute Herpetic Gingivostomatitis Scaling and Root-Surface Instrumentation (Non-Surgical
Treatment Planning for Periodontitis Treatment)
Furcation Surgery
Outcomes of Periodontal Treatment
Tunnel Preparation
The Stepwise Approach to Periodontal Treatment
Root Resection
Step 1
Step 2 Summary

This chapter outlines treatment planning for gingivitis, acute gingival conditions, periodontitis and the management of furcation-involved teeth.
By the end of the chapter the reader should: The chapter covers the following topics:
• Understand the aims of periodontal treatment and how • Introduction
these öt into the overall dental treatment plan • Management of simple plaque-induced gingivitis
• Be familiar with the stepwise approach to periodontal care • Acute gingival conditions and their management
and how this is reøected in periodontal treatment planning • Outcomes of periodontal treatment
• Be able to formulate a treatment plan for the management • The stepwise approach to periodontal treatment
of gingivitis and periodontitis • Structuring periodontal treatment
• Recognise the presentation of acute gingival conditions and • Achieving the ideal end points of treatment
outline their management • Periodontal reassessment
• Describe the treatment options for furcation-involved multi- • Management of furcations
rooted teeth. • Summary
Introduction “cure” patients with a course of treatment; rather, the aim is

to control disease. e short-term responses to active treat-
is chapter looks at the treatment of acute periodontal con- ment may not entirely resolve the patient’s clinical signs of the
ditions and considers the treatment planning of gingivitis and disease. Also, long-term stability relies heavily on the patient’s
periodontitis. Chronic periodontal diseases provide a particu- own eorts with home care. As a result, the management of
lar challenge in treatment planning in that clinicians do not periodontitis often relies on a staged approach where patients
125
126 SECTION 3 Periodontal Treatment Planning
undergo a course of treatment, and the response to each stage

of treatment is assessed before decisions about the next stage
can be made. It is essential that adequate time is given for the
tissues to respond to therapy before a reassessment is made
and worth remembering that the supporting tissues include
epithelium, connective tissue and bone.
KEY POINT 1
Periodontal diseases provide a particular challenge in their
treatment planning in that clinicians do not “cure” patients with
a course of treatment; instead the aim is to control disease.
Long-term stability relies heavily on the patient’s own efforts
with home care.
Management of Simple • Figure 3.1.1 Interproximal calculus hampering plaque control.
Plaque-Induced Gingivitis
Gingivitis is an inammatory response of the marginal gin- including easily accessible calculus, in conjunction with
giva. Dental plaque as the primary cause is supported by oral hygiene instruction. Poor restoration margins should
overwhelming evidence from clinical, microbiological and be corrected, where possible, by reducing and polishing of
epidemiological studies. Management involves the consis- overhangs (Figure 3.1.2) or the placement of temporary or
tent and eective removal of the plaque biolm at the gin- permanent restorations. e patient then needs to be given
gival margin. A classic experimental gingivitis study by Löe the tools they require to achieve an adequate level of plaque
etal. (1965) showed that eective oral hygiene will resolve control (see Chapter 4.1). It is essential that the patient is
gingivitis in as little as 7–10 days. reviewed to ensure that they have managed to improve their
As explained in Chapter 2.2, the basic periodontal exam- home care in accordance with the instructions given and
ination (BPE) identies gingivitis in BPE codes 1 and 2. that the gingivitis has resolved as a result.
Code 1 is dened as bleeding after probing, with no prob- To assess the response to this treatment, a reassessment
ing depths over 3.5 mm. As such, this common condition should be scheduled after an appropriate time to allow the
should respond to improvements in oral hygiene to remove gingivitis to resolve, or for the plaque to re-establish if the
plaque biolm from the critical gingival marginal area. patient’s oral hygiene is still not adequate. is normally
Code 2 describes the presence of plaque-retentive factors takes at least 2 weeks.
in areas that may reduce the eectiveness of oral hygiene
techniques by the patient. Plaque-retentive factors are local
conditions in the mouth that increase the amount of biolm Acute Gingival Conditions and Their
that forms in an area or inhibits self-performed plaque con- Management
trol, promoting biolm accumulation.
Such plaque-retentive factors include calculus, which may • Periodontal abscess
interfere with a patient’s ability to clean inter-proximally • Necrotising gingivitis
(Figure 3.1.1) and which also presents as a rough surface • Acute herpetic gingivostomatitis
that may be more dicult to clean. Other plaque-retentive
factors include anything that creates an area inaccessible to Periodontal Abscess
clean or a surface that is harder to render plaque-free, such
as a poor restoration margin, an overhang, a marginal dis- In this context, the periodontal abscess (Figure 3.1.3) is
crepancy, a rough restorative surface or a carious lesion. one that originates in a pre-existing periodontal pocket as
opposed to one originating primarily from a necrotic pulp,
KEY POINT 2 which can, on occasion, track coronally to drain via the gin-
Although a BPE score of 2 indicates the presence of a plaque- gival crevice or present laterally due to the presence of a
retentive factor, sufcient plaque to cause gingival bleeding lateral canal (the so-called perio-endo lesion).
may not be present at up to a third of sites with this score. A periodontal abscess may occur when the coronal margin
of a periodontal pocket becomes blocked, preventing drain-
Where plaque-retentive factors are present, they need to age of a pre-existing chronic lesion. is can result from the
be corrected as part of the management of plaque-induced impaction of a foreign body or food debris becoming lodged
gingivitis. Clinicians must do what they can to ensure that in the pocket. Alternatively, improved gingival health after
the mouth is more easily cleansable for the patient. is periodontal treatment may result in the marginal tissue
means removing any plaque-retentive factors where possible, around the neck of the tooth becoming tighter, preventing
CHAPTER 3.1 Treatment Planning – Gingivitis and Periodontitis 127
drainage from the pocket and, if plaque-retentive factors per- characterised by a white slough of necrotic tissue supercially
sist at the base of the pocket, an acute response can occur. adjacent to the teeth and an adjacent zone of red inamed tis-
ere may also be an increased tendency towards the for- sue. e necrotic area tends to start at the papillae tips. Patients
mation of periodontal abscesses in patients who are immu- with necrotising gingivitis frequently exhibit an oensive oral
nocompromised, especially in poorly controlled diabetic odour. e causal organisms for necrotising gingivitis have
patients (Herrera etal. 2000). e aetiology and manage- been described as made up of a “constant ora” and a “vari-
ment of periodontal abscesses is shown in Box 3.1.1 able ora”. e constant ora includes spirochaetes such as
Borrelia vincentii and bacteria such as B. intermedius and Fuso-
KEY POINT 3 bacterium spp., and the variable ora consists of other spe-
A periodontal abscess is one that originates in a pre-existing cies of micro-organisms, the exact mix of which varies from
periodontal pocket, as opposed to one originating primarily patient to patient and site to site (Loesche etal. 1982).
from a necrotic pulp. ere are particular predisposing factors that render a
patient more susceptible to necrotising gingivitis. ese
include stress and smoking. In the First World War, over
Necrotising Gingivitis 50% of troops serving in the trenches developed the infec-
Necrotising gingivitis (Figure 3.1.4 and Box 3.1.2) is an tion, and in the Second World War, it was very prevalent
acute infection aecting the marginal gingival tissues around among submariners. ere is also an increased incidence of
the teeth. It has a very particular clinical picture that is necrotising gingivitis in patients who are HIV positive.
e management of necrotising gingivitis should include
the treatment of acute infection and of the underlying predis-
posing factors to reduce the risk of recurrence. Recurrent epi-
sodes of necrotising gingivitis can lead to interdental cratering
where the interdental tissues have been lost (Figure 3.1.5).
Treatment involves gentle cleaning and the use of mouth-
washes, such as hydrogen peroxide or chlorhexidine (see
Box 3.1.2). Necrotising gingivitis responds well to antibi
otics, particularly the penicillins and metronidazole. How-
ever, these should be considered an adjunct to mechanical
debridement (Hartnett & Shiloah 1991). It is worth noting
that although necrotising gingivitis is associated with spe-
cic bacteria, it is not a contagious condition and cannot be
passed between individuals.
KEY POINT 4
Although necrotising gingivitis is associated with specic
• Figure 3.1.2 A restoration overhang at LR7 distally which acts as a bacteria, it is not thought to be a contagious condition and
plaque-retention factor.
cannot be passed between individuals.
A B
• Figure 3.1.3 A periodontal abscess.
• BOX 3.1.1 Aetiology of Periodontal Abscesses • BOX 3.1.2 Presentation and Management of
Necrotising Gingivitis
Causes of Periodontal Abscess
• Pre-existing periodontal pocket Predisposing Factors
• Foreign body impaction, including food, in periodontal • Pre-existing gingivitis
pocket • Poor oral hygiene
• Response to incomplete periodontal therapy • Smoking
 • Improvement in marginal tissue health before pockets • Stress
fully debrided
 • Plaque or calculus pushed into tissues during Signs and Symptoms
instrumentation • Ulceration of the papillae tips or gingival margin
• Compromised immune system • Formation of a pseudo-membrane
 • Poorly controlled diabetes • Pain
• Halitosis
Signs and Symptoms of Periodontal Abscess
• Pain Treatment
• Localised swelling over the tooth • Debridement, though this may be painful
• Pus may come from the gingival margin on probing or • Mouthwashes can help, particularly chlorhexidine or
pressure on local soft tissues hydrogen peroxide based
• There may be an increase in mobility • Antibiotics may be prescribed. Metronidazole is the drug of
• Deep periodontal probing depth choice
• Evidence of a susceptibility to periodontal disease • When the acute phase has been treated, address the
predisposing factors to reduce the chance of recurrence
Treatment of Periodontal Abscess
• Drainage of the abscess is usually achieved by periodontal
instrumentation
• Local anaesthesia and thorough root-surface debridement
• Antibiotics should not routinely be required but may be
considered where there is an underlying systemic medical
factor
• Figure 3.1.5 Interproximal cratering following an episode of necrotis-

ing gingivitis.
• Figure 3.1.4 Necrotising gingivitis.
A more aggressive form of necrotising gingivitis can occur

that extends to the underlying supporting bone and attach- • BOX 3.1.3 Presentation and Management of Acute
ment. So-called necrotising periodontitis may be associated Herpetic Gingivostomatitis
with an underlying immune deciency, particularly HIV
(Robinson 1998) or malnutrition. While the destruction Signs and Symptoms
is far more signicant, the principles of treatment are the • Usually pre-school children
same. • Painful oral ulceration
• Pyrexia
• Increased saliva
Acute Herpetic Gingivostomatitis
Treatment
Primary herpetic gingivostomatitis (Box 3.1.3) is an • Treat symptoms
acute local infection by the herpes simplex virus. It  • Anti-pyretic medication
presents as multiple small vesicles that can coalesce to  • Maintain uid intake
• Wait for infection to run its course, usually 1–2 weeks
produce larger irregular ulcerated lesions surrounded by
erythema (Figure 3.1.6). Lesions may be limited to the
• BOX 3.1.4 Overall Treatment Outcomes in

Periodontal Therapy
• Denitive – leading to a denite end point
• Provisional – leading to an intermediate stage in
treatment to allow further consideration
• Compromise – leading to a less-than-ideal end point
because of unfavourable factors
Patients should be aware of the aims of treatment and
understand why uncertainty may be an issue.
• BOX 3.1.5 Ideal Treatment Outcomes in

• Figure 3.1.6 Irregular ulceration and erythema in herpetic
Periodontal Therapy
gingivostomatitis. •All pockets 4 mm or less
•Bleeding on probing less than 10%
•Plaque score less than 15%
gingiva or include other mucosal areas of the mouth. •No furcations probeable
Historically, in the United Kingdom, the condition was As dened by the British Society of Periodontology and
usually seen in young children where it is associated with Implant Dentistry, these are the ideal end points of treatment as
they are associated with periodontal stability. These end points
herpes simplex virus (HSV) 1. However, increasingly, it
may not be achievable in some cases and a compromise may
is seen in young adults where it tends to be associated have to be accepted.
with HSV-2.
Transmission is by direct contact with the infected lesions
or saliva of an individual with an infected lesion.
KEY POINT 5
Treatment Planning for Successful treatment of periodontitis can only be judged in
the long term by stable attachment levels and the retention of
Periodontitis teeth.
Outcomes of Periodontal Treatment

For periodontitis, one approach is to divide the phases of
Much of dentistry involves planning for treatment where treatment into:
the result can be predicted with some certainty, such as • Cause-related therapy – generally speaking, non-surgi-
the placement of a restoration in a tooth with a small- or cal treatment aimed at managing the cause of the dis-
medium-sized carious lesion. Some situations are less pre- ease and resulting in clinical improvements in the soft
dictable both in the short-term response to treatment and tissues
the longer-term success of that treatment. • Corrective therapy – surgical procedures such as pocket
e management of periodontitis often falls into this reduction or elimination that aim to re-establish a nor-
more unpredictable category, and clinicians therefore sched- mal dento-gingival anatomy, albeit at a dierent position
ule reassessment appointments to monitor what has been around the tooth
achieved by treatment to date and to plan the next stage • Supportive periodontal therapy – ongoing regular peri-
(Box 3.1.4). Ultimately, the aim is to achieve a benecial odontal therapy aimed at maintaining periodon-
outcome for the patient; however, successful treatment of tal health and reducing or preventing further disease
periodontitis can only be judged in the long term by stable progression.
attachment levels and the retention of teeth. e diculty is is not to say that one phase of treatment neces-
with this approach is that success is being judged retrospec- sarily progresses to the next, rather that these are staged
tively. When treating patients or trying to assess the clinical approaches in managing the disease. With a high level of
success of treatment, surrogate measures, which are associ- patient compliance, many periodontal conditions may sta-
ated with periodontal stability, are used. e most com- bilise with cause-related therapy alone. e best approach
monly reported measure with the greatest predictive ability for an individual patient, or clinical situation, will depend
for tooth loss is probing pocket depth. e British Soci- on the patient’s attitude as well as the oral ndings. e
ety of Periodontology and Implant Dentistry has produced European Federation of Periodontology (EFP) produced the
guidelines that outline the ideal end points of the treatment S3 Clinical Practice Guideline for the Treatment of Stage
of periodontitis (Box 3.1.5). ese are helpful for the clini- I-III Periodontitis (Kebschull & Chapple 2020, Sanz etal.
cian as they set the aims for any course of periodontal treat- 2020). is applied evidence-based clinical recommenda-
ment and also set standards against which the patient can be tions as a stepwise approach to treatment (see Chapter 4.3
judged during reassessment. for further details).
Table 4 Stepwise approach
Step of therapy Periodontitis Periodontitis Periodontitis stage III (and stage IV

stage I stage II in BSP implementation plan)
Step 1: Control of risk factors Always
Step 2: Subgingival Only in affected teeth Only in affected teeth, possibly with
instrumentation adjunctive measures
Step 3: Corrective surgery N/A Only in affected teeth after re-evaluation

of step 2 procedures; specialists/dentists
with specific training; subjects with
adequate biofilm control
Supportive periodontal therapy Always
• Figure 3.1.7 The stepwise approach to treating periodontitis. (Reprinted by permission from Springer
Nature: Br. Dent. J. Evidence-based, personalised and minimally invasive treatment for periodontitis
patients - the new EFP S3-level clinical treatment guidelines, Kebschull, M., Chapple, I., copyright 2020.)
The Stepwise Approach to Periodontal (PMPR). Consideration should also be given to systemic
Treatment factors, such as smoking cessation advice or diabetes
control.
e stepwise approach (see Appendices 3 and 4) breaks
treatment down into a series of stages which follow the KEY POINT 6
classic management strategy for periodontitis and maps Optimal oral hygiene has been shown to be critical to the long-
them to the new classication system developed in 2017. term stability of any post-treatment improvements.
e extent to which a patient is likely to progress along the
stepwise approach can be estimated by their classication
(Figure 3.1.7). Step 2
e rst stage of treatment is considered the pre-requisite is is the cause-related therapy mentioned previously and
to therapy and referred to as step 0 (see Appendix 3). is involves disruption of the biolm by subgingival instru-
includes the initial examination and subsequent diagnosis mentation, possibly including the use of local or systemic
and classication of the periodontal condition. Risk factors adjunctive measures if appropriate (such as local delivery
should be assessed, and the patients educated on the causes antiseptics or systemic antibiotics).
of the disease and relevance of those risk factors. From there, Subgingival instrumentation is aimed at removing
a personal care plan should be developed. plaque and plaque-retentive factors, such as subgingival cal-
culus, from root surfaces. Signicant probing depth reduc-
tion can be achieved by non-surgical periodontal treatment,
Step 1
which is almost invariably the rst line of treatment. is
Step 1 is aimed at motivating the patient and establishing is technically demanding and requires scheduling sucient
the behaviour changes required for successful periodon- time to allow the treatment to be done thoroughly. ere
tal treatment. Optimal oral hygiene has been shown to be are dierent ways of approaching the appointment sched-
critical to the long-term stability of any post-treatment ules (see Chapters 5.1 and 5.2), depending upon the extent
improvements (Axelsson et al. 2004). Optimal supragin- and severity of the disease, the clinician’s preferred approach
gival plaque control is also required to reduce subgingival and the patient’s acceptance of treatment. ere is little
recolonisation by the periodontal pathogens associated evidence to support one approach over another (Eberhard
with the disease (Magnusson etal. 1984). For this reason, etal. 2008).
ideally, an optimal level of oral hygiene should be estab- Adjunctive use of specic antibiotics may be prescribed
lished before undertaking subgingival instrumentation. As for specic cases where the disease is particularly aggressive,
a patient’s home care improves, there should be a reduc- such as generalised periodontitis stage III in a young adult.
tion in inammation, and this will lead to a reduction in If adjunctive antibiotics are used, then it is essential that all
probing depths. Oral hygiene is covered in more detail in the root-surface instrumentation is completed during the
Chapters 4.1 and 4.3 course of antibiotics (see Chapter 5.3).
Local risk factors should be addressed, such as the
removal of supragingival plaque-retentive factors, as Step 3
mentioned in the section on the management of gingi- Step 3 follows a periodontal reassessment after a suitable
vitis, along with professional mechanical plaque removal time is allowed for a response to the non-surgical therapy.
Diagnosis:
Periodontitis stage/grade
Periodontal factors to consider General factors to consider

• Smoker? • Caries management
• Do hopeless teeth need extracting? • Extractions – need replacement?
• Adjunctive antibiotics? • Definitive or provisional?
• Possible systemic factors? • Local factors need addressing?
• Local factors need addressing? • Ability to commit for treatment
• Is surgery likely? • Contributing medical history
• Should I refer?
Overall treatment plan
• Figure 3.1.8 Factors to consider when a diagnosis of periodontitis has been made.
When there are sites where the end points have not been TABLE Factors to consider when assessing
met, then further treatment, as outlined in step 3, is consid- 3.1.1 prognosis
ered. is may involve further non-surgical therapy when Assessing prognosis
further improvements could or should be expected, or sur-
gical intervention where anatomical considerations such as Tooth factors Patient factors
vertical bone loss or furcation involvements limit the like- Restorative condition Susceptibility
lihood of success by simpler means. Periodontal surgery
Endodontic condition Oral hygiene ability
should not be considered in the absence of adequate level of
plaque control by the patient. Periodontal condition Dexterity
Attachment level Motivation
Step 4
Bone height Systemic disease
Step 4 represents supportive periodontal therapy (SPT),
which is aimed at maintaining periodontal stability. It can be Root length Smoking status
hoped that the periodontally involved sites have responded Root shape/divergence
to the treatment provided in either step 2 or step 3,
Site of defect
and the ideal end points have been achieved. e patient
can then be put into an SPT regime appropriate for their Plaque-retentive factors
needs (Chapter 5.4). Furcation involvement
Structuring Periodontal Treatment

e stepwise approach helps structure the management of hospitals are divided into departments. However, in den-
periodontitis, but this still needs to be tailored to the indi- tal practice, patients will often present with multiple oral
vidual needs of the patient. Figure 3.1.8 gives examples of problems, and a decision has to be made about the priori-
the factors that could inuence the overall treatment plan. tisation of treatment and how to break down the treatment
As the complexity of a case increases, so does the importance into a manageable, logical structure. is will ensure that
of assessing the prognosis as part of the planning process all the oral problems are considered in a systematic way
(Table 3.1.1). e prognosis can relate to individual teeth, (Box 3.1.6).
based on factors that may be favourable or unfavourable, or
to patient factors that will inuence the response to treat-
ment. Estimation of prognosis will allow the clinician to Achieving the Ideal End Points of
make judgements on the likely outcome of treatment both Treatment
at a tooth level and patient level. Prognosis is covered in
detail in Chapter 2.5 e aims of periodontal treatment have been outlined in
It is also worth considering where periodontal treat- Box 3.1.5. ese treatment outcomes do not eliminate
ment ts into the overall management of a dental patient. the risk of disease progression but are all associated with
Dental education can compartmentalise dentistry into its maximising the likelihood of stability and a reduced risk of
various specialities and disciplines. ere is an obvious progression. A treatment plan for the management of peri-
benet to this, particularly when considering that teaching odontitis is aimed at achieving these outcomes. e success
• BOX 3.1.6 A Treatment Path for Patients with • BOX 3.1.7 Management Options for Furcation-
Multiple Dental and Oral Problems Involved Teeth
1. Relief of acute symptoms Grade I Furcation Involvement
2. Oral hygiene instruction, diet analysis, disease prevention • Scaling and debridement
3. Addressing active disease • Surgery
a. Extraction of hopeless teeth  • Improve access by tissue reshaping and bone removal
b. Provision of immediate prostheses  • To facilitate debridement
 c. Correction of local risk and plaque-retentive factors • Regular maintenance
 d. Treatment of caries and pulp symptoms
e. Occlusal therapy Grade II Furcation Involvement
4. Non-surgical periodontal treatment
5. Reassessment • Scaling and debridement (maintenance)
6. Corrective therapy • Surgery
a. Root canal treatment
 • Improve access by tissue reshaping and bone removal
b. Periodontal surgery
 • To facilitate debridement
c. Orthodontic therapy
• Periodontal regenerative surgery
7. Denitive restorative treatment – xed/removable • Tunnel preparation – conversion to grade III to facilitate oral
prosthodontics hygiene
8. Recall/maintenance/supportive periodontal therapy • Root resection
• Extraction
Grade III Furcation Involvement

• Scaling and debridement (maintenance)
of each phase of treatment, or after treatment during SPT, • Tunnel preparation
is judged on the reassessment which should be scheduled • Root resection
within an appropriate time frame. • Extraction
Periodontal Reassessment
Clinicians do not cure patients of periodontal diseases; is residual inammation or where there is a thin tissue bio-
rather they aim to control the disease. As such, there is no type that can be expected to recede, leading to probing
actual end to treatment, and the long-term maintenance depth reduction, or where tissue shrinkage as a result of the
of periodontal health is an ongoing process (see Chapter initial therapy has improved access to residual contaminated
5.4). e purpose of a reassessment appointment is to assess root surface and calculus deposits. Periodontal surgery still
whether the desired clinical end points have been achieved has a place and can be considered when it is appropriate (see
and to decide what the next stage of treatment is for the Chapter 6.1).
patient. is may be further active treatment or the pre-
scription of a supportive periodontal maintenance regimen Management of Furcations
and setting of a recall period, when a formal periodontal
review will be performed. e time between active treat- Furcation involvements can pose a particular challenge in
ment and reassessment should be sucient for the tissues to their management. e positions of the furcation entrances
respond. Badersten etal. (1984) showed that there may be are often in less accessible areas of the mouth, making treat-
improvements for up to 9 months following non-surgical ment and access for plaque control more awkward. Furca-
treatment. However, most of the change will have occurred tions are associated with complex tooth shapes within the
and be recordable at 8–12 weeks. erefore, reassessment furcation leading to an unfavourable anatomy for plaque
appointments are often scheduled 8–12 weeks after active control as well as adversely aecting the healing potential.
treatment. ere is less scope for a reduction in the probing depths
e reassessment appointment involves gathering all the after treatment. e classication of furcation involvements
relevant periodontal data once again so that these can be is covered in Chapter 2.2. e management options for the
compared to previous periodontal examinations. Improve- treatment of furcations are summarised in Box 3.1.7
ments in clinical parameters, as well as assessment of further
disease progression or stability, will all be considered when Scaling and Root-Surface Instrumentation
deciding what the next stage of treatment should be. is
(Non-Surgical Treatment)
might involve further oral hygiene instruction with the aim
of improving the long-term stability, further subgingival Scaling and root-surface instrumentation can be particu-
debridement or periodontal surgery. larly challenging in furcation-involved teeth because of the
Further non-surgical treatment is considered if further additional diculties in accessing the root surface. Teeth
improvements can be expected. is may occur when there with narrow furcation entrances and close roots can be very
• Figure 3.1.9 Osteoplasty in the furcation area to improve access for • Figure 3.1.10 Access between the roots in this class III furcation
plaque control. allows the patient to clean with an interdental brush.
dicult to clean thoroughly, and the tooth surface may have survival of teeth that had had tunnel procedures and found
concavities within the furcation that cannot be accessed the main reason for failure in teeth treated in this way was
by even the smallest curette or ultrasonic tip. Furcation caries in the furcation.
entrances may also be interproximal in the case of upper
rst premolars.
Root Resection
Furcation Surgery Root resection is an option for converting an uncleansable
furcation defect into one that can be maintained by divid-
Periodontal surgery to furcation entrances can help over- ing the tooth and either removing one root (root resection),
come the diculties associated with non-surgical manage- one half of the tooth (hemisection) or converting a molar
ment of furcation entrances. Access to the root surface for unit into two premolar-sized units by dividing the crown
debridement is improved by raising a periodontal ap. e and restoring each root as individual premolar-sized units
local tissues can also be adjusted where possible to improve (premolarisation) (Figures 3.1.11 and 3.1.12). ese can
postoperative maintenance. e furcation entrance itself can be complicated treatment options as the tooth needs to be
be carefully opened by means of judicious use of a water- root-treated before the roots can be sectioned and removed,
cooled handpiece. is local osteoplasty (bone removal) and and often the tooth will need to be restored with a full cov-
ap modication can improve the postoperative access for erage crown afterwards. Lee et al. (2012) recently showed
maintenance (Figure 3.1.9). that the average lifespan of a root-resected tooth is around 7
Periodontal regenerative surgery is a technique that aims years, so it should still be considered as a possible treatment
to stimulate bone growth in intra-bony defects. In theory option to prolong the life of a severely compromised tooth.
this could occur between the roots to close the furcation.
Whilst regenerative surgery is recognised as a possible treat-
ment option, this has proven to be an unpredictable way of Summary
managing furcations.
Periodontal treatment, and periodontal treatment planning,
should always be considered in the context of the patient’s
Tunnel Preparation
overall treatment needs. Once any acute problems have been
e tunnel preparation aims to convert a grade II or grade resolved, periodontal treatment planning then aims to control
III furcation into an open grade III furcation that can be the destructive processes that characterise periodontitis. Fol-
maintained by the patient (Figure 3.1.10). It will usually lowing a stepwise approach to periodontal treatment planning
involve raising buccal and lingual aps and reshaping the should ensure a successful and stable periodontal outcome.
tissues to leave the furcation open for interproximal brush- Central to successful periodontal outcomes is the patient’s
ing. Occasionally, persistent oral hygiene can convert a self-care as well as long-term professional supportive care.
grade II or III furcation involvement to one that can be Multiple choice questions on the contents of this chapter
maintained in this way. Hellden etal. (1989) looked at the are available online at Elsevier eBooks+
A B
C
• Figure 3.1.11 A root-resected lower molar tooth: (A) the tooth on presentation, (B) radiograph and (C)
clinical appearance 10 years after surgery.
Eberhard J, Jervøe-Storm PM, Needleman I, Worthington H, Jepsen

S. Full-mouth treatment concepts for chronic periodontitis: a sys-
tematic review. J Clin Periodontol. 2008;35:591–604.
Hartnett AC, Shiloah J. e treatment of acute necrotizing ulcerative
gingivitis. Quintessence Int (Berl). 1991;22:95–100.
Hellden LB, Elliot A, Steennsen B, Steensen JEM. Prognosis of
tunnel preparations in the treatment of class III furcations. A fol-
low-up study. J Periodontol. 1989;60:182–187.
Herrera D, Roldan S, Sanz M. e periodontal abscess: a review. J
Clin Periodontol. 2000;27:377–386.
Kebschull M, Chapple I. Evidence-based, personalised and minimally
invasive treatment for periodontitis patients - the new EFP S3-level
clinical treatment guidelines. Br Dent J. 2020;229(7):443–449.
Lee KL, Corbet EF, Leung WK. Survival of molar teeth after resec-
tive periodontal therapy – a retrospective study. J Clin Periodontol.
2012;39:850–860.
• Figure 3.1.12 A hemisected lower molar tooth.
Löe H, eilde E, Jenson SB. Experimental gingivitis in man. J Peri-
odontol. 1965;36:177–187.
Loesche WJ, Syed SA, Laughon BE, Stoll J. e bacteriology of acute
necrotising ulcerative gingivitis. J Periodontol. 1982;53:223–230.
References Magnusson I, Lindhe J, Yoneyama T, Liljenberg B. Recolonization of
a subgingival microbiota following scaling in deep pockets. J Clin
Axelsson P, Nyström B, Lindhe J. e long-term eect of a plaque Periodontol. 1984;11:193–207.
control program on tooth mortality, caries and periodontal disease Robinson PG. Which periodontal changes are associated with HIV
in adults. Results after 30 years of maintenance. J Clin Periodontol. infection? J Clin Periodontol. 1998;25:278–285.
2004;31:749–757. Sanz M, Herrera D, Kebschull M, Chapple I, Jepsen S, Beglundh
Badersten A, Nilveus R, Egelberg J. Eect of non-surgical periodon- T, Sculean A, Tonetti M. Treatment of stage I-III periodontitis-
tal therapy II. Severely advanced periodontitis. J Clin Periodontol. e EFP S3 level clinical practice guideline. J Clin Periodontol.
1984;11:63–76. 2020;47(suppl 22):4–60.
3.2
The Management of
Mucogingival Conditions
(Gingival Recession)
DAV I D G I L L A M A N D W E N DY T U R N E R
CHAPTER OUTLINE
Introduction Tooth Movement
Denitions Smoking
Healing after Periodontal Treatment
Gingival Recession
Restorative Dentistry
Dentine Hypersensitivity
Removable Partial Dentures
Prevalence of Gingival Recession and Dentine Self-Inøicted Trauma/Chemical Trauma
Hypersensitivity Clinical Outcomes of Gingival Recession
Mechanisms for Gingival Recession Dentine Hypersensitivity
Aesthetics
Mechanisms for Sensory Transmission of Dentine
Plaque Retention and Gingival Inøammation
Hypersensitivity Sensitivity
Tooth Abrasion
Aetiology of Gingival Recession and Dentine Hypersensitivity Root Caries and Non-Carious Cervical Lesions
Classication of Gingival Recession Management and Treatment of Gingival Recession Defects
Predisposing Factors for Gingival Recession and Dentine Hypersensitivity
Anatomical Recession (Tooth Position) Non-Surgical Management of Gingival Recession and
Quantity of Attached Gingiva Dentine Hypersensitivity
Periodontal (Gingival) Biotype 1. Preventive Care
Bone Morphology 2. Non-Surgical Correction of Recession Defects
Malocclusion Surgical Treatment of Gingival Recession Defects
High Attachment of Frenum Pedicle Soft Tissue Grafts
Free Soft Tissue Grafts
Precipitating Factors for Gingival Recession
Guided Tissue Regeneration
Plaque, Calculus and Periodontal Diseases
Summary
Toothbrush Trauma

After providing denitions, this chapter describes the prevalence of gingival recession and dentine hypersensitivity, mechanisms for gingival
recession and dentine hypersensitivity, aetiology, classication, predisposing and precipitating factors and management of these conditions.
By the end of the chapter the reader should: • Mechanisms of sensory transmission of dentine
• Understand the causes of gingival recession and dentine hypersensitivity
hypersensitivity • Aetiology of gingival recession and dentine hypersensitivity
• Be able to manage these conditions using a non-surgical • Classiöcation of gingival recession including the updated
approach. guidelines from the World Workshop 2017
The chapter covers the following topics: • Predisposing factors for gingival recession
• Precipitating factors for gingival recession
• Introduction • Management – treatment of gingival recession defects and
• Deönitions dentine hypersensitivity
• Prevalence of gingival recession and dentine hypersensitivity • Summary.
• Mechanisms for gingival recession
135
A
• Figure 3.2.2 Clinical features of gingival recession with associated
dentine hypersensitivity.
Definitions
Gingival Recession
A marginal tissue recession is characterised by the displace-
ment of the location of marginal periodontal tissues api-
cal to the cemento-enamel junction (American Academy
of Periodontology 2001). Gingival recession, dened as
an apical shift of the gingival margin with respect to the
B cemento-enamel junction (CEJ), is associated with clinical
• Figure 3.2.1 Clinical features of (A) gingival recession defect with attachment loss (CAL) and exposure of the root surface to
so-called toothbrushing trauma and (B) gingival recession associated the oral environment (Cortellini & Bissada 2018).
with localised plaque-induced inammation lesion. Source: Lindhe J,
Lang NP & Karring T, eds: Lindhe’s Clinical Periodontology and Implant
Dentistry, 2 Volume Set, 7th Edition, 2021. Dentine Hypersensitivity
Introduction Pain from dentine hypersensitivity is generally one of the main
symptoms of gingival recession together with patients’ aesthetic
According to the published epidemiological studies, expo- concerns. Dentine hypersensitivity has been dened as “being
sure of the root surface may be a consequence of: characterised by short sharp pain arising from exposed dentine
1. Overzealous or improper oral hygiene habits in popula- in response to stimuli (typically thermal, evaporative, tactile,
tions and patients with high standards of oral hygiene osmotic or chemical) and which cannot be ascribed to any
where gingival recession and dentine hypersensitiv- other form of defect or disease” (Canadian Advisory Board on
ity predominantly aects the buccal surfaces of upper Dentin Hypersensitivity 2003). From a clinical perspective, the
canines, premolars and molars (Figure 3.2.1A) denition of dentine hypersensitivity is essential when treating
2. Progression/treatment of periodontal diseases in popula- the condition and is important when considering a dierential
tions and patients with poor plaque control or who have diagnosis of tooth-related pain (Figure 3.2.2).
been deprived of professional dental care and education
where recession defects may be more widely distributed
around all four surfaces of the aected tooth (Figure Prevalence of Gingival Recession and
3.2.1B). Dentine Hypersensitivity
Patients may also become aware of the problems asso-
ciated with gingival recession: for example, aesthetics, the ere are limited data on studies that specically look at
appearance of triangular interdental spaces, pain from den- gingival recession and dentine hypersensitivity. Generally
tine hypersensitivity and a fear of losing teeth which, in speaking, the two conditions are investigated separately in
turn, may have an impact on their quality of life. the published literature and, consequently, there is an over-
lap of information when discussing aetiology, predisposing
KEY POINT 1 factors and clinical features of the two conditions (Kassab
Exposure of a root surface may be the consequence of & Cohen 2003, Kamal 2005, Gillam & Orchardson
overzealous/improper oral hygiene habits and/or progression/ 2006). A study by Colak etal. (2012) reported that 7.6%
treatment of periodontal diseases.
of Turkish patients experienced dentine hypersensitivity
CHAPTER 3.2 The Management of Mucogingival Conditions (Gingival Recession) 137
upon testing, most of these sensitive teeth had associ- Stimulus:

ated buccal gingival recession of up to 3 mm. A study by thermal, mechanical,
West et al. (2013) reported an association between clini- evaporative, chemical
cally elicited dentine hypersensitivity, erosive tooth wear Acts on
and gingival recession in 18–35-year-old European adults.
Secondary analysis on 350 UK participants enrolled in the
Exposed dentine;
main European study indicated that while each partici- open tubules
pant exhibited at least one tooth with gingival recession,
many of these teeth did not exhibit dentine hypersensi-
tivity despite prevalent recession and severe erosive tooth Increase rate of
wear (Seong etal. 2018). dentinal fluid flow
Mechanisms for Gingival Recession

Generation of
Baker and Seymour (1976) proposed a hypothesis that action potentials in
intradental nerves
would explain gingival recession caused by: (1) good oral
hygiene practice (e.g. overzealous toothbrushing) and (2)
periodontitis. It is plausible that toothbrushing leads to Action potentials pass
subclinical inammation by epithelial permeability, and to brain to cause PAIN Dentine
both the gingival biotype and quality of the underlying
bone may inuence the degree of localised destruction of Pulp
the gingival crest. Similarly, the presence of plaque may lead
to inammatory changes within the connective tissue space
and subsequent destruction and remodelling of the gingival Nerve
crest. e resultant clinical appearance of this remodelling
will be determined by the periodontal (gingival) biotype;
a thin gingival biotype may result in recession whereas, in • Figure 3.2.3 Outline of the hydrodynamic mechanism by which stim-
thick gingival biotypes, the inammation may be conned uli activate interdental nerves to cause pain. Source: Orchardson, R.,
to the region of the gingival sulcus and persist as a periodon- Gillam, D.G., 2006. Managing dentine hypersensitivity. J. Am. Dent.
Assoc. 137,990–998.
tal pocket.
Aetiology of Gingival Recession and

Mechanisms for Sensory Transmission of Dentine Hypersensitivity
Dentine Hypersensitivity Sensitivity
Gingival recession should be considered a multifacto-
Several mechanisms are described for the transmission of rial periodontal condition. ere are several contributory
various stimuli across dentine to the pulp, for example: (1) predisposing and precipitating factors which may interact
nerves in dentine, (2) the odontoblast as a sensory receptor or to cause gingival recession and dentine hypersensitivity
transducer and (3) the hydrodynamic theory. Currently, the (Figure 3.2.4). e aetiological factors associated with den-
hydrodynamic theory, as proposed by Brännström (1963), is tine hypersensitivity may initiate two specic biological
considered the main mode of stimulus transmission across processes, namely, lesion localisation and lesion initiation.
dentine. Briey, the hydrodynamic theory describes the pro- Lesion localisation occurs when the dentine is exposed due
cess whereby rapid uid movement (towards the pulp or away to the loss of enamel and/or soft tissue (including the loss
from the pulp) in the dentinal tubules responds to either a of cementum). Once the dentine is exposed, patent dentine
cold, hot or osmotic stimulus on the exposed dentine surface tubules will be exposed to the oral environment and lesion
and subsequently activates the A-δ bres in the pulp–dentine initiation may occur. e predominant factor in this process
area by a mechanoreceptor action (Figure 3.2.3). appears to be acid erosion.
Evidence from scanning electron microscopy studies has e role of gingival recession in dentine hypersensitiv-
demonstrated the presence of open dentine tubules on the ity therefore should be considered as a predisposing factor
outer surface of sensitive teeth. In addition, the number and rather than the primary cause. For example, areas of gingival
width of the open dentinal tubules in sensitive and non- recession may dictate where lesions are initiated; however,
sensitive dentine may have a signicant impact on the rate dentine hypersensitivity may occur when erosion opens up
of uid ow through dentine. the exposed dentine tubules.
KEY POINT 2
Dentine hypersensitivity is mediated by a hydrodynamic KEY POINT 3
process. Gingival recession is a multifactorial periodontal condition.
Faulty toothbrushing+
Oral piecing+
Occlusal injury+
Mechanical forces
Bone dehiscence* Orthodontic movement+

Anatomy Iatrogenic factors
Malocclusion+ Restorative dentistry+
Tooth position+
Gingival biotype* Recession
Aberrant fraenal
attachment*
Quantity of attached Plaque-induced
Ageing Pathological factors
gingiva* inflammation (smoking+)
• Figure 3.2.4 Examples of contributory predisposing* and precipitating + factors associated with a mar-
ginal tissue recession defect. Source: Kassab, M.M., Cohen, R.E., 2003. The etiology and prevalence of
gingival recession. J. Am. Dent. Assoc. 134,220–225.
Attached gingiva
Mucogingival junction
Alveolar mucosa
Class I
Class II Class III Class IV

• Figure 3.2.5 Miller’s classication of gingival recession (Miller 1985a).
Classification of Gingival Recession surgical techniques (Pini-Prato 2010, Cortellini & Bissada
2018). e classication (RT1–RT3) described by Cairo
Several classications have been previously proposed in the et al. (2011) is a treatment-oriented classication which
published literature to facilitate both a diagnosis and a tem- forecasts the potential for root coverage through the assess-
plate for a therapeutic strategy. Currently, the classication ment of both the recession depth and the interdental CAL
mainly used by clinicians in root-coverage procedures is the (Table 3.2.2). is classication system for recession has
Miller classication system (I–IV) (Miller 1985a). One of been recommended by the 2017 World Workshop (Cortel-
the advantages of this classication is the ability to corre- lini & Bissada 2018).
late treatment prognosis/outcome and anatomical features, In the Cairo RT1 classication (Miller class I & II) 100%
whereas previous classication systems used either ana- root coverage can be predicted. In the Cairo RT2 classica-
tomical features or treatment prognosis only (Figure 3.2.5, tion (overlapping Miller class III) several randomised clini-
Table 3.2.1). However, it should be acknowledged that this cal trials indicate the limit of interdental CAL within which
classication was proposed when root-coverage techniques 100% coverage is predictable when applying dierent root
were in their infancy and as such the forecast of potential coverage procedures. In the Cairo RT3 classication (over-
root coverage in the Miller classication (I–IV) no longer lapping Miller class IV) full root coverage is not achievable
matches the treatment outcomes of the most advanced (Cortelinni & Bissada 2018).
TABLE
3.2.1 Miller’s classication of marginal tissue recession defects
Classification Distinguishing feature Description

Miller (1985a) Takes into consideration Class I Marginal tissue recession that does not extend to the mucogingival
factors that may inuence junction with no interproximal tissue loss
both treatment and
anticipated therapeutic junction, with no periodontal attachment loss in the interdental area
outcomes Class III Marginal tissue recession that extends to or beyond the
mucogingival junction, with periodontal attachment loss in the interdental
area or malpositioning of teeth
Class IV Marginal tissue recession that extends to or beyond the
mucogingival junction, with severe bone or soft tissue loss in the
interdental area, to a level apically to the buccal/labial soft tissue margin
and/or severe malpositioning of teeth (see Figure 3.2.5)
(Miller 1985a)
TABLE The recession classication system (Cairo plaque accumulation and lead to both recession and pocket
3.2.2 etal. ) as recommended by the World formation. ere is no published evidence, however, to sug-
Workshop  gest that a lack of an “adequate” zone of attached gingiva
results in an increased incidence of soft tissue recession in
Recession patients maintaining a proper level of plaque control (Cor-
type (RT) Clinical features telinni & Bissada 2018).
RT1 Gingival recession with no loss of A recent consensus concluded that a minimum amount
interproximal attachment. Interproximal of keratinised tissue is not needed to prevent attachment
CEJ is clinically not detectable at both loss when adequate plaque control is being maintained.
mesial and distal aspects of tooth. However, attached gingiva is important to maintain gingival
RT2 Gingival recession associated with loss of health in patients with suboptimal plaque control (Cortel-
interproximal attachment. The amount of inni & Bissada 2018).
interproximal attachment loss is less than
or equal to the buccal attachment loss.
Periodontal (Gingival) Biotype
RT3 Gingival recession associated with loss of
interproximal attachment. The amount of Soft tissue biotype can aect the outcome of periodontal
interproximal attachment loss is higher
treatment and root-coverage procedures. Several investigators
than the buccal attachment loss.
have dened a thin tissue biotype as a thickness of <1.5 mm
Source: Reprinted from Journal of Clinical Periodontology 45:(Supple- and a thick tissue biotype as a tissue thickness >2 mm (Claey
& Shanley 1986). Clinicians traditionally have used a probe
permission from John Wiley & Sons.
to discriminate thin from thick gingiva based on the transpar-
ency of the probe through the gingival tissues, although this
method may have inherent aws (Fu etal. 2010). Recent stud-
Predisposing Factors for Gingival ies examining tissue biotype and its relation to the underlying
bone morphology would appear to suggest that periodontal
Recession (gingival) biotype is signicantly related to labial plate thick-
Anatomical Recession (Tooth Position) ness, alveolar crest position, keratinised tissue width, gingival
architecture (thickness), tooth dimension and probe visibility
Several anatomical factors are associated with gingival recession: but is unrelated to gingival recession (Cook etal. 2011, Cor-
• Tooth position in the dental arch (e.g. a prominent buc tellini & Bissada 2018). Examples of normal, thin and thick
cally positioned upper canine) gingival tissues can be seen in Figure 3.2.6. Table 3.2.3 shows
• Overcrowding with tooth displacement out of the arch management options for thick and thin periodontal (gingival)
(with bone dehiscence) biotypes in the absence and presence of gingival recession.
• Bulbous root structure
• Enamel pearls.
KEY POINT 4
Quantity of Attached Gingiva The new classication system for gingival recession
recognises the importance of the periodontal (gingival) biotype,
Historically, it has been suggested that the absence of an interproximal attachment loss and the characteristics of the
root surface
adequate width of attached gingiva may reduce resistance to
Bone Morphology
e alveolar bone crest is usually approximately 1–2 mm
apically to the CEJ, but tooth position in the arch can aect
the bone morphology around a tooth. Clinically, gingival
recession is often accompanied by an alveolar bone dehis-
cence, although it is not clear whether the underlying bone
dehiscence develops before, or in parallel with, gingival
recession.
A Malocclusion
Angle’s class II division II malocclusion has been associated
with direct trauma on the labial gingival margins of lower
incisors and on the palatal margins of upper incisors. is
particular incisor relationship may therefore generate reces-
sion defects at these areas, often resulting in indentations in
the gingiva (Tugnait & Clerehugh 2001). A deep overbite
in the absence of adequate overjet may also lead to the strip-
ping of the gingival margins. Severe class III malocclusions
combined with a deep bite and occlusal trauma caused by
upper teeth to lower anterior teeth may also result in dam-
B
age to the gingival margin.
High Attachment of Frenum

Several investigators have previously suggested that a high
fraenal attachment may predispose a site to gingival reces-
sion, for example, when the attachment close to the gingival
margin compromises the plaque removal from the area by
the patient (Marini etal. 2004, Ustun etal. 2008). Accord-
ing to Chapple & Hamburger (2006), contrary to popular
belief, there is no evidence in the published literature for
a direct eect from so-called frenal pull in the initiation
C of gingival recession, as the frenum rarely has any muscle
• Figure 3.2.6 Clinical pictures of (A) normal, (B) thin and (C) thick gin- bres.
gival biotypes.
TABLE
3.2.3 Management options for dierent periodontal (gingival) biotypes
Presence/
absence Periodontal
of gingival (gingival)
recession phenotype Management options
Absence of gingival Thick gingival biotype Prevention through good oral hygiene and monitoring.
recession
thin gingival biotype, mucogingival surgery should be considered to prevent
orthodontics, restorative dentistry or implant therapy are planned.

Presence of gingival Thick biotypes Conservative clinical approach – charting and monitoring periodontal and root
recession surface lesions.
Thin biotypes and Mucogingival surgery for root coverage and CEJ reconstruction when needed.
when motivated by This applies especially in cases in which additional orthodontics, restorative
patient concern dentistry or implant therapy are planned.
Precipitating Factors for Gingival

Recession
According to Marini etal. (2004) there are several factors
that may contribute to the onset of gingival recession (see
Figure 3.2.4).
Plaque, Calculus and Periodontal Diseases

Published studies would appear to correlate the prevalence
of generalised recession with high levels of bacterial deposits
around teeth and the presence of active or past periodontitis.
Attachment loss may therefore manifest either as recession
of the gingival margin, pocket formation or their combina-
tion. A localised plaque-induced inammatory lesion may
also induce development of a recession defect as observed • Figure 3.2.7 Gingival recession following orthodontic treatment
(Courtesy of Prof. Georgios N. Belibasakis).
in Figure 3.2.1B
Toothbrush Trauma adaptive immune response and (2) topically reduced tissue
vascularity inuencing any subsequent wound healing of
Gingival recession has been reported to be relatively com- the aected tissues.
mon in populations with high standards of oral hygiene,
where it is usually located at buccal surfaces of canines, pre- Healing after Periodontal Treatment
molars and molars (see Figure 3.2.1A) and associated with
wedge-shaped hard tissue defects. Results from these stud- Pocket reduction following non-surgical periodontal treat-
ies would suggest that potentially overzealous or improper ment is achieved by the control of inammation which may
toothbrushing habits may be associated with gingival reces- result in gingival recession. Surgical treatment of periodon-
sion. However, there is no evidence of a cause-and-eect tal defects may also result in more recession postoperatively
relationship between toothbrushing and gingival recession. (Lindhe & Nyman 1980). Patients should therefore be
warned about the possibility of post-treatment recession in
Tooth Movement all forms of periodontal therapy.
Labial tooth movement may result either from occlusal Restorative Dentistry
trauma accompanied by periodontal diseases or from orth-
odontic movement (Tugnait & Clerehugh 2001) (Figure Subgingival and overhanging restoration margins can be
3.2.7). According to Wennström (1996), provided the considered a local risk factor in the development of peri-
tooth is moved within the envelope of alveolar bone, gingi- odontal diseases. Any subgingival placement of restorations
val recession will not occur irrespective of the quality (vol- (llings, crowns, etc.) may therefore produce an inamma-
ume) and quantity (width) of attached gingiva. However, if tory lesion in response to plaque accumulation which can
labial tooth movement results in the development of alveo- impinge on the supracrestal tissue attachment (biological
lar bone dehiscence, there is a greater risk of gingival reces- width) of the connective tissue, possibly resulting in loss of
sion. e use of computerised tomography to visualise the attachment or enlargement of the gingival tissues (Figure
morphology of the buccal or lingual bone plates in the plan- 3.2.8).
ning phase of orthodontic therapy may help prevent gingi-
val recession during orthodontic therapy, as the thickness of Removable Partial Dentures
the bone around individual teeth and any bony dehiscences/
fenestrations can be identied before treatment is initiated. Several investigators have suggested that removable partial
dentures may compromise every aspect of the periodontal
Smoking health of abutment teeth, including the incidence of gingi-
val recession. For example, poorly designed removable par-
Smoking is a signicant risk factor for the development of tial dentures may traumatise the periodontal tissues either
periodontal diseases. Increased prevalence and severity of physically or as a result of plaque accumulation (Tugnait
recession has also been reported in populations who either & Clerehugh 2001, Ercoli & Caton 2018). According to
smoke or use smokeless tobacco (Robertson et al. 1990, Wright and Hellyer (1995), however, the accumulation of
Banihashemrad etal. 2008). Several mechanisms have been plaque may be considered the main causative factor associ-
proposed for the eect of smoking on gingival recession, ated with gingival recession rather than any aspect of den-
for example, (1) systemically compromising the innate and ture design per se.
may be sucient when dealing with dierent forms of post-

operative sensitivity. Identication of the exact cause of den-
tine hypersensitivity is paramount if successful treatment is
to be achieved. is process will involve taking a thorough
history of the complaint together with a clinical examination
to eliminate any other possible dental cause, such as defec-
tive restoration margins or dental caries (dierential diagno-
sis). e use of a cold air syringe and an explorer probe may
help in the detection of sensitive areas of the tooth.
KEY POINT 5
• Figure 3.2.8 Inammatory response of the gingivae following the Dentine hypersensitivity is, by denition, a diagnosis of
subgingival placement of restoration margins. exclusion.
Aesthetics
A high smile line is usually a predisposing factor that con-
tributes to the patient’s concerns regarding the appearance of
gingival recession. Elongation of the clinical crowns of teeth
contrasts with the darker root dentine and, additionally, the
presence of “black triangles” as a consequence of generalised
recession is often seen in patients with periodontitis and often
compromises the aesthetics (Figure 3.2.10). ese elements
may generate psychological issues which are further aggra-
vated by the established association of recession with ageing.
Concern about the aesthetic eects of recession is often one
of the main reasons for patients attending the dental clinic.
• Figure 3.2.9 Gingival recession due to trauma caused by a lower lip
stud. Source: Reprinted by permission from Springer Nature: Br. Dent. J. KEY POINT 6
Gingival recession due to trauma caused by a lower lip stud, JJ Aesthetics and pain arising from dentine hypersensitivity are
O’Dower et al., Copyright 2002. key motivators for a patient to see a dentist.
Self-Inflicted Trauma/Chemical Trauma Plaque Retention and Gingival Inflammation

Case reports detailing the eects of patient behaviour, Receding gingival margins are often exposed to plaque accu-
such as ngernail picking at the gingival margin, or lip mulation due to patients’ inability to perform oral hygiene
and tongue piercings, have shown localised gingival reces- eectively at those sites. is may be due to either discom-
sion (Figure 3.2.9) (O’Dwyer & Holmes 2002). Similarly, fort associated with dentine hypersensitivity or diculties
topical cocaine application can also promote rapid gingival in cleaning the gingival margin of the recession defect.
recession and dental erosion (Kapila & Kashani 1997).
Tooth Abrasion
Clinical Outcomes of Gingival Recession
It has been suggested that aggressive toothbrushing may
Common clinical outcomes reported to be associated with cause exposure of the root surface which could continue if
gingival recession include: the brushing technique is not corrected. Other toothbrush-
• Dentine hypersensitivity ing characteristics have also been reported to increase the
• Aesthetic concerns risk of abrasion, for example, lament nishing and sti-
• Plaque retention and inìammation ness, in contrast to other studies that suggest abrasives in
• Tooth abrasion toothpastes are more likely to lead to loss of tooth or gingi-
• Root caries and non-carious cervical lesions (NCCL). val tissue than toothbrushing per se.
Dentine Hypersensitivity Root Caries and Non-Carious Cervical Lesions

Dentine hypersensitivity is usually one of the main symp- According to Banting (2001), the location of root caries has
toms of gingival recession that may encourage patients to been positively associated with age and gingival recession,
seek advice from a dental professional. Generally, this pain is and this is consistent with the concept that root caries occur
transient in nature, and simple monitoring and reassurance in a location adjacent to the crest of the gingiva where dental
periodontal probe. e use of study casts and clinical pho-

tographs may also be helpful in monitoring any progression
of gingival recession over time.
Non-surgical periodontal therapy and oral hygiene
advice are the two cornerstones of periodontal therapy. Gin-
gival recession may be the result of plaque accumulation due
to incorrect oral hygiene habits, and subsequent correction
would therefore contribute to the stability of the gingival
margin.
Additionally, patients should receive advice and/or treat-
A ment to alleviate symptoms arising from gingival recession
outcomes, mainly dentine hypersensitivity. Dietary advice
on the consumption of acidic drinks commonly associated
with erosion and on high-sugar-concentration products
that provide the nutritional environment for root car-
ies lesions may also be provided. Instructing the patient
to use an atraumatic brushing oral hygiene technique or
changing from a manual to a powered toothbrush may
also be benecial. Smoking cessation advice may also be
appropriate for some patients. Dentine hypersensitivity
arising from periodontal therapy may be initially allevi-
ated by the application of desensitising polishing pastes
B prior to the provision of a desensitising toothpaste for
• Figure 3.2.10 (A) Contrast of darker root dentine and enamel and home use. Application of desensitising products, such as
(B) interdental soft tissue loss leading to the appearance of “black toothpastes and bonding agents to occlude or seal the den-
triangles”. tine tubules, have also been proposed for the treatment
of dentine hypersensitivity. High uoride concentration
plaque accumulates. High counts of Streptococcus mutans and varnishes and dentifrices may be used in treating both
high plaque scores at the gingival margin have been associ- dentine hypersensitivity and root caries (see Table 3.2.3).
ated with the initiation of root caries lesions. Non-carious Following the initial management of gingival recession,
cervical lesions (NCCL) have also been associated with orthodontic therapy may also be indicated to correct
gingival recession and can be classied according to their malpositioned teeth or replacement of xed or removable
appearance (wedge-shaped, disc-shaped, attened and irreg- prosthesis to allow the patient to maintain a healthy oral
ular areas). Several studies have indicated that the prevalence environment.
and severity of NCCL increases with age, and the presence of
these dental lesions with subsequent concavities on the root 2. Non-Surgical Correction of Recession Defects
surface may obliterate the CEJ (Cortellini & Bissada 2018). When recession defects cannot be treated by surgical root
coverage procedures, for example, when the recession defect
is due to periodontitis, restorative techniques may be used.
Management and Treatment of e presence of “black triangles” can be masked by using a
Gingival Recession Defects and Dentine exible silicone gingival veneer. e use of a tooth-coloured
Hypersensitivity composite as a minimally invasive adhesive restoration may
also be recommended to resolve associated carious lesions
e management and treatment of gingival recession defects and alleviate pain symptoms from dentine hypersensitivity.
and associated dentine hypersensitivity may be based on Restoration of cervical defects with glass ionomer cements
non-surgical and surgical treatment strategies (Table 3.2.4). may also have the added advantage of uoride release over a
prolonged period of time. Aesthetic concerns raised by the
Non-Surgical Management of Gingival presence of recession defects may thus be resolved by either
non-surgical or surgical correction.
Recession and Dentine Hypersensitivity
Management may comprise: Surgical Treatment of Gingival Recession
1. Preventive care Defects
2. Non-surgical correction of the defects.
e main techniques that have been described in the pub-
1. Preventive Care lished literature for the treatment of gingival recession by
Once a diagnosis of gingival recession has been conrmed, root coverage include pedicle soft tissue grafts, free soft tis-
the degree of recession may be measured clinically using a sue grafts and guided tissue regeneration.
TABLE Non-surgical and surgical interventions for patients with gingival recession and dentine
3.2.4 hypersensitivity
Non-surgical treatment Surgical treatment

Periodontal ap surgery/periodontal plastic
In-surgery procedures techniques
Clinical measurement of the gingival recession defect and taking study casts and Guided tissue regeneration
clinical photographs to monitor condition over time Coronally advanced ap +/− enamel matrix
Identication and correction of predisposing or precipitating factors derivatives
Dietary and oral hygiene advice Coronally advanced ap + connective tissue
Manufacture of silicone gingival veneers graft
Orthodontic treatment Free gingival graft (acellular dermal matrix
Restorative correction of recession defect and subgingival margins of llings and allograft)
crowns
Desensitising polishing pastes
Desensitising gels for bleaching procedures
Polymers: Sealants/varnishes/resins/dentine bonding agents
Laser obturation of dentinal tubules
Bleaching gels + desensitising agent
Pulpal extirpation (root canal treatment)
Over-the-counter (toothpastes and mouth rinses)
Strontium chloride/strontium acetate
Potassium nitrate/chloride/citrate/oxalate
Calcium compounds:
Calcium carbonate and arginine and casein phosphopeptide + amorphous
calcium phosphate
Bioactive glass
Hydroxyapatite
Fluoride in higher concentration
Amine/stannous uoride
2012). According to Cortellini & Bissada (2018) there is

Pedicle Soft Tissue Grafts currently insucient evidence to conclude that root cover-
e two main procedures in this category are the laterally age procedures predictably reduce dentine hypersensitivity.
positioned pedicle graft and the coronally advanced ap
which is often used with enamel matrix derivatives, connec- KEY POINT 7
tive tissue graft or acellular dermal matrix allograft material, Treatment of a patient with gingival recession is usually
depending on the amount of remaining keratinised tissue. non-surgical.
Free Soft Tissue Grafts

Free soft tissue grafts are used for root coverage procedures Summary
either as epithelial (free gingival grafts) or subepithelial con-
nective tissue grafts. e management of gingival recession and any associated
sequelae, such as dentine hypersensitivity, caries, NCCL or
Guided Tissue Regeneration aesthetics, may be based on either a non-surgical or surgi-
Guided tissue regeneration procedures using resorbable or cal approach depending on the extent and severity of the
non-resorbable membranes with or without enamel matrix problem. e implementation of a preventive treatment
derivatives. approach that incorporates the identication and subse-
According to Miller (1985b) complete root coverage quent treatment or management of both the aetiological
can be anticipated in Miller class I and II recession defects, and predisposing factors is essential irrespective of whether
whereas only partial root coverage can be expected when a non-surgical or surgical approach is proposed. Monitoring
part of the interproximal tissue is lost (Miller class III). Root the condition over time to maintain the status quo and pre-
coverage is not predictable in Miller class IV. vent any further deterioration of the problem is an essential
From the published literature, the optimal result of a root component of the management strategy.
coverage procedure would be the complete resolution of the Dentine hypersensitivity is essentially a diagnosis of
marginal tissue recession defect as measured on the denuded/ exclusion, and as such a dierential diagnosis should be
covered root surface, with minimal probing depths in con- initiated to determine the exact cause of the patient’s pain.
junction with an acceptable chromatic and texture harmony Identication of the exact cause is imperative if subsequent
of the treated with the adjacent sites (Cortellini & Prato treatment is to be eective.
Fu J-H, Yeh C-Y, Chan H-L, Tatarakis N, etal. Tissue biotype and
KEY POINT 8 its relation to the underlying bone morphology. J Periodontol.
Management of both gingival recession and dentine 2010;81:569–574.
hypersensitivity is by implementation of prevention and
Gillam DG, Orchardson R. Advances in the treatment of root den-
corrective strategies together with a realistic monitoring
tin sensitivity: mechanisms and treatment principles. Endod Top.
programme which is simple to adopt in a practice environment.
2006;13:13–33.
Kamal H. Prevalence of dentine hypersensitivity in gingival recession-
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are available online at Elsevier eBooks+. 27–29th Abstract presentation); 2005.
Kapila YL, Kashani H. Cocaine-associated rapid gingival recession
and dental erosion. A case report. J Periodontol. 1997;68:485–
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3.3
TREATMENT PLANNING:
PERIODONTAL PROBLEMS
IN CHILDREN AND
ADOLESCENTS
VA L E R I E C L E R E H U G H A N D A R A D H N A T U G N A I T
CHAPTER OUTLINE
Introduction Use of Radiographs
Periodontal Diseases that can Aect Children and Periodontal Diagnosis
Adolescents Treatment Planning and Periodontal Therapy
Periodontal Health EFP S3 Level Clinical Practice Treatment Guidelines and BSP
Gingivitis Implementation for UK Clinical Practice
Plaque-Induced Gingivitis Step 1 Building Foundations for Optimal Treatment
Necrotising Gingivitis Outcomes
Non-Plaque-Induced Gingival Lesions Step 2 Subgingival Biolm & Calculus Control/Removal
Periodontitis Step 3 Management of Non-Responding Sites (≥4 mm with
Incipient Periodontitis BOP or ≥6 mm)
Stage II, III or IV Grade C Periodontitis in Younger Age Step 4 Maintenance/Supportive Periodontal Therapy
Groups Plaque Control
Necrotising Periodontitis Toothbrushing and Motivation
Recession Flossing
Gingival Overgrowth Non-Surgical Periodontal Therapy
Periodontal History, Examination and Simplied Basic Management of Gingivitis and Periodontitis
Periodontal Examination Role of Systemic Antimicrobials
Management of Recession
Periodontal History and Examination
Management of Gingival Overgrowth
Simpliöed Basic Periodontal Examination (sBPE)
sBPE Codes Treat or Refer

This chapter outlines the dierent periodontal diseases that can aect children and adolescents and outlines the principles for periodontal
screening and management of children and adolescents under 18 years of age.
By the end of the chapter the reader should be able to: • Understand the factors that may inøuence the decision to treat
• Outline the various key periodontal diseases that can aòect young patients in a general dental practice or refer to a specialist.
children and adolescents e chapter covers the following topics:
• Understand the role of periodontal screening using the • Introduction
simpliöed basic periodontal examination (sBPE) in patients • Periodontal diseases that can aòect children and adolescents
under 18 years old • Periodontal history, examination and simpliöed basic
• Explain the diòerent steps of periodontal therapy based on periodontal examination (sBPE)
the European Federation of Periodontology (EFP) S3-level • Treatment planning and periodontal therapy for the younger
clinical practice guidelines and the British Society of age groups
Periodontology and Implant Dentistry (BSP) implementation • The decision to treat in general dental practice or refer to a
of them specialist.
146
CHAPTER 3.3 Treatment Planning: Periodontal Problems in Children and Adolescents 147
Introduction • BOX 3.3.1 Classication of Periodontal Diseases/

Conditions in Children/Adolescents
A wide range of periodontal diseases can aect children based on 0 World Workshop
and adolescents, just as in adults (Clerehugh & Tugnait Classication of Periodontal and Peri-
2001, Clerehugh et al. 2004, Clerehugh 2008), but the Implant Diseases and Conditions (Caton
2017 World Workshop on the Classication of Periodon- etal. 08)
tal and Peri-implant Diseases and Conditions (Caton etal.
2018) reects that our understanding of them has changed Periodontal health, gingival diseases/conditions
since the previous 1999 International Workshop classica- Periodontal health and gingival health
tion (Armitage 1999) (see Box 3.3.1). Furthermore, a new Gingivitis, dental plaque biolm induced
Gingival diseases, non-dental plaque biolm induced
method for staging and grading periodontitis was agreed
upon that inuences the management of patients, whether Periodontitis
they are children, adolescents or adults (Tonetti etal. 2018). Necrotising periodontal diseases
e BSP has published an implementation plan for peri- Periodontitis
odontal diagnosis in the context of the 2017 classication Periodontitis as a manifestation of systemic disease
for clinical practice in the United Kingdom (Dietrich etal.
Other conditions affecting the periodontium
2019), along with guidance on implementation of the EFP
Systemic diseases or conditions affecting the periodontal
S3-level evidence-based guidelines for stage I–III periodon- supporting tissues
titis in UK clinical practice (West etal. 2021). Periodontal abscesses and endodontic–periodontal lesions
Mucogingival deformities and conditions
KEY POINT 1 Traumatic occlusal forces
Many different periodontal diseases can affect children and Tooth and prosthesis-related factors
adolescents (see Box 3.3.1) but the 2017 World Workshop Reprinted from Journal of Clinical Periodontology, 30(10):15, Caton, J.G.,
Classication on Periodontal and Peri-implant Diseases Armitage, G., Berglundh, T. et al. (2018), with permission from John Wiley
and Conditions reects that our understanding of them has & Sons.
changed since the previous 1999 classication.
is chapter will focus on:

•Gingivitis Periodontal health was classied for the rst time in the
•Periodontitis 2017 World Workshop Classication on Periodontal and
•Necrotising periodontal diseases Peri-implant Diseases and Conditions (Caton etal. 2018)
•Recession that replaced the previous 1999 international classication
•Gingival overgrowth. (Armitage etal. 1999). According to the 2017 World Work-
Early diagnosis and treatment planning are essential to shop Classication, a case of periodontal health on an intact
ensure successful management in the younger age groups, periodontium is dened by the absence of inammation
and periodontal screening is a key aspect of this. In 2012, (i.e. bleeding on probing [BOP] at less than 10% sites) and
BSP and the British Society of Paediatric Dentistry (BSPD) the absence of attachment loss and bone loss from previous
jointly produced guidelines for periodontal screening and periodontitis, with probing depths ≤3 mm); there is also a
management of children and adolescents under 18 years of category which acknowledges periodontally healthy tissues
age, and these were updated in 2021 (Clerehugh & Kin- on a reduced and stable periodontium arising from histori-
delan 2021, www.bsperio.org.uk) using a simplied ver- cal successfully treated periodontitis (Chapple etal. 2018).
sion of the basic periodontal examination used in adults
(sBPE). e principles of periodontal management need
Gingivitis
to be applied to the younger age groups when treating the Plaque-Induced Gingivitis
conditions in Box 3.3.1, and the decision needs to be taken If supragingival plaque accumulates, an inammatory cell
whether to treat in the primary dental care setting or to refer inltrate develops in the gingival connective tissue and the
to a specialist. weak junctional epithelial attachment is disrupted, leading
to an increase in gingival sulcus depth and formation of a
Periodontal Diseases that can Affect false gingival pocket, in which subgingival plaque can col-
lect; supragingival calculus and subgingival calculus may
Children and Adolescents form on the clinical crown. is is entirely reversible with
Periodontal Health eective plaque biolm and calculus removal supragingi-
vally and subgingivally. At this stage, the most apical extent
In children and adolescents with a healthy periodontium, of the junctional epithelium (JE) is still at the CEJ, and
the gingival sulcus is typically 0.5–3 mm deep on a fully there is no periodontal loss of attachment or bone loss.
erupted tooth, and the alveolar crest has been shown to be Epidemiological studies report a low prevalence of
between 0.4 and 1.9 mm apical to the cement–enamel junc- plaque-induced gingivitis in preschool children, reaching a
tion (CEJ) in teenagers (Hausmann etal. 1991). peak in prevalence around puberty. Puberty gingivitis is the
increased inammatory gingival response to dental plaque • BOX 3.3.2 Local and Systemic Periodontal Risk
mediated by the hormonal changes associated with puberty, Factors
perhaps also in association with changes in the bacterial
composition of the dental plaque (Bimstein & Eidelman Local
1988, Bimstein & Matsson 1999). e 2013 Child Den- • Anatomical factors
tal Health Survey in England, Wales and Northern Ireland • Overhanging/poorly contoured restorations
• Removable partial dentures
found that out of a representative sample of 13,628 chil- • Orthodontic appliances
dren aged 5, 8, 12 and 15 years, only 22% of 5-year-olds • Root fractures and cervical root resorption
had visible gingival inammation, compared with 46% of • Calculus
8-year-olds, 60% of 12-year-olds and 52% of 15-year-olds • Local trauma
(Pitts etal. 2015). • Fraenal attachments
• Mouth breathing and lack of lip seal
According to the 2017 World Workshop Classication, a
case of gingivitis on an intact periodontium and on a reduced Systemic
periodontium without a history of periodontitis is dened as • Smoking
>10% bleeding sites with probing depths <3 mm (Chapple • Poorly controlled type 1 and type 2 diabetes mellitus
etal. 2018). Localised gingivitis is dened as 10–30% bleeding • Ethnic origins
sites; generalised gingivitis is dened as >30% bleeding sites. • Genetics
• Male gender
Importantly from an epidemiological perspective, a periodon- • Polymorphonuclear leucocyte function
titis case cannot simultaneously be dened as a gingivitis case. • Socio-economic status (low educational level)
is means that a patient with a history of periodontitis with • Acquired systemic infection (e.g. HIV)
gingival inammation is still classed as a periodontitis case. • Severe malnutrition
From a clinical perspective, successfully treated periodontitis
patients may achieve a reduced, stable periodontium where
probing depths are ≤4 mm and there is an absence of clini-
cal inammation (BOP). However, BOP may occur at certain Periodontitis
sites, and where probing depths are ≤3 mm, this would be clas-
sied as gingival inammation in a stable periodontitis patient; e key features of periodontitis are:
close monitoring is required due to the potential for relapse and • Loss of attachment of the periodontal connective tissues
high risk of recurrence of periodontitis. • Apical migration of the JE beyond the CEJ and transfor
mation of the JE to pocket epithelium (often thin and
Necrotising Gingivitis ulcerated)
Necrotising gingivitis (NG) has a fusiform-spirochaetal • Alveolar bone loss.
microbial aetiology and is more generally found in patients Local and systemic periodontal risk factors can inu-
in developing countries who typically exhibit various risk ence the rate, severity and extent of progression of peri-
factors, including smoking, immunosuppression – in par- odontitis (Box 3.3.2). e system of staging and grading
ticular HIV-positive status – stress, malnourishment or periodontitis was introduced for the rst time in the 2017
poor diet (Herrera etal. 2018). Extreme living conditions World Workshop on Classication (Tonetti etal. 2018), see
and severe (viral) infections such as measles, herpes viruses, Chapter 2.1 and Appendices 1 and 2. Risk factors have not
chicken pox, malaria or febrile illnesses may be predisposing previously been included in the classication of periodon-
conditions in children (Papapanou etal. 2018). Key diag- titis, but the 2017 World Workshop scheme allows for the
nostic features include: presence of recognised periodontal risk factors (especially
• Pain smoking and diabetes; see Box 3.3.2) to be able to modify
• Necrosis and ulceration of the interdental papillae which the assigned grade of periodontitis (Tonetti etal. 2018). It
have a “punched out” appearance is also important to incorporate current disease status into
• Bleeding, which may be spontaneous the periodontitis diagnosis (stable, unstable or in remission)
• Secondary fetor oris by considering the presence of true probing pocket depths
• Pseudo-membrane may be present (PPD) of 4 mm or more and BOP, which reect the inam-
• May manifest in children and teenagers matory status and drive treatment planning (Chapple etal.
• May progress to necrotising periodontitis (NP). 2018, Dietrich etal. 2019). Details can be found in Chapter
NG is the only form of gingivitis for which systemic anti 2.1 and Appendix 2
biotics may normally be indicated as part of the treatment. Although current evidence, as documented in the 2017
World Workshop (Caton etal. 2018), does not support the
Non-Plaque-Induced Gingival Lesions distinction between the conditions previously classied as
Children may also present with non-plaque-induced gin- chronic and aggressive periodontitis in the 1999 Interna-
gival lesions. For such lesions, a specialist referral may be tional Classication (Lang etal. 1999), it is important for
indicated (Clerehugh etal. 2004, Clerehugh & Kindelan the dental practitioner to be able to identify those adoles-
2021). cents at an incipient (early) stage of periodontitis who are
amenable to treatment in general dental practice (typically to a prevalence of 37% at 16 years and 77% at 19 years.
stage I, grade A) and those minority of cases who would pre- Periodontal pathogens typical of those found in the sub-
viously have been classied as aggressive periodontitis with gingival microora of adults with periodontitis have also
a more severe, rapidly progressing, destructive form of peri- been found in the subgingival plaque of adolescents with
odontitis who would now be categorised typically as stage incipient periodontitis, including Porphyromonas gingiva-
II, III or IV, grade C and who would benet from referral lis, Prevotella intermedia, Aggregatibacter actinomycetem-
to a specialist (Wadia et al. 2019, Walter et al. 2019a, b, comitans and Tannerella forsythia (Clerehugh et al. 1997,
Clerehugh & Kindelan 2021). Hamlet etal. 2004).
Radiographic bone loss has been observed around the
primary dentition in some children, and this reinforces the Stage II, III or IV Grade C Periodontitis in Younger
notion that periodontitis can develop at an early age (Mats- Age Groups
son etal. 1995, 1997). e condition that would previously have been diagnosed as
In the mixed dentition, it is important to be aware of localised aggressive periodontitis, although not deemed in
the potential problem of false pocketing occurring around the 2017 World Workshop on Classication to have a su-
partially erupted teeth. ciently well-dened aetiology or pathophysiology to have its
own classication, has in fact been acknowledged to have a
Incipient Periodontitis well-recognised clinical presentation: typically with an onset
In the permanent dentition, the transition from gingivitis around puberty and localised rst molar/incisor presentation
to the early stages of periodontitis, namely incipient peri- with interproximal clinical attachment loss which is much
odontitis, can occur in the early teenage years, aecting a more severe and more rapidly destructive than expected and
substantial number of teenagers. It is characterised by 1–2 inconsistent with the levels of plaque biolm deposits pres-
mm loss of clinical attachment interproximally, periodontal ent. Historically it has typically been found in adolescents
pockets 4–5 mm deep and crestal alveolar bone loss of about from Africa/Middle East with Aggregatibacter actinomy-
0.5 mm which is usually horizontal (Figure 3.3.1). cetemcomitans as the implicated infecting agent (Fine etal.
A 5-year longitudinal study of 167 adolescents (Clere- 2018, Papapanou etal. 2018). A. actinomycetemcomitans
hugh etal. 1990) showed that 3% had attachment loss of is very adept at evading the host defences and can be dif-
1 mm or more on at least one of the molar, premolar or cult to eradicate (Figure 3.3.2). Hence the management
incisor teeth when examined at age 14 years, increasing may well involve adjunctive systemic antimicrobials at the
CAL Clinical attachment loss
CEJ Cemento-enamel junction
Pocket
4−5 mm
CEJ
Inflammatory
CAL
infiltrate
1−2 mm
Bone loss
• Figure 3.3.1 Incipient periodontitis.

Aggregatibacter actinomycetemcomitans
Stages of bacterial
Examples of virulence factors
pathogenicity
Autotransporter proteins
1 Attaches to host tissues Fimbriae
PGA polysaccharide
2 Multiplies Bacteriocins
Chemotactic inhibition factors

Leukotoxin
3 Evades host defences Immunosuppressive factors
to IgG, IgM
4 Invades tissues Cytolethal distending toxins
Activation of T-helper and

5 Destroys tissues B-cells
Collagenases
Lipopolysaccharide
• Figure 3.3.2 Aggregatibacter actinomycetemcomitans.
cause-related corrective phase of therapy, but careful consid- Factors associated with recession, especially if the gingiva
eration would be required on a case-by-case basis. is thin, are:
Within the staging system there is a category for describ- • Anatomy
ing the extent and distribution of periodontitis as localised • Tooth position, or orthodontic tooth movement, which
(up to 30% of teeth aected) or molar/incisor (Tonetti etal. may be associated with fenestration or dehiscence in the
2018, Wadia et al. 2019, Walter et al. 2019a) for young- thin bone covering the root (Figure 3.3.3)
sters who would previously have been diagnosed as localised • Trauma, e.g. overzealous toothbrushing
aggressive periodontitis, whilst for adolescents who would • Traumatic habits, e.g. ënger picking of the gingival
previously have been diagnosed as generalised aggressive margin
periodontitis, they would typically be categorised as stage • Local plaque-retention factors, e.g. supragingival calcu
II, III or IV, grade C, generalised periodontitis – that is, lus and frenal pull/high muscle attachments
30% or more of teeth aected (Tonetti etal. 2018, Walter • Periodontitis
etal. 2019a). e additional descriptor of periodontitis that  • Loss of attachment associated with periodontitis can
is “currently unstable” may also apply to these cases (Wadia lead to the periodontal pocket margin being located
etal. 2019, Walter etal. 2019a) (Table 2.1.5). apical to the cement–enamel junction, with the devel-
opment of periodontal pockets and alveolar bone loss
Necrotising Periodontitis  • Smoking is a further risk factor for recession
Although uncommon in young people in developed coun-  • Treatment of periodontitis can also lead to recession
tries like the UK, necrotising periodontitis (NP): as a consequence of reduced marginal inammation.
• May be an extension of NG A treatment-oriented classification of gingival reces-
• Features necrosis of the gingival tissues, periodontal liga sion with reference to interdental loss of attachment was
ment and alveolar bone. proposed by Jepsen et al. (2018), along with a clinical
diagnostic approach which takes account of gingival
Recession phenotype, gingival recession and associated cervical
lesions.
During the early years, after eruption of the permanent
tooth, an increase in the width of the attached gingiva takes Gingival Overgrowth
place (Bimstein & Eidelman 1988).
As explained in Chapter 3.2, gingival recession is dened A greater incidence of gingival overgrowth is seen in
as the apical migration of the gingival margin beyond the puberty, and the severity is more intense in children than
cement–enamel junction, resulting in exposure of the root in adults with similar amounts of dental plaque (Tiainen
surface. etal. 1992).
Fenestration
Dehiscence
• Figure 3.3.3 Fenestration and dehiscence may be associated with gingival recession, especially where
overlying gingiva is thin and subjected to trauma, e.g. from overzealous toothbrushing.
ere are a number of contributing factors to gingival calculus deposits should be noted. Local periodontal risk
overgrowth: factors – e.g. plaque-retention factors, location of high
• Usually associated with plaque-induced inìammation fraenal attachments, malocclusion, the presence of mouth
• Drugs: phenytoin for management of epilepsy; ciclospo breathing and incompetent lip seal – should be identied.
rin (immunosuppressant); calcium channel blockers Mouth breathing, increased lip separation and decreased
• Hormonal (pregnancy; contraceptive pill) upper lip coverage have all been associated with higher
• Hereditary gingival ëbromatosis levels of plaque and gingival inammation. e inuence
• Neoplasia, including leukaemia of mouth breathing tends to be restricted to palatal sites,
• Scurvy, vitamin C deëciency whereas decreased lip coverage inuences gingival inam-
• Mouth breathing, which can exacerbate existing plaque- mation at both palatal and labial sites (Wagaiyu & Ashley
induced gingivitis. 1991). Radiographs and sensitivity tests may be necessary.
e enlarged gingival tissue may be dicult to clean, Just as for adults, periodontal screening is recommended
thereby acting as a plaque-retention factor, and aesthetics in children and adolescents, but a simplied version of the
may be a concern. basic periodontal examination (BPE) has been developed
for the under 18-year-old group (sBPE), and guidelines on
Periodontal History, Examination its use have been updated by Clerehugh and Kindelan in
association with the BSP and the BSPD in 2021 (Clerehugh
and Simplified Basic Periodontal & Kindelan 2021) (Figure 3.3.4).
Examination
Simplified Basic Periodontal Examination
Periodontal History and Examination
(sBPE)
KEY POINT 2 Periodontal screening using the simplied BPE (sBPE) is
A thorough history and examination are necessary for appropriate for children and adolescents under 18 years of
periodontal diagnosis and subsequent treatment planning and age seen in general dental practice and community and hos-
will identify systemic and local periodontal risk factors (Box 3.3.2). pital settings.
e routine dental examination of children and adolescents KEY POINT 3

should include an extra-oral and intra-oral assessment. A simplied version of the BPE (sBPE) is a quick, acceptable
Variables to note are gingival colour, contour, swelling, the method for periodontal screening in the under 18-year-old age
presence and location of inammation, recession or sup- group in general dental practice and community and hospital
settings.
puration. Oral hygiene and the presence of supragingival
• Index teeth (WHO partial

recording for adolescents):
UR6, UR1, UL6
LR6, LL1, LL6
• Walk probe around 6

sites per tooth:
db, b, mb, dl, l, ml
• Record worst finding in box
• Figure 3.3.4 Simplied basic periodontal examination (sBPE) index teeth.
sBPE Codes
gingiva, calculus and/or overhangs of llings, i.e. sBPE
0 Healthy (no bleeding on probing, no calculus/overhangs codes 1 and 2 only, to avoid the problem of false pockets
or pocketing ≥3.5 mm detected). Black band entirely vis- on the erupting/recently erupted rst permanent molar
ible. and incisor teeth
1 Bleeding on probing (no calculus/overhangs or pocket- 2. At 12–17 years of age, the full range of sBPE codes can
ing ≥3.5 mm detected). Black band entirely visible. be used on the six index teeth. It would be unusual to
2 Calculus (supragingival and/or subgingival) or plaque- nd periodontal breakdown at other teeth without the
retention factor (no pocketing ≥3.5 mm detected). Black index teeth being aected
band entirely visible. 3. An sBPE should be undertaken in all new child or ado-
3 Shallow pocket (4 mm or 5 mm), i.e. probing depth ≥3.5 lescent patients and prior to commencing orthodontic
mm but ≤5.5 mm. Black band partially visible. treatment in the under 18s
4 Deep pocket (6 mm or more), i.e. probing depth >6 mm. 4. Whether in the mixed or permanent dentition stage, the
Black band disappears. examination of these index teeth is quick, easy and well
* Furcation tolerated and is sucient to identify children who would
benet from a more detailed examination.
KEY POINT 4 Although a brief periodontal examination similar to the
sBPE is performed on six index teeth (UR6, UR1, UL6, sBPE has been reported to be acceptable for children as
LL6, LL1 and LR6) using a WHO 621 probe with a 0.5 mm young as 3 years of age (Rapp et al. 2001), it would not
spherical ball on the tip and a black band at 3.5–5.5 mm to normally need to be undertaken in the primary dentition.
delineate healthy sulcus (probing depth 3 mm or less) from
pockets (probing depth 4 mm or more), employing a light
As a guide for when to do sBPE:
probing force of 20–25 g. • If sBPE = 0, screen again at routine recall visit or within
1 year, whichever is sooner
e sBPE is performed on the following six index teeth: • If sBPE = 1 or 2, treat and screen again at routine recall
UR6, UR1, UL6, LL6, LL1 and LR6 using the WHO 621 or after 6 months, whichever is sooner
probe with a light probing force of 20–25 g. is has a 0.5 • If sBPE = 3, undertake initial periodontal therapy, includ
mm spherical ball on the tip and a black band at 3.5–5.5 ing any other aected teeth in the involved sextant(s).
mm to delineate healthy sulcus depth (<3.5 mm) and peri- After 3 months, do a full periodontal assessment, includ-
odontal pockets of 4 mm or more (see Figure 3.3.5). ing 6-point probing pocket depths on the index tooth
ere are, however, certain points that need to be con- and other teeth in the involved sextant(s).
sidered when adapting this for use in children and ado- • If sBPE = 4 or * on any index tooth, do a full periodon
lescents (Clerehugh 2008, Clerehugh & Kindelan 2021, tal assessment, including 6-point probing pocket depths,
www.bsperio.org.uk): throughout the entire dentition. Consider referral to a
1. At 7–11 years of age, in the mixed dentition phase, the specialist. Undertake initial periodontal therapy as for
index teeth should only be examined for bleeding of the code 3 in the meantime (Figure 3.3.5).
Code 3
Black band
partially visible
Code 4
Black band
disappears
within pocket
Code *
Furcation involvement
• Figure 3.3.5 Section through tooth - diagram of sBPE codes 3, 4, *.
Please see Table 3.3.1 for guidance on the interpretation A radiographic report should be included in the patient’s
of sBPE codes for clinical practice. case notes. In addition to caries and other pathology, nd-
ings of periodontal signicance to record include:
Use of Radiographs • Bone levels/loss
• Type of bone loss (horizontal or vertical)
In health, the alveolar bone crest is 0.4–1.9 mm from the • Calculus
CEJ around permanent teeth but may be greater than • Furcations
2 mm in primary teeth. is distance may increase with • Apical pathology
facial growth and if an adjacent primary tooth is lost or a • Endodontic-periodontal lesion
neighbouring permanent tooth erupts. Horizontal bite- • Root caries
wing radiographs for the detection of caries can be useful • Deëcient or overhanging restoration margins
in assessing a young patient’s periodontal condition on pos- • Poorly contoured restorations
terior teeth (Faculty of General Dental Practitioners 2018). • Widened periodontal ligament space.
Selected periapical radiographs may be indicated for the
anterior and/or posterior teeth. Panoramic lms are com- KEY POINT 5
monly used for orthodontic purposes to assess the state of For sBPE codes of 3, 4 or *, consideration should normally be
the developing dentition. e chance to assess bone levels given to a radiographic examination when it is justied and has
on intra-oral or panoramic lms should always be seized, the potential to change the management or prognosis, in line
with best radiological practice. Assessment of bone loss is a
even if the lm was not originally taken to assess the peri- core component of staging and grading of periodontitis.
odontal condition.
For sBPE codes of 3, 4 or *, consideration should nor-
mally be given to a radiographic examination when it is jus- Periodontal Diagnosis
tied and has the potential to change the management or
prognosis, taking account of best available radiological prac- e diagnosis of any periodontal conditions present in
tice. Assessment of bone loss is a key aspect of staging and a child or adolescent will follow the history, examination
grading periodontitis and reaching a periodontal diagnosis and any special tests; a treatment plan can then be drawn
(see Chapter 2.1 and Appendices 1 and 2). up. Guidance on periodontal diagnosis in the context of
TABLE Summary guidance on interpretation of • Corrective therapy: various therapeutic measures, includ
3.3.1 simplied BPE (sBPE) codes ing further non-surgical therapy or, in selected cases,
periodontal surgery, adjunctive local or systemic antimi-
sBPE
crobials, orthodontics or any denitive restorative work.
code Summary
• Supportive therapy: prevention of disease recurrence and
0 No periodontal treatment maintenance of periodontal health, with tailored recall
Screen again at routine recall or within 1 year, visits.
whichever is sooner
l Oral hygiene instruction (OHI) EFP S3 Level Clinical Practice Treatment
Screen again at routine recall or within 6
months, whichever is sooner
Guidelines and BSP Implementation for UK
Clinical Practice
2 OHI as for code 1. Supragingival/subgingival
professional mechanical plaque removal Following the 2017 World Workshop on Classication
(PMPR). Remove/manage plaque-retention
(Caton et al. 2018), the EFP developed a set of stringent
factors
Screen again at routine recall or within 6 S3-level, evidence-based clinical recommendations (CRs)
months, whichever is sooner for the management of stage I–III periodontitis. ese were
based on 15 systematic reviews and a moderated consen-
3 OHI as for codes 1 and 2. Supragingival/
subgingival PMPR, with particular emphasis sus process from representative stakeholders (Sanz et al.
on subgingival PMPR in shallow 4 mm–5 mm 2020). Please see Chapter 4.3 and Appendix 3 for further
pockets. Remove/manage plaque-retention details and an explanation of the development of the EFP
factors S3 guidelines. e BSP adapted these EFP S3-level guide-
After 3 months, do a full periodontal
lines for clinical use in the UK healthcare system and pro-
assessment, including 6-point probing pocket
depth (PPD) chart, in affected sextants duced UK Clinical Practice Guidelines for the Treatment of
Periodontal Diseases, illustrating the four-step sequence for
4 or * Unusual in young patients. Do a full periodontal the practitioner to follow for the treatment of periodontal
assessment, including 6-point PPD chart,
throughout the entire dentition diseases, covering the spectrum from periodontal health to
gingivitis and periodontitis (see Appendix 4).
therapy, as code 3 Preventive advice, health education and oral hygiene
instruction are key to successful management of plaque-
Table reproduced from Clerehugh & Kindelan (2021)
induced gingivitis and prerequisites to the successful man-
and Implant Dentistry (www.bsperio.org.uk/publications). agement of periodontitis in the younger age groups. e
young patients and their families/caregivers should have a
diagnosis and discussion of the causes of the child/young per-
son’s periodontal condition, treatments options, risk-benets
the 2017 World Workshop Classication of periodontal and a care plan. e following steps 1–4 can then provide a
diseases and conditions and its implementation in clini- stepwise approach for successful treatment outcomes of their
cal practice has been produced by the BSP (Dietrich etal. periodontal diseases/periodontitis (Appendices 3 and 4).
2019). Appendix 2 shows how to reach a diagnosis in con-
junction with use of the periodontal screening systems used Step 1 Building Foundations for Optimal
in the UK (appropriate for both BPE for adults and sBPE Treatment Outcomes
for children under 18), and then shows the use of staging Step 1 aims to lead to behaviour change/motivation to suc-
and grading for periodontitis cases, assessment of current cessfully control the plaque biolm (OHI); uses possible
periodontitis status, risk factor assessment and nally reach- adjunctive therapies for gingival inammation; uses pro-
ing a diagnosis statement in clinical practice. fessional mechanical plaque removal (PMPR) to remove
supragingival plaque and calculus and also any subgingival
plaque and calculus on the crown of the tooth; employs risk
Treatment Planning and factor control.
Periodontal Therapy Step 2 Subgingival Biofilm & Calculus
Periodontal therapy has traditionally been undertaken in Control/Removal
three phases: initial, corrective and supportive, each with a Step 2 aims to control (reduce/eliminate) the subgingival
number of associated stages: plaque bioëlm and subgingival PMPR to remove subgin
• Initial therapy: cause related; targeted at controlling the gival plaque biolm and subgingival calculus from the root
plaque biolm, managing any modiable periodontal surface; may also involve the use of: adjunctive physical or
risk factors and completing the initial phase of non-sur- chemical agents; adjunctive local or systemic host-modulat-
gical periodontal therapy in order to control the infec- ing agents; adjunctive subgingival locally delivered antimi-
tion and inammation and halt the progress of disease. crobials; adjunctive systemic antimicrobials.
Step 3 Management of Non-Responding Sites (≥4 complementary to dentistry (Siam et al. 1980). ere is
mm with BOP or ≥6 mm) strong reinforcement of this message in the Public Health
Step 3 aims at treating non-responding sites (probing depth England/Department of Health’s Delivering Better Oral
>4 mm with BOP or >6 mm); aims to gain access to fur- Health (DBOH) evidence-based toolkit for prevention,
ther subgingival instrumentation or to achieve regeneration now in its third edition (2017); a fourth edition is currently
or resection in lesions (infrabony or furcation) that increase being compiled (Public Health England 2020).
complexity in managing periodontitis.
Toothbrushing and Motivation
Step 4 Maintenance/Supportive Periodontal Plaque biolm-induced gingivitis in children and ado-
Therapy lescents can be managed by thorough mechanical plaque
Step 4 aims to maintain periodontal stability through support- removal and good oral hygiene (Oh et al. 2002, Needle-
ive periodontal care in all treated periodontitis patients; com- man et al. 2005), which has additional benets in terms
bines preventive/therapeutic interventions from steps 1 and 2; of reduced risk of caries. Public Health England/Depart-
requires regular recall intervals, tailored to patient’s individual ment of Health Guidelines on Delivering Better Oral
needs; should be managed as a recurrent disease with updated Health should be followed (2017); they recommend com-
diagnosis and treatment plan; requires compliance with OHI mencing toothbrushing as soon as the rst primary tooth
regimens and healthy lifestyle, which are integral. erupts. Children under 3 years of age should use a tooth-
paste containing no less than 1000 ppm uoride, whilst a
KEY POINT 6 family toothpaste (1350–1500 ppm uoride) is indicated
Preventive advice, health education and oral hygiene for maximum caries control in children above 3 years of
instruction are key to successful management of plaque- age, ensuring adequate parental supervision for use of small
induced gingivitis and are also prerequisites to the successful amounts. As manual dexterity to carry out good plaque con-
management of periodontitis in the younger age groups.
The BSP UK Clinical Practice Guidelines for the Treatment
trol for themselves varies from child to child, guidance from
of Periodontal Diseases provides a stepwise approach for the DBOH toolkit (Public Health England 2017) is that
successful treatment outcomes of periodontal diseases/ parents/caregivers should brush/supervise toothbrushing at
periodontitis in the under 18 age group. ages 0–3 years and supervise children 3–6 years of age. No
particular technique of toothbrushing has been shown to be
better than any other, rather the need to systematically clean
KEY POINT 7 all tooth surfaces should be emphasised by the clinician. e
All phases of periodontal therapy require ongoing guidance on patient’s existing toothbrushing technique may need to be
oral hygiene practices to control gingival inammation.
modied to achieve this. It is recognised that disclosing tab-
lets can help to indicate areas that are being missed. It is
recommended that toothbrushing is carried out twice a day
Plaque Control
with a uoridated toothpaste.
According to the Children’s Dental Health Survey of 2013 An appropriately sized toothbrush should be recom-
(Tsakos etal. 2015), twice daily toothbrushing was reported mended for children and adolescents; the DBOH toolkit
in 79% of 12-year-olds (compared with 76% in 2003) and (Public Health England 2017) has recommended a small-
in 84% of 15-year-olds (versus 80% in 2003); between headed toothbrush with medium texture bristles. e 2013
37%–49% of children in all age groups reported using Child Dental Health Survey has shown that around 40%
an electric toothbrush. e use of dental oss, although of children overall used an electric toothbrush (39% of
small, was evident, with 21% of 15-year-olds reporting its 5-year-olds, 49% of 8-year-olds, 37% of 12-year-olds, 41%
use. Mouthwash use was reported in all age groups, rising of 15-year-olds). Although there is evidence that some pow-
from 22% of 5-year-olds up to 67% of 15-year-olds. Oral ered toothbrushes, with a rotation-oscillation action, may be
health messages for the child population should incorpo- more eective for plaque control than manual toothbrushes
rate relevant information about the use of these common (Robinson et al. 2003, 2005, Deacon et al. 2010, Yaacob
oral hygiene adjuncts. Smoking prevalence was very low etal. 2014), it is probably more important that the tooth-
(2%) in 12-year-olds, but because 11% of 15-year-olds brush, whether manual or powered, is used eectively twice
reported being a current smoker and 29% reported having daily. e practitioner can thus recommend good, eective
ever smoked cigarettes, smoking cessation advice is of para- brushing with a manual or powered toothbrush twice daily
mount importance in these teenage years. using a uoridated toothpaste. e choice of toothbrush
Under optimal conditions, the careful and regular may be inuenced by patient preference.
removal of dental plaque biolm can prevent the occurrence Professional support to patients and parents in the form
and progression of early periodontal diseases (Badersten of preventive or educational programmes has been shown
etal. 1975, Agerbaek etal. 1977, Axelsson & Lindhe 1977, to improve patient motivation, leading to improved levels
Hamp etal. 1978, Ashley & Sainsbury 1981). It is however of oral health (Hochstetter etal. 2007). A recent systematic
recognised that attainment and maintenance of optimal oral review with meta-analysis involving adolescents and moth-
hygiene requires reinforcement by dentists or professionals ers of young children, as well as adults, showed that mobile
applications and text messages compared with conventional Although the eects of plaque on the gingival and
oral hygiene instructions were a useful adjunct in improv- periodontal tissues may be transient for the duration of
ing oral hygiene and oral health knowledge and reducing the orthodontic therapy (Ristic etal. 2007), high plaque
gingival inammation (Toniazzo etal. 2019). e reader is accumulation can develop in patients undergoing xed
directed to Chapter 4.3 on patient adherence to healthcare orthodontic treatment (Atack etal. 1996, Turkkahraman
advice and some of the diculties to be overcome when et al. 2005) which can result in demineralisation of the
motivating patients to clean their teeth to a higher standard. adjacent enamel and gingival inammation (Lovrov etal.
2007). Patients accepted for orthodontic treatment, par-
Flossing ticularly xed appliance therapy, should demonstrate an
Although evidence relating to the eectiveness of ossing in adequate level of oral hygiene. Toothbrushing using the
children for the improvement in gingival and periodontal Bass technique with use of approximal brushes and inter-
health is sparse, it may be benecial to recommend super- space brushes (Goh 2007) is recommended by orthodontic
vised ossing of children’s teeth for those at high risk of specialists. Reminder therapy has been shown to be a valu-
caries. e Public Health England DBOH toolkit (2017) able strategy in contributing to the reduction of plaque
recommends for children aged 12–17 years to clean daily and gingival indices and white spot lesions in patients
between the teeth to below the gum line before toothbrush- undergoing orthodontic treatment according to a system-
ing, using dental oss or tape for small spaces between the atic review and meta-analysis of high-quality evidence
teeth, or, for larger spaces, using interdental brushes. (Lima etal. 2018). A systematic review showed some lim-
e BSP have produced an infographic for children ited evidence that use of mobile phones can be eective in
called, “Let’s keep children smiling,” portraying the message improving adherence to oral hygiene advice in orthodon-
that they should be ecient at ossing or using interdental tic patients (Sharif etal. 2019). e daily use of a 0.05%
brushes at around the age of 10 years (available at www.bs sodium uoride mouthwash (225 ppm) should be advised
perio.org.uk). at a dierent time from toothbrushing for patients under-
going xed appliance therapy (Benson etal. 2004, Public
Non-Surgical Periodontal Therapy Health England 2017).
Management of Gingivitis and
Periodontitis Role of Systemic Antimicrobials
Step 1 of the stepwise approach contains the key elements Systemic antimicrobials are not indicated for the manage-
for the management of plaque-biolm-induced gingivitis ment of plaque-induced gingivitis or the cases of incipient
in the child or adolescent (see Chapter 4.3 and Appendi- periodontitis (typically stage I, grade A) that may be found
ces 3 and 4). It is directed at the removal of supragingival in adolescents who would normally be treated in the pri-
and subgingival plaque and calculus deposits on the clinical mary dental care setting in general dental practice. ere are
crown of the tooth via PMPR, in conjunction with risk fac- some specic exceptions:
tor control and patient education and engagement in tai-
lored home plaque control measures; adjunctive therapeutic 1. Severe, rapidly destructive disease
agents to help control inammation may also be indicated Stage II, III, IV, grade C periodontitis in young individu-
(Sanz et al. 2020, West et al. 2021). Management of any als who would previously have been diagnosed as aggres-
modiable risk factors needs to be incorporated into treat- sive periodontitis in the old classication (Armitage et al.
ment planning, including smoking cessation advice if appli- 1999) may be considered for adjunctive systemic antibiotic
cable to children and teenagers. therapy, but such cases are often best managed by specialists
For periodontitis cases, step 1 needs to be successfully (Clerehugh & Kindelan 2021), including:
completed before progressing on to step 2. is involves • molar-incisor pattern of periodontitis aêecting ërst
reinforcement of oral hygiene measures, risk factor control molars/incisors that may occur in adolescents around
and behaviour change before proceeding with subgingival puberty, which would previously have been classied as
PMPR. Incipient periodontitis (stage I, grade A) in teen- localised aggressive periodontitis.
agers can often be managed in dental practice. e more • localised pattern of periodontitis in young people, which
challenging cases (stages II, III, IV, Grade C) in the younger would previously have been classied as localised aggres-
age groups and consideration for adjunctive use of systemic sive periodontitis.
antimicrobials may best be undertaken by a specialist to • generalised periodontitis, grade C in young adults, which
whom referral may be appropriate (Clerehugh & Kindelan would previously have been diagnosed as generalised
2021). Re-evaluation of the outcome of step 2 drives the aggressive periodontitis.
decision to move to step 3 (managing non-responding sites) In these situations, systemic antimicrobials would only
or to step 4 (supportive periodontal therapy [SPT]) (see be administered as adjuncts to disruption of the biolm
Chapter 5.4 for further information on this topic). achieved through subgingival PMPR (Teughels etal. 2020,
Younger patients are able to comply with this treatment, West etal. 2021) (Figure 3.3.6). According to a recent sys-
but more attention may need to be paid to behavioural tematic review and meta-analysis (Teughels et al. 2020),
aspects (see Chapter 4.3) to acclimatise them to treatment. the best treatment outcomes have been observed using a
Evidence-based recommendation (2.16)

A. Due to concerns about patient’s health and the impact of systemic antibiotic use to
public health, its routine use as adjunct to sub-gingival instrumentation in patients
with periodontitis is not recommended.
B. The adjunctive use of specific systemic antibiotics may be considered for specific
patient categories (e.g. generalised periodontitis grade C in young adults).
Supporting literature Teughels et al. [45]
Qualityof evidence RCTs (n=28) with a double-blind, placebo-controlled, parallel design.
Risk of bias was low for 20 of the studies, while 7 studies had a high risk. PPD reduction
at 6 months; MET+AMOX: n=8, 867 patients. PPD reduction at 12 months; MET+AMOX:
n= 7, 764 patients, MET: n=2, 259 patients.
A. Grade of recommendation grade A - ↓↓
B. Grade of recommendation grade 0 - ↔
A. Strength of consensus consensus (0% of the group abstained due to potential Col)
B. Strength of consensus consensus (0% of the group abstained due to potential Col)
BSP implementation
This evidence-based recommendation (A) is adopted.
A. We do not recommend the routine use of systemic antimicrobials as an adjunct to
sub-gingival instrumentation in patients with periodontitis, due to concerns with
overuse of systemic antimicrobials on individual patient health and on the wider
aspects of public health.
This evidence-based recommendation (B) is adopted.
B. The adjunctive use of specific systemic antibiotics may be considered for specific
patient categories (e.g. periodontitis grade C 2 in younger adults where a high rate
of progression is documented)
Updated evidence: No new applicable evidence was identified
Strength of consensus: Unanimous consensus (0% abstentions due to potential Col)
• Figure 3.3.6 Do adjunctive systemic antibiotics improve the clinical outcome of subgingival instrumenta-
tion? (Reprinted from West N et al. BSP implementation of European S3 - level evidence-based treatment
guidelines for stage I-III periodontitis in UK clinical practice. Journal of Dentistry 2021;106:1–72:103562.)
combination of adjunctive systemic amoxicillin (adult .niced.org.uk/treatment-summary/oropharyngeal-infections-

dose, 250 mg or 500 mg three times per day) plus met- antibacterial-therapy.html); doses should be scaled pro rata
ronidazole (adult dose, 200 mg or 400 mg three times per for children/adolescents according to age as per the BNF.
day), although no conclusive consistent evidence emerged
for optimum duration which ranged from 3–14 days in 3. Periodontal abscess with systemic involvement
the studies cited; to a lesser extent metronidazole alone or When local measures are not sucient, treatment should
azithromycin alone also showed signicant clinical benets include the administration of phenoxymethylpenicillin
in terms of probing pocket depths, clinical attachment 500 mg four times daily, or alternatively amoxicillin 500
level, bleeding on probing, frequency of pocket closure mg three times daily (or, if penicillin allergy, clarithromycin
and residual pockets. e debate as to whether to use in 500 mg twice daily) for up to 5 days, review at 3 days, plus
the initial phase of treatment or after 3 months subgingi- metronidazole 400 mg three times per day if signs of spread-
val PMPR is ongoing, and the need for cautious and judi ing infection, e.g. lymph node involvement. Doses pro rata
cious use of systemic antimicrobials is paramount because according to age in younger age groups.
of antibiotic resistance and potential side eects from their
use (Teughels etal. 2020).
KEY POINT 8
Systemic antimicrobials are not indicated for the management
2. Necrotising gingivitis of plaque-induced gingivitis or for most cases of periodontitis
Treatment includes an adult dose of metronidazole 400 mg in young people, with a few specic exceptions: uncommon
three times per day for 3 days, in association with debride- but severe and rapidly destructive forms of periodontitis in
ment, to target the fusiform-spirochaetes in the subgingival young patients (typically staged and graded as stage II, III or
plaque, as in British National Formulary guidance by National IV, grade C); necrotising gingivitis; periodontal abscess with
systemic involvement.
Institute for Health and Care Excellence (NICE) (https://bnf
Periodontist Paediatric dentist
Treat or refer
Dentist factors Patient-centered factors Complexity of case
Practice and profile Patient’s compliance Diagnosis
Training and experience Periodontal risk factors Severity and extent
Initial therapy done? Medical history Multi-disciplinary care
• Figure 3.3.7 The decision to treat or refer young cases in practice depends on a number of factors.
Management of Recession improvement, resective (gingivectomy) surgery (step 3) may

e recession should be monitored and management should be necessary to correct the gingival contour where function
use a two-tiered approach: and aesthetics are a concern, especially with respect to drug-
1. Aimed at halting the recession by taking account of the induced gingival overgrowth. e management of such
aetiological factors patients may require referral to dental paediatric or peri-
2. Managing the consequences of recession. odontal specialists who will liaise with appropriate medical
When considering the aetiological factors, the patient colleagues.
needs:
• An atraumatic brushing technique Treat or Refer
• Advice on habits associated with gingival trauma (e.g.
nger-picking habits), replacement of poorly designed e decision to treat young patients in a primary dental care
partial dentures setting or refer to a specialist is dependent on a number of
• Orthodontic treatment planning – avoidance of move factors (Figure 3.3.7).
ment which might lead to thinning of the buccal or lin- As per the updated BSP Guidelines for Periodontal
gual plate, especially where the gingiva is thin Screening and Management for Children and Adolescents
• Treatment of periodontitis and oral health education on under 18 years of age (Clerehugh & Kindelan 2021), the
prevention of further destruction periodontal conditions and cases that may be considered for
• Smoking cessation advice. referral include:
When managing the consequences of recession, the clini- • Stage II, III periodontitis not responding to treatment
cian needs to treat: • Grade C or stage IV periodontitis
• Dentine hypersensitivity • Medical history that signiëcantly aêects periodontal
 • Anti-sensitive teeth dentifrices; dietary advice; topical treatment or requires multi-disciplinary care
uorides; restoration(s) • Periodontitis as a direct manifestation of systemic disease
• Root caries • Systemic/genetic diseases that can aêect periodontal sup
 • Topical ìuorides; dietary advice; restoration(s) porting tissues
• Restoration of aesthetics • Root morphology/furcation defects adversely aêecting
 • Findings from the literature suggest that mucogingi prognosis on key teeth
val surgery is not needed before the patient reaches • Non-plaque-induced conditions requiring complex or
adulthood (Bosnak etal. 2002). Referral to a specialist specialist care
in paediatric dentistry or periodontology should be • Cases requiring diagnosis/management of rare/complex
considered by the primary care clinician. clinical pathology
• Drug-induced gingival overgrowth needing surgery
Management of Gingival Overgrowth • Cases requiring evaluation for periodontal surgery
Treatment for gingival overgrowth should begin with rigor- Multiple choice questions on the contents of this chapter
ous home care for optimal plaque biolm control and fre- are available online at Elsevier eBooks+
quent appointments for PMPR as in steps 1 and 2 of the A series of videos demonstrating how to assess the peri-
S3-level treatment approach. Although this often leads to odontium are also available online.
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3.4
REFERRAL TO A PERIODONTAL
SPECIALIST
AL A N WO O D M A N
CHAPTER OUTLINE
Introduction How to Refer
Why Refer? What to expect from a Referral
Who to Refer What to Expect as a Referring Clinician
How to Prepare your Patient
What to Refer
After Referral
Clinical Criteria
Radiographic Criteria The Specialist’s Report
Restorative Criteria Legal and Ethical Issues
Implants On Conclusion of Specialist Care
When to Refer Managing the Patient Who Declines Referral
Where to Refer

This chapter explains the who, what, why, when, where and how of periodontal referrals.
It incorporates the British Society of Periodontology and Implant e chapter covers the following topics:
Dentistry (BSP) guidance on referral and associated dento-legal • Introduction
issues. • Why refer?
By the end of the chapter, and aer having completed the online • Who to refer to
questions and exercises, the reader should: • What to refer – radiographic criteria, restorative criteria,
• Understand the indications for the referral of periodontal implants
patients • When to refer
• Appreciate the mechanisms of eòective referral • Where to refer
• Be conödent in explaining to patients the beneöts and • What to expect from a referral
possible outcomes of referral • After the referral
• Be able to construct a satisfactory referral letter • Dento-legal issues.
• Understand the long-term relationship between the referrer,
referee and the patient.
Introduction this long-term outcome cannot be overstated. However, a

small proportion of patients may either initially present
For most patients, the early recognition and treatment to the clinician with a more advanced condition, because
of periodontal diseases allows clinicians to achieve a pre- of previous non-attendance or lack of appropriate treat-
dictable outcome and a stable periodontium. is can ment, or display a high level of susceptibility or show
be maintained for life with continued supportive care a greater disease complexity due to health, behavioural,
and allows for the successful provision of other dental anatomical or dental complications. Such patients may
treatment. e important role of the hygienist in achieving seem to the receiving clinician to demand, or deserve,
161
particular skills which they themselves feel unable to GDP

oer, and thus referral to a specialist in periodontics is exam
deemed desirable.
is chapter aims to advise the clinician on the rationale
for periodontal referral and the practical aspects of achiev- Hygienist
Patient
ing a successful result for the patient. e referral should be treatment
seen as a shared, continuing and cyclical partnership among
the several participants (Figure 3.4.1).
KEY POINT 1 Hygienist

GDP
Early recognition of periodontal diseases will minimise the need review
for late referral.
Periodontal
specialist
Why Refer?
• Figure 3.4.1 The participants in periodontal care and treatment.
A decision to refer to a colleague will be based upon:
• ɨe clinician’s experience, conëdence and perceived abil
ity to manage the patient’s condition • ɨe patient’s preference or request to see a specialist
 • If the situation is carefully explained to the patient  • Patients have become increasingly aware of treatment
and a choice clearly given, most patients only see alternatives via the internet and other media and may
referral as a positive beneët, not as a “failure” in their demand another approach if, in their view, existing
clinician, but it is important to be able to answer their treatments seem unsuccessful
initial queries about the referral  • Such a request should not be assumed to be a criti
 • In the medical environment, patients do not expect cism, but it must carefully be discussed to determine
their general practitioner (GP) to handle all their the reasons for the patient’s decision and to maintain
problems and referral is common a professional relationship post-referral
• ɨe age and general health status of the patient  • ɨe specialist will always be discreet and tactful when
 • Periodontitis presenting in a younger patient is gener replying to the patient’s inevitable query, “Why has this
ally regarded as a greater concern – aggressive disease at not been done before, by my dentist/hygienist . . . ?”
any age justiëes referral, but referral is essential for the
adolescent patient KEY POINT 2
 • Concurrent health problems may inìuence the onset The dental hygienist or therapist may be the backbone of
of periodontal diseases and their treatment outcomes, successful periodontal care but will always provide more
effective support with good general dental practitioner (GDP)
particularly: input and interest.
Unstable diabetes
Drug-induced gingival enlargement (DIGE), which is
increasingly prevalent as more patients receive calcium KEY POINT 3
channel blockers as part of anti-hypertensive therapy It is very important that the specialist maintains proper
professional respect when dealing with such patient queries
A history of head and neck radiotherapy to ensure that the long-term relationship between the referrer,
A known signiëcant bleeding dyscrasia/disorder patient and specialist remains mutually supportive.
A signiëcant immunocompromised or suppressed state
• ɨe complexity of the treatment likely to be required. Who to Refer
For example:
 • Multiple deep infra-bony lesions, where surgical care ree broad groups of patients may be regarded as suitable
is likely to be recommended for referral:
 • ɨe presence of suspected posterior perio-endo • Patients with concurrent complicating medical condi
lesions, where complex endodontic treatment, or pos- tions, discussed previously, but most commonly:
sible root resection, is required  • Unstable diabetes
 • Extensive pocketing associated with tooth mobility,  • ɨose presenting with DIGE, especially those tak
where splinting may be indicated ing calcium channel blockers (e.g. nifedipine) for
 • Isolated pockets aêecting important abutment teeth hypertension
 • ɨe presence of concurrent muco-gingival disease • Compliant but non-responding patients:
 • ɨe presence of peri-implant disease or the close prox  • Non-smokers – who have made good eêorts with
imity of implants to the disease site(s) their oral hygiene but failed to achieve the outcome
 • A requirement for intramuscular (IM) or intrave expected after initial hygienic phase treatment
nous (IV) medication as a component of clinical  • Smokers – who show a poor response to initial treat
management ment, but they must be advised that:
CHAPTER 3.4 Referral to a Periodontal Specialist 163
Initial patient examination with Medical complications

GDP
Younger patient with

Specialist periodontist
aggressive periodontitis
Patient with advanced

chronic periodontitis
Initial non-surgical treatment

Non-responding patient,
with GDP or dental hygienist/
compliant with OHE
dental therapist
Advise smokers
Review with GDP Non-responding patient,

and re-assessment non-compliant with OHE,
(at 6–12 weeks) but demanding
Improving and responding

patient managed within
General Dental Practice
• Figure 3.4.2 Protocol for referral.
the outcome of treatment will be less predictable, time). Patients suited to referral will usually show some of
whoever undertakes it, the following features:
progress will be slower to achieve, and • Non-resolving sites, either as multiple pockets or isolated
surgical treatment may not be a practical option if deep lesions
they continue to smoke • Pocket depth ≥5 mm
advising a patient to seek smoking cessation advice • Signiëcant anatomical diïculty such as:
prior to referral makes a very valuable contribution to  • the close proximity of roots, either due to closely
their care, both in the short and long term. approximated teeth, or
• Non-compliant but demanding patients:  • narrow furcation spaces
 • ɨese patients have not adequately complied with oral  • “extra” roots, such as third roots in upper premolars,
hygiene advice during initial or maintenance therapies, or lower molars, fourth roots in upper molars or, less
and thus show little or no improvement, yet demand commonly, biëd roots in canines or incisors
further treatment but will not accept extractions  • thick crestal bone
 • Referral of such patients is not ideal, but some may  • thick, obstructive, gingival tissues
respond to a dierent approach or dierent clinician. • Mobility of grade 1 or 2
If they still do not respond after specialist care, an • If mobility exceeds this, i.e. grade 3, extraction is the
alternative strategy must be adopted, usually involv- most likely outcome and referral is rarely justiëed unless
ing the extraction of teeth splinting is proposed
 • It may be that simply giving a second (specialist) • Persistent bleeding on probing from pockets – in spite of
opinion will suce and convince the patient to accept good oral hygiene
the original GDP proposals • Persistent desquamative gingival surfaces
 • Providing a comprehensive history of the treat • History of periodontal abscess(es)
ment attempted is particularly important for these • Suspected perio-endo/endo-perio lesion
patients, to assist the specialist in making a reasoned • Unstable furcation involvement – i.e. a furcation to
judgement about any possible treatment options. which access is denied by either the gingival tissues or an
A protocol for referring periodontal patients is shown in unfavourable root anatomy
Figure 3.4.2  • Furcations which show roots divergent by >30 degrees
may be maintained in the long term and are suitable
for referral
What to Refer  • A convergence or divergence of <30 degrees is
Clinical Criteria unpredictable
 • If further complicated by mobility or occlusal stresses
Certain features of periodontal diseases are logical prerequi such convergent teeth should not be the subject of
sites for referral (but not all have to be present at the same referral
 • If a furcation has become cleansable and patent due Implants

to gingival recession, it can be regarded as stable and
should not need referral e increasing use of osseo-integrated implants has resulted,
• Unacceptable gingival architecture – which will compli inevitably, in more peri-implant disease, which has tended
cate the application of eective oral hygiene methods to fall into the hands of the periodontist for remedial action.
 • Gingival enlargement – especially DIGE At present, there are no universally agreed methods of coping
Calcium channel–blocking medications have become with these problems, other than gentle debridement, anti-
increasingly common anti-hypertensives in favour of biotic therapy and continued good oral hygiene, although
beta-blockers in recent years there are claims that regenerative surgical techniques can
ey are now a more common cause of gingival over- be successful in improving the bone contours around the
growth than anti-epileptics (epanutin/Dilantin) and ëxtures. It is certainly appropriate to refer such cases to the
anti-rejection drugs (cyclosporin, tacrolimus) specialist periodontist, even though debate continues about
eir use usually has to be tolerated periodontally, as the precise nature of the “disease” occurring around the fail
the medical beneëts outweigh the gingival disadvantages ing ëxture.
and GPs show understandable reluctance to change the An increasing number of periodontists undertake the
prescription surgical placement of implants. is has added a useful
• Gingival recession, which treatment modality when teeth are beyond periodontal care
May have developed progressively over time and extraction is deemed inevitable and may, in some cir-
May be associated with fraenal attachments cumstances, inìuence the treatment planning for referred
May have occurred as a complication of successful treat patients. Gaining periodontal stability of the remaining
ment teeth is generally considered a prerequisite for successful
Leaves the patient concerned about aesthetics or implant placement and thus periodontal care usually must
Permits persistent cervical sensitivity, resistant to topical precede the implant phase.
therapies
• Elective “crown-lengthening” surgery to improve the KEY POINT 4
restorability of teeth. You may not wish to undertake periodontal treatment yourself,
but remember that your dental hygienist/therapist is specically
trained to undertake non-surgical periodontal therapy.
Radiographic Criteria In all but the most severe cases, let the hygienist/therapist
carry out some initial treatment rather than assuming the worst
It is expected that patients referred to a specialist would outcome!
exhibit at least one of these features:
• >30% loss of bony support
 • which can only be judged if the radiograph shows the KEY POINT 5
whole tooth, thus Clear, concise and comprehensive records on paper or
 • peri-apical or orthopantomogram (OPT) views are computer are absolutely essential in periodontal therapy and
essential for conërmation of diagnosis facilitate any referrals.
• Irregular (vertical) bone loss Such records also offer medico-legal protection to the
clinician.
• Infra-bony lesions
Make a record of all discussions, communications and
• Perio-endo/endo-perio lesion(s) advice given to patients about their problems and treatment.
• Concurrent but unrelated endodontic lesion(s) on peri
odontally aected teeth.
When to Refer
Restorative Criteria
As with any medical condition, early referral is the ideal.
Prior to referral, it is important to consider the restorability However, the timing of the presentation of the case is not
of periodontally aected teeth. ere is no point in carry- always within the clinician’s control and most cases are
ing out complicated periodontal treatment to retain a tooth referred later than the specialist would prefer.
which cannot then be restored. Unless the patient presents with an established aggres-
However, the presence of periodontal lesions in certain sive periodontitis, it is usually appropriate for the GDP or
circumstances assumes priority for complex care, where the dental hygienist to carry out some initial hygienic phase
alternative, tooth loss, would have serious consequences for therapy, which is the accepted start of all periodontal
the existing restoration or prostheses: treatment.
• Abutment teeth for existing bridges/dentures • Referral should be considered if, following review of such
• Last functional molar in any quadrant initial hygienic phase therapy after 3 months, extensive
• Teeth complicated by suspected occlusal co-factors pocketing remains with bleeding from the pockets
• Potential loss of posterior support if tooth/teeth lost. • If pockets reappear after a period of stability
• If, on presentation, prior to initial treatment, a new  • Since the creation of a specialists list by the General
patient shows basic periodontal examination (BPE) code Dental Council (GDC), such periodontal specialists
4 in several sextants, especially in the younger or medi- have become available but, as they are exclusively prac-
cally challenged patient tising under private contract, this may prove expensive
• If the patient has advanced chronic periodontitis for many potential patients.
• If the restorative co-factors are challenging in addition to  • It is essential that referring clinicians discuss the pos
the poor periodontal condition. sibility and extent of fees which could be incurred for
ɨe BPE may be regarded as a guide to referral, but initial consultation when recommending referral and
clinicians are strongly recommended to undertake a full that they ensure patients understand their liabilities.
periodontal assessment and comprehensive periodontal Most specialists will provide a guide to their fees.
examination (CPE) to justify referral and to enhance their  • Subsequent fees will be discussed between the spe
own records of the patient’s condition at referral for dento- cialist and the patient following the consultation.
legal prudence, particularly if the patient is a poor complier Referring clinicians should avoid discussion with the
with oral hygiene advice and appointments. patient about specialists’ fees for treatment.
It is likely that patients considered suitable for referral will  • If there is certainty about the availability of spe
have demonstrated a BPE code of 4 in one or more sextants; cialists in a particular area, the British Society of
however, a widespread distribution of code 3 may also initi- Periodontology and Implant Dentistry website
ate referral, especially as this may be associated with DIGE. (www.bsperio.org.uk) oers a suitable search capabil-
e relationship between the complexity of treatment ity. ɨe GDC Specialists List, contained in the dentists
and the BPE is explained in the British Society of Periodon register, also has similar information (https://www.gdc-
tology and Implant Dentistry (BSP) document “Referral uk.org/registration/your-registration/specialist-lists).
Policy and Parameters of Care”, which attempts to outline
complexity in terms of the types of patient, condition, com- KEY POINT 6
plications and potential treatments to assist in making a There is no fast track to periodontal health.
decision to refer. Paying privately for periodontal treatment does not
Ultimately, the timing of the referral will be the referring necessarily equate to better treatment, but usually means that
more time is spent with the clinician.
clinician’s decision and will be made after discussion with Remember the time spent on periodontal health education
the patient. is as rewarding clinically as the active treatment.
Where to Refer
KEY POINT 7
In the UK, the options available to the GDP and patient, In the UK (and other countries with state-funded care), there
which are limited by location and professional demography, are strict budgetary restraints on all expenditure within the
are as follows: National Health Service.
This may limit some surgical procedures involving
• University dental school periodontal or restorative expensive regenerative materials, even within the dental
consultant schools, unless research funding is available.
 • ɨis is inconvenient for those living outside the main
cities
 • ɨe cases required for undergraduate training are usu KEY POINT 8
ally only moderately severe Never assume the nancial status or commitment of your
 • ɨe dental school need for complex cases will be pro patients.
portionate to the number of postgraduates undertak- Always give the patient the full choice of options for referral.
Many patients will choose to prioritise their personal spending
ing treatment on dental care so that they may keep their teeth for longer.
 • However, if available, treatment will be free.
• NHS general hospital restorative consultant
 • Unfortunately, such departments rarely have funding How to Refer
for prolonged treatments and hygienist support, but
advice and treatment planning may be, at best, avail- Essential information required in any communication,
able but will be free either online, by email or by letter should contain:
• Community dental service periodontal specialist • Referring clinician’s details and contact information
 • Such posts are few and far between but will usually be • Patient’s details, date of birth and address
free • Patient’s contact information and availability
• Dentist with special interest in periodontics (DWSIs) • Medical alert/status of the patient
 • A small number of GDPs have followed this route in • Patient’s original complaint/wishes
practice and may be able to provide an enhanced peri- • Brief description of periodontal and general dental condition
odontal service locally. is is most likely to be under • Speciëc concerns, especially related restorative complica-
private terms tions or plans
• Private specialist in periodontics • Outline of treatment provided and response, if any
• Copies of charts, radiographs (new and old) and study • BOX 3.4.1A Results of a 6-Year Audit of Activity
casts if available of a Specialist in Periodontics
• Purpose of referral – is this for:
New patient consultations 2036
 • Second opinion
Initial non-surgical treatment by the 997
 • Treatment planning, or
periodontist
 • Treatment.
Initial non-surgical treatment by dental 959
Examples of suitable formats for referral and referral
hygienist
exercises are included in the online section of this chapter.
Patients receiving occlusal analysis 993
Patients subsequently provided with an 91
KEY POINT 9
acrylic occlusal splint
Always state:
• Why they are coming Patients proceeding to surgical care after 523
• What you have tried review of initial treatment
• What the patient wants Supportive care reviews with the periodontist* 4710
• Where any specic sites are to be found Supportive care reviews with the dental 12256
• What medical issues might be a compromise to
hygienist
treatment.
Patients receiving acrylic labial gingival 178
veneers for aesthetics
KEY POINT 10 Periodontal splints applied (webbing/ 334
Always try to send: composite)
• Previous CPE chart(s) Periodontal splint repairs subsequently 639
• Relevant radiographs or copies (old radiographs are
undertaken
particularly useful to provide a historical record of
disease progression) Metal (Rochette/Maryland) splints applied 61
• Photographs of acute sites
• Models – if occlusal or recession problems are the *Joint appointments with the dental hygienist.
subject of the referral.
KEY POINT 11 • Always ensure that the alternatives to further periodontal
Always provide: treatment are explained
• Clear details of: • Do not assume that a surgical approach will be undertaken
Your address & contact • Do not second-guess what the specialist will say – let the
Patient’s address
specialist outline the treatment needs in due course
Patient’s contact
Patient’s availability • If appropriate, warn the patient of the likelihood of a
• Give the patient details of: poor response to treatment in the presence of modiëable
Who they are seeing risk factors, such as smoking and poor oral hygiene.
Any possible cost Many specialists in periodontics undertake a broad spec
Why you want them to go
trum of periodontal and closely allied treatments, such as
implant dentistry, occlusal therapies and apical surgery.
What to expect from a Referral Others restrict their practice to “pure” periodontics.
e choice of specialist will depend upon the referring
What to Expect as a Referring Clinician clinician’s undergraduate teaching, interests and beliefs, the
perceived needs of your patient and the availability of a spe-
• Probably more initial non-surgical “re-treatment”
cialist in the local area.
• A period of review and reassessment usually 6 weeks to 3
e clinical audits (Box 3.4.1A and B) illustrate the
months post-treatment
activities typical of a specialist in periodontics, showing the
• Possibly endodontic co-treatment may be recommended
varied tasks undertaken within a “broad spectrum” special
(undertaken by the referrer or another specialist)
ist periodontal practice over a 6-year period (2004–2010).
• Possibly occlusal co-treatment (by the specialist or, less
likely, by the referrer)
• Possibly a recommendation for surgical treatment KEY POINT 12
• ɨe need for continued long-term hygienist sup The patient should receive:
• A clear statement of the problem
port, either initially or permanently within the referral • The objectives of treatment
practice. • A clear plan of proposed treatment
Including:
• The number of appointments planned
How to Prepare your Patient • Who will be treating the patient
• An estimate of costs
• Always try to explain the origins of their disease, the rea • The anticipated treatment time.
sons for your concern and the need for referral
• BOX 3.4.1B Specialist in Periodontics: Surgical • Occlusal or orthodontic treatment in complex cases.
Activities Over a 6-Year Period Such treatments may be undertaken either by the
referring clinician or managed by the specialist or
Surgical treatments 523 another specialist colleague, depending upon the com-
Including tissue regeneration with: plexity and wishes of the patient and the referring
Emdogain (nil teeth lost) 20 clinician.
Ceramic (5% teeth lost) 34 e report may also indicate where the necessary sup-
BioOss/Gide (3% teeth lost) 187 portive periodontal treatment (SPT) should be under
Also: taken after initial treatment – within the specialist
Frenectomies 31 practice or the referring clinician’s practice. However,
Connective tissue grafts 7 most specialist periodontists prefer to keep the patient
And: under their close supervision for a recovery period of at
least 1 year.
Apicectomies 48
SPT, the longer-term outcome of all periodontal treat
Vital root resections 63
Number requiring subsequent:
ment, is usually undertaken by the dental hygienist under
the supervision of the referring clinician. Many periodon
Endodontic treatment 14 tists, however, prefer to keep SPT under their control. ɨere
Extraction 6 is reliable research evidence that such long-term care in spe-
cialist practice is more successful in reducing subsequent
tooth and attachment loss than that carried out in general
dental practice.
If the patient remains under the care of the specialist for
After Referral a long period of time, it is customary to provide the refer-
The Specialist’s Report ring clinician with a periodic review of the patient’s status,
especially if a change in the treatment plan is proposed,
Following consultation, the specialist will provide the referring for example, progress to surgical therapy or the need for
clinician (and the patient) with a report on the condition of the extractions.
patient, the ëndings, diagnosis and proposed treatment. Examples of such reports and estimates can be found in
is may be a copy of a report prepared for the patient or the online section which complements the printed part of
a separate report. Many specialists will copy all correspon this book.
dence to the patient and referring dentist to each party, thus
enabling complete transparency regarding any fees involved Legal and Ethical Issues
and the treatment oered.
If paying for treatment, the patient will receive an esti Guidance on these issues can be found in the GDC docu
mate of the likely fees involved for any proposed treatment ment: Standards for the Dental Team (http://www.gdc-
within the specialist practice. uk.org/Dentalprofessionals/Standards/Documents/Standa
Patients may seek to discuss these reports (and the esti- rds for the Dental Team.pdf ).
mate of likely fees) with the referring clinician for guidance As dentistry has entered increasingly litigious times,
and/or reassurance before committing to treatment. ɨis is the frequency of complaints against practitioners for
quite reasonable, although most patients will agree to treat- failing to diagnose and/or treat periodontal diseases has
ment at or shortly after their consultation. risen considerably, and the various defence organisations
In essence the specialist report should outline: regularly remind their clients of the need for compre-
• ɨe current dental status of the patient hensive record keeping, early recognition of disease and
• ɨe current periodontal status of the patient good communication with their patients to minimise
• ɨe particular periodontal sites of concern risk.
• Any concurrent restorative concerns From an ethical standpoint, the patient has a right to
• Any concurrent endodontic concerns expect referral for any condition if their primary care cli-
• Any observed soft tissue concerns nician feels unable to provide treatment to a satisfactory
• Any observed occlusal concerns standard. us, ignoring or delaying necessary periodontal
• Any medical contraindications or co-factors treatment cannot be excused when the option of referral to
• A proposed treatment plan, which must also be clear to a colleague is available.
the patient. Similarly, a failure to take adequate steps to diagnose and
Any perceived concurrent treatment requirements will be thus subsequently fail to treat periodontal diseases will be
discussed, for example: deemed unacceptable by regulating authorities.
• Endodontic • Responsibility for recognising the need for referral lies
• Restorative – new or replacement prostheses/restorations with the diagnosing clinician
• Responsibility for providing the appropriate care after recommendations for SPT closely and ensure that the treat
referral lies with the specialist ment provided is adequate.
• ɨe specialist will work under diêerent conditions from
the generalist:
 • ɨey are expected to undertake more complex tasks Managing the Patient Who Declines
 • ɨey are assumed, by deënition, to be more experi Referral
enced and competent in their ëeld
 • ɨus, any failure of treatment will be judged a more Not all patients will accept the need for referral. ɨis may
serious breach of their “duty of care”. be for many reasons:
• Patients’ expectations will be higher when receiving spe • anxiety
cialist treatment; thus to avoid disappointment: • lack of understanding
 • Setting realistic and clearly understood goals is essen • lack of interest in keeping teeth
tial at the outset of specialist care • ënancial concerns
 • Gaining informed consent must be achieved • other health issues
 • Having ensured that all options for treatment have • lack of time
been fully explained. • loss of time from work, etc.
e referring clinician has often known the patient for In such cases, it is imperative that the patient’s records are
a considerable time and has been able to establish a good fully annotated with the referral oered, the reasons why refer-
rapport. It is worth remembering that the specialist is meet ral was recommended and the reasons for this being declined.
ing and treating a stranger and such rapport will take time Keeping a statement of these facts signed by the clinician
to build. e interpersonal skills of the specialist are as and the patient is a prudent action and may limit possible
important as their clinical skills in ensuring a harmonious future dento-legal diculties.
relationship between them, their patient and their referring
clinicians. KEY POINT 13
If a patient declines referral always make a full record of this
On Conclusion of Specialist Care and their reasons for saying no!
• It is essential that the specialist informs the referring cli Multiple choice questions on the contents of this chapter
nician of the outcome of treatment, the likely future care are available online at Elsevier eBooks+.
required and the prognosis for the patient’s periodontal A series of case studies and referral letters are also avail-
and general dental condition as a result of the treatment able online.
provided.
• After surgical procedures there may be a recommended References and Further Reading
interval for radiographic reviews.
• A clear statement of the oral hygiene advice given and Baker P, Needleman I. Risk management in clinical practice. Part 10.
continuing techniques expected will be beneëcial for Periodontology. Br Dent J. 2010;209:557–565.
future dental hygiene support. Dental Protection Society. Riskwise. 2012;43.
e specialist must always remain available for advice or Gaunt F, Devine M, Pennington M, Varnazza C, Gwynnett E, Steen
N, Heasman P, et al. e cost-eectiveness of supportive peri-
remedial treatment, even though they may have returned
odontal care for patients with chronic periodontitis. J Clin Peri-
the patient to the referring clinician. odontol. 2010;35(8 Suppl):67–82.
Problems can occur when care is shared between the spe- General Dental Council, 2005. Standards for dental profession-
cialist and, for example, the dental hygienist in the origi- als. Accessed from: www.gdc.org-uk (on 22 October 2012) and
nal referring practice, often during the supportive phase of http://www.gdc-uk.org/Newsandpublications/Publications/Publ
care. Should the patient’s condition deteriorate, an awkward ications/StandardsforDentalProfessionals[1].pdf (on 24 October
situation can arise. It is advisable to follow the specialist’s 2010).
SECTION 4
The Role of Self-Care and Oral

Hygiene Methods
169
4.1
PATIENT EDUCATION
AND SELFPERFORMED
BIOFILM CONTROL
EL A I N E T I L L I N G
CHAPTER OUTLINE
Introduction Interdental Cleaning
Patients’ Health Beliefs Elastomeric Toothpicks
Floss
Motivating Patients to Clean Optimally
Flossing Techniques
Tailoring Oral Health Advice Interdental Brushes
Techniques for Oral Hygiene Oral Irrigators
Subgingival Cleaning
Self-Assessment of Home Plaque Control
Adjunctive Antiseptic Agents
Delivery of Oral Hygiene Advice
Dentifrices (Toothpastes)
Toothbrushing Mouth Rinses
Manual Chlorhexidine
Brushing Technique Conclusions
Powered Brushes

This chapter explains the role of self-care in periodontal therapy, oral hygiene methods, the pivotal role of the patient in the long-term success
of periodontal management and the complexity of behavioural change in health.
• Understand the impact of factors aòecting compliance and • Introduction
motivation in self-performed bioölm control • Patients’ health beliefs
• Describe the practical application of the key principles of • Motivating patients to clean optimally
the Health Belief Model in relation to self-performed bioölm • Tailoring oral healthcare advice
control • Techniques for oral hygiene
• Be able to demonstrate the various techniques for the • Delivery of oral hygiene advice
mechanical disruption of bioölm using a range of oral • Toothbrushing
hygiene tools • Interdental cleaning
• Recognise the pivotal role of the patient in the outcome of • Dentifrices
periodontal treatment • Mouthwashes
• Describe the role of some of the active ingredients in • Conclusions.
commercially available dentifrices and mouthwashes.
171
172 SECTION 4 The Role of Self-Care and Oral Hygiene Methods
Introduction Patients’ Health Beliefs

e strategic focus of many health education interven- e Health Belief Model (HBM), developed in the 1950s
tions has been on clearly dened diseases and targeted by a group of American Public Health Service psycholo-
at changing the behaviours of high-risk individuals. e gists, focuses on compliance and the relationship between
concept of health as a collective responsibility is not new, patients’ beliefs and their behaviour. e HBM, modied
but the growing emphasis on the critical role of the indi- later by Rogers (1998), also considers social and economic
vidual in their general health and well-being is increas- factors. However, like all models, it has its shortfalls, as
ingly recognised. e health educational model for the human behaviour is not always rational!
promotion of oral health emphasises lifestyle and behav- e practical use of this model can take dierent formats
ioural change through educational awareness. Health pro- and utilise some or all of the principles of: perceived suscep-
fessionals tend to dominate in this top-down, disease-led tibility, perceived severity, motivation to change, perceived
focus. It has been popular within the dental profession barriers and perceived benets, which are summarised in
as it ts with the clinical approach in the care and treat- Table 4.1.1
ment of individual patients. However, this model has its
limitations, as it underestimates the dynamic complexity Motivating Patients to Clean Optimally
of motivation for behavioural change. Establishing and
maintaining eective biolm (plaque) control is not just A biolm of dental plaque will build on a clean tooth sur-
about having the manual dexterity to clean eectively face within 24 hours and causes gingivitis in 48 hours (Löe
but about the many factors that strongly inuence com- et al. 1965). Some of the early clinical signs of gingival
pliance and motivation. ese factors include attitude, inammation (redness of the gingival margin, swelling and
understanding, beliefs and lifestyle, all of which need to spontaneous bleeding) rarely manifest in chronic gingivitis,
be taken into consideration when trying to eect perma- leading to underestimation of disease levels by both patients
nent change in a patient’s habits. ere is some debate and practitioners (Lang etal. 2009). e lack of pain and
regarding the impact of self-performed biolm control for associated bleeding serve to relegate the importance of
chronic periodontitis. A systematic review (Hujoel etal.
2005) highlighted the lack of consistent epidemiological TABLE
evidence on the role of plaque/biolm in the aetiology of 4.1.1 Principles of the Health Belief Model
periodontitis. With many medical conditions, including
periodontal diseases, the behaviour of the individual in Perceived In practice, advising the patient
terms of modifying risk factors associated with disease is susceptibility that they have a largely incurable
chronic disease (in a sensitive
increasingly becoming part of care pathways. In patients manner) gains their attention.
diagnosed with periodontal diseases, the pivotal role of Then, by informing them of the
the individual in oral biolm control is recognised in the prevalence of periodontal disease
clinical recommendations (CR) detailed in Figure 4.3.3 within the population, they can
in Chapter 4.3. e stepwise approach mapped to the new begin to see that they are different
to the majority
classication system for periodontal and peri-implant dis-
eases by the World Workshop in 2017 (see Chapter 2.1 Perceived severity Using the radiographs, periodontal
for full details) is described in Chapter 4.3 and illustrated charting and bleeding indices can
show the patient the extent of the
in Figure 4.3.2. From this it is clear that the responsibility disease affecting them
for daily plaque removal is placed rmly on the patient,
and supportive periodontal care provided by the clinician Motivation to Encouraging the patient to respond
change positively to their oral health needs
is dependent upon the individual’s adherence to eec- can be tackled by directly relating
tive daily home care. e ecacy of the plethora of oral their own disease levels to the
hygiene aids and methods of use are subject to constant likely outcomes using a variety of
change of clinical opinion. However, in the absence of risk assessment tools
further evidence and professional consensus, the prag- Perceived barriers Establishing that the exceptionally
matic and reasonable stance, based upon the weight of high level of plaque control
evidence for the association between oral biolm and required is far more than for
gingival inammation, is that the regular and thorough the “average patient” helps the
patient understand the level of
removal of the biolm using a range of oral hygiene aids commitment required by them
remains the mantra for all.
Perceived benets Reduction in discomfort, tooth
mobility and tooth loss as well as
KEY POINT 1 the potential benets to overall
Adequate daily plaque control is key to the prevention and/ health are all realistic outcomes of
or stabilisation of periodontal diseases, and this is the successful treatment
responsibility of the patient.
CHAPTER 4.1 Patient Education and Self-Performed Biolm Control 173
oral hygiene in our day-to-day lives despite the generally cognitive behavioural principles and the adaptation for each
accepted understanding that twice daily toothbrushing with of the participants was based on their thoughts, medium-
uoridated toothpaste is the best way to reduce the risk of and long-term goals and oral health status. e eect of the
both caries and periodontal diseases. e words of MacK- programme on gingival index (GI), plaque indices (PIl),
intosh still have relevance today: “Everybody says that pre- self-reporting, and the participants’ own global rating of
vention is better than cure and hardly anyone acts as if they treatment was evaluated 3 and 12 months after oral health
believed it” (MacKintosh 1953). education and non-surgical treatment. Between baseline
Given the prevalence and nature of periodontal diseases, and the 12-month follow up, those in the experimental
instruction in self-performed, mechanical plaque removal group improved both GI and PIl more than in the con-
has been the bedrock of oral disease prevention for the past trol group, reported higher frequency of daily interdental
century; maintaining a good level of oral hygiene is the key cleaning and were more certain that they could maintain the
to sound oral health and prevention of periodontal diseases attained level of behavioural change. e largest dierence
for the majority of patients. Ensuring patient adherence was seen at interproximal surfaces (Jonsson etal. 2009).
with oral hygiene advice, to reduce the risk of oral disease
and maintain oral health, is a dicult and demanding goal
for the dental profession. Indeed, one of the most debated Techniques for Oral Hygiene
issues in public health is that of the eectiveness of health Self-Assessment of Home Plaque Control
education. Although there is evidence that oral health educa-
tion/promotion can be eective in bringing about change in Ensuring that a patient can assess the eectiveness of their
patients’ knowledge and in improving patients’ oral health, own home care is critical in helping the patient to under-
there is good evidence that bespoke or tailored oral hygiene stand that they are able to take responsibility for their long-
advice appears to be the most eective means of delivery term oral hygiene. e use of disclosing agents to check
of oral hygiene advice, particularly for long-term adherence brushing techniques and identify problem areas or by moni-
and patients with chronic periodontitis (Schou 1998). toring visible gingival inammation can be eective tools
Research indicates a number of factors that inuence for empowerment. Explanation of the role of inammation
adherence with oral hygiene advice. ey include: and bleeding as disease indicators can aid compliance by
• Patients who present with good levels of oral hygiene challenging the patient to reduce or eliminate them. e
are more likely to comply with advice than patients who choice of “empowerment tool” or aid to understanding is
present with poor oral hygiene at the start of treatment a matter of individual choice and tailored to the patient’s
(Borkowska etal. 1998) level of understanding and often the stage in their treat-
• Socio-economic status is consistently related to oral ment. Disclosing the biolm is a simple and eective way of
hygiene levels and other health-related behaviours establishing “missed areas” at the start of treatment – link-
(Schou 1998) ing the presence of bleeding to the role of inammation in
• Patients who believe that they have some personal con the disease process may have more impact and acceptance
trol over their health which may inuence outcome are during the maintenance phase of treatment. Patients often
the most likely to comply with advice (Kyak etal. 1998) believe that they are getting bleeding from “brushing too
• Non-life-threatening chronic conditions tend to inspire hard”, which often results in patients brushing less. Taking
less compliance with health advice than life-threatening the time and eort to explain the disease process and what
illness (Wilson 1987). to do about it on a one-to-one basis is essential whichever
empowerment tool is used. Educational literature can be a
Tailoring Oral Health Advice useful endorsement of the advice given but should not take
the place of a detailed verbal explanation (see Figure 4.3.6).
Oral hygiene advice should:
• Take into account the individual’s personal needs and Delivery of Oral Hygiene Advice
background factors
• Involve the patient in the instructional process, for Eective delivery of healthcare messages requires two
example with the use of digital or printed self-instruction core competencies: technical and specialist skills, as well
materials as knowledge and the ability to communicate and edu-
• Be followed up by a bespoke maintenance programme. cate. e use of commercially available tools and visual
Studies indicate that individually tailored oral health aids, such as anatomical models and diagrams, can aid
educational advice can be extremely eective in improving patient understanding of the complex concepts such as
long-term adherence to oral hygiene in periodontal treat- demonstrating cleaning techniques for furcation sites.
ment. One such study (Jonsson etal. 2009), which was a Just as simple and eective is the use of your hands and
randomised evaluator-blinded, controlled trial, used two the patient’s sleeve to explain the more dicult concepts
dierent active treatments with 113 adult subjects allocated of subgingival cleaning for example (Figure 4.1.1). Edu-
to an experimental or a control group. e individually cational psychologists from the Michigan State Univer-
tailored oral health educational programme was based on sity and the University of Iowa who studied the use of
KEY POINT 3
“With what”: While evidence for efcacy of specic oral hygiene
aids must be considered, often what the patient prefers to use
and is therefore more likely to use is the more effective option.
Adaptation of tools and cleaning techniques can be achieved
with time and effort.
KEY POINT 4
“How”: The actual techniques used to accomplish biolm
control will vary according to the specic needs of the patient
and can depend upon, for example: manual dexterity, gingival
architecture, physical access to the oral cavity, depth of
pockets, size of the tongue, frenal attachments.
The timing of the clinical intervention should be tailored
A to the individual and clinical need; patients are more likely to
appreciate the importance of their own home care if they see
the positive results of reduction in inammation, discomfort
and pocket depths without any initial clinical intervention.
KEY POINT 5
Patient-focused interventions that encourage self-management
of the patient’s own oral health are key to positive clinical
outcomes.
Toothbrushing
is may be manual or powered and should take into
account the patients’ abilities, preference and needs.
B
• Figure 4.1.1 (A) Using the patient’s sleeve to demonstrate a periodon- Manual
tal pocket; (B) using the same model to demonstrate gingival recession.
e plethora of manual toothbrushes now available can
serve to confound selection by their very number and diver-
gesturing in teaching complex mathematical theory con- sity in terms of design, size, shape and lament type, length
cluded that gestures clarify or provide conceptual infor- and density. Studies have failed to establish clinical supe-
mation that is not readily apparent in the accompanying riority for almost every characteristic examined (Frandsen
speech (Cook et al. 2013). e use of readily available 1985).
props such as your hands also has the benet of being Most modern manual toothbrushes use a nylon lament
completely free (Figure 4.1.1). type. Nylon, as a polymer with good chemical resistance,
Establishing a mutual cooperation and responsibility hard wearing and has antistatic properties (more hygienic),
between the patient and the clinician for the management is the lament type that predominates the toothbrush mar-
of periodontal diseases is critical to a successful clinical out- ket in the developed world. e laments of a toothbrush
come. e patience and time required to establish this for are usually arranged in roughly 40 tufts in three or four
both parties should not be underestimated. rows.
e “when”, “with what” and “how” part of the advice is e lament texture of choice should be soft, as the la-
more eectively received if tailored to the individual patient. ment diameter should be able to penetrate the gingival sul-
No single method, cleaning tool or cleaning programme for cus unlike the larger lament diameters of the hard lament
biolm control suits all. brushes. e harder laments can traumatise the soft tissues
and can contribute to tooth surface loss by abrasion. Soft
KEY POINT 2 laments should be recommended to all patients because
“When”: Oral hygiene measures can be undertaken at any they minimise soft tissue trauma and toothbrush abrasion
time of the day and should t in with the patient’s daily routine. while maximising biolm removal, particularly around the
It is the time spent cleaning and thoroughness rather than gingival margins and in the gingival crevice. A toothbrush
frequency of technique that is the most important factor with a small-to-medium head with soft, round-ended nylon
(Honkala etal. 1986).
laments is recommended.
• Figure 4.1.2 Modied Bass technique.
Features of a recommended toothbrush: accessible surfaces is key to this and any other technique
• Small head: small enough to be used eêectively every employed. Time spent on establishing an eective brush-
where in the mouth to ensure full quadrant coverage ing technique with the patient will have a positive impact
• Ergonomic handle: providing a comfortable stable grip on clinical outcome and should be established before any
for manoeuvring treatment intervention. Empowering the patient to reduce
• Nylon round-ended soft-to-medium ëlament. inammation with an eective oral hygiene regimen can
have a lasting impact on their motivation to improve their
Brushing Technique oral health. Moreover, the resolution of gingival inamma-
tion as a result of eective home care will reduce the dis-
Many brushing techniques have been advised over the years, comfort of any future clinical intervention – a motivator
but the basic requirements of an eective toothbrushing in itself.
technique are few:
e technique should: Powered Brushes
• Clean all accessible surfaces
• Be atraumatic to both hard and soft tissues Now well accepted as part of home care, electronic tooth
• Be simple and easy to learn and perform brushes have become a mainstay in oral hygiene support
• Be methodical in its application to ensure full mouth programmes. Systematic reviews of studies of powered
cleaning. toothbrushing using oscillating-rotating heads, compared
One of the most frequently recommended methods is the with manual toothbrushing in patients undergoing the
modied Bass (mini-scrub) (Figure 4.1.2). is technique initial phase of periodontal therapy, have found that sub-
aims to clean the gingival crevice, and so the brush head is jects using a power toothbrush during initial treatment had
held at 45 degrees to the axes of the teeth, with the end of the reduced supragingival plaque to lower levels and showed sta-
laments pointing into the gingival crevice. Gentle pressure tistically less bleeding on probing than subjects using a man-
is applied towards the gingiva and then the brush is moved ual toothbrush (Robinson etal. 2003). Timing mechanisms
in small backwards and forwards movements, so the la- alerting the user to the recommended 2-minute brushing
ments are forced gently into the crevice and embrasure sites. duration are also a feature of some powered brushes and
Working with the patient to determine the actual pattern serve to reinforce the 2-minute brushing time that studies
of cleaning in terms of covering all the quadrants and all the have indicated is required for optimal biolm control.
• Figure 4.1.3 Use of a powered (counter-rotational) brush. • Figure 4.1.4 Interdental woodsticks.
Patients need to be taught to use power toothbrushes, sucient interdental space. Bergenholtz etal. (1974) dem-
as the placement and angulation of the brush head is criti- onstrated the superiority of triangular wood points over
cal to eectiveness and is entirely dierent from a manual round or rectangular ones.
brushing technique – the oscillating laments provide the
biolm disruption on the tooth surface and into the gin-
Elastomeric Toothpicks
gival crevice, but the toothbrush head needs to be angled
and positioned correctly to maximise the oscillating action e modern version of the wooden toothpick is made from
(Figure 4.1.3). a plastic core and often covered with a silicon or rubber
cleaning surface. Usually conical in shape, these devices
Interdental Cleaning are available in a size range of small, medium and large;
they do not require specic sizing for individual patients
Although toothbrushing is regarded as the most important or sites. ey oer an eective option for supragingival
oral hygiene measure, the regular use of interdental clean- plaque control for patients that are new to interdental
ing aids is important for all adult patients but particularly cleaning.
for patients with periodontitis. For eective and atraumatic
interdental cleaning to be achieved, time and care should be
Floss
devoted to helping patients select the best product to t the
interdental site and the correct technique for its use (Slot In the UK, dental oss was rst recommended for inter-
etal. 2020). Because the interdental area is the site of great- dental cleaning at the end of the 1960s (Drum 1968). For
est plaque retention, gingival inammation usually starts patients with gingivitis, ossing is recognised as an eec-
in the interdental papilla and spreads around the gingival tive method for removing approximal plaque, with studies
margin. Interdental cleaning is therefore an essential part of reporting daily use of oss resulting in reduction of plaque
home-care regimens for all, but especially for patients with scores and gingivitis (Cronin & Dembling 1996). Floss-
periodontitis. Research has shown that periodontal patho- ing is not supported as an eective method for interdental
gens can re-establish within 4 to 8 weeks in the numbers cleaning for patients with diagnosed periodontal diseases
observed before professional debridement (Sbordone etal. undergoing supportive care (Slot etal. 2020).
1990), and therefore maintenance of regular self-performed Dental oss can be waxed or unwaxed, thread-like or
biolm disruption is crucial to a successful clinical outcome. tape, and impregnated with avouring or antibacterial and/
Given that periodontitis and gingivitis lesions are pre- or anti-caries products. Little evidence supports the superior
dominantly interdental and that the interdental sites are ecacy of any specic type of oss (Lamberts etal. 1982)
most frequently coated in plaque (Hugoson et al. 1986), – most of the evidence for the eectiveness of oss lies with
regular, thorough interdental cleaning is essential for pre- the benets of supragingival biolm disruption in patients
vention of disease. that have not been diagnosed with periodontal diseases.
Of the products specially designed for interdental clean- Implant oss is a specic type of oss that has a sti
ing, toothpicks have been available for the longest time threading end and includes a thicker/often spongey tex-
(Kashani 1998). A wide range of toothpick products, both tured section to clean under prostheses. is is often the
wooden and plastic, are currently available on the market only option that allows patients to clean around implant
(Figure 4.1.4). Toothpicks can only be used where there is abutments.
• Figure 4.1.5 Flossing technique. • Figure 4.1.7 Use of a oss holder.
• Figure 4.1.6 Use of a oss loop. • Figure 4.1.8 An interdental brush.
Flossing Techniques Interdental Brushes

To be eective, the oss needs to be adapted to the tooth e growth in the popularity of interdental brushes is largely
surface by gently wrapping the oss around the tooth once attributed to ease of use and eectiveness (Figure 4.1.8). If a
past the contact site. patient can use a pen, then they can usually manage to use
e anchorage method of wrapping the oss around the an interdental brush eectively. Biolm disruption in the
ngers to prevent slipping is useful for some (Figure 4.1.5), interdental area can be simply achieved using an interden-
but the method of tying the oss in a circle and using the tal brush, with studies reporting the superiority of biolm
oss between thumb and forenger on a continuous loop is removal over that of oss and interdental sticks (Waerhaug
a little easier (Figure 4.1.6). at said, ossing does not suit 1976, Christou etal. 1998, Worthington etal. 2019).
all patients as the dexterity required is sometimes beyond Available in an ever-increasing number of ISO standard
the capability or certainly the patience of many. sizes 0–8, it is important for the clinician to ensure that
Devices to make ossing a little easier do exist and vary the correct size of brush for the site is used. e maximum
in design and complexity, some of which allow the oss biolm disruption is achieved if the laments of the brush
to be used in the recommended way (Figure 4.1.7). Well- t the interdental space fully. Studies have shown that the
designed oss holders can make ossing easier and therefore regular use of interdental brushes can keep the proximal
more likely to be carried out regularly. surfaces and some subgingival surfaces free from biolm
to a depth of 2.5 mm below the gum margin (Waerhaug
KEY POINT 6 1976). Adapting the wire core of the brushes by bending
It is important to emphasise to patients that all interdental aids, allows the brushes to be used comfortably without catching
such as interdental brushes, oss and single-tufted brushes, can the soft tissue on the opposing side of the interdental space.
be highly effective but are best used following professional advice. Interdental cleaning should be carried out once a day before
toothbrushing. For patients undergoing supportive peri-

odontal care interdental brushes are recommended along-
side toothbrushing wherever anatomically possible.
Oral Irrigators
Oral irrigators or water ossers use water under pressure to
ush the interdental sites. Oral irrigators were rst designed
to be used supragingivally, applying water pressure to dis-
place and remove plaque, relying on pressure to irrigate sub-
gingival regions (Goyal 2012). Since then, various tips have
been designed that may be used subgingivally and several
manufacturers provide products that enable subgingival use.
Whilst these have gained in popularity, consensus for their
clinical ecacy is sparce, with only weak evidence suggest-
ing oral irrigators may reduce gingivitis at 1 month but not • Figure 4.1.9 A single-tufted brush being used for subgingival plaque
at 3 or 6 months (Worthington etal. 2019). control.
Subgingival Cleaning
anti-gingivitis eects, are useful adjuncts to self-performed
In deeper periodontal lesions, improved plaque control mechanical plaque removal (Stephen etal. 1990). Research
alone can have very little eect on the gingival condition, suggests that the combined use of a triclosan/copolymer
pocket depth or the subgingival ora (Corbett & Davies dentifrice may be eective in reducing or controlling gingi-
1993), and so for these patients, tailored oral hygiene edu- vitis in those areas demonstrating the most gingival inam-
cation and methods are often delivered in conjunction with mation. Typical ingredients of toothpastes are listed in Table
professional subgingival debridement. 4.1.2
In addition to interdental cleaning, the introduction of
single-tufted brushes to clean subgingivally can signicantly Mouth Rinses
enhance clinical outcome (Kinane 1998) (Figure 4.1.9).
e chemical control of plaque biolm can be aided by the
KEY POINT 7 use of mouth rinses. Mouth rinses were rst mass-produced
Periodontitis is predominantly an interdental lesion. in the late 1800s and are used for a number of purposes,
Toothbrushing alone cannot adequately disrupt the biolm in which include:
the interdental spaces, making the use of an interdental aid an • To clear the mouth of food debris
essential part of home care.
• As a carrier of antibacterial agents
• As a carrier of anti-caries agents
Adjunctive Antiseptic Agents • To reduce the activity of odour-producing organisms.
e simplest and possibly the most frequently used
Toothpastes and mouth rinses are widely accepted by mouth rinse is a warm, dilute saline solution recommended
patients as part of their daily oral hygiene routine. ere are for postsurgical care. However, the commercial availability
also several other chemical plaque control formulations that of a plethora of mouth rinses attests to public demand for a
have been marketed in recent years, although none have perceived easy option for home care. Excluding profession-
been shown to oer any signicant benet over the estab- ally recommended mouthwashes, clinicians need to make it
lished toothpastes and mouth rinses. clear that mouthwashes should only be used as an adjunct
to mechanical removal of the biolm. Many combinations
Dentifrices (Toothpastes) of formulations exist to achieve the objectives and are listed
in Table 4.1.3
Dentifrice was originally used to promote better oral
hygiene by chemical cleaning of the teeth. With advances Chlorhexidine
in product formulation, it has become a valuable vehicle for
delivering a variety of both health and cosmetic benets. Of the agents listed in Table 4.1.3, chlorhexidine gluconate
e widespread use of dentifrice has played a signicant role is by far the most eective agent against the oral biolm.
in the practice of good oral hygiene and promotion of good It is a bis-biguanide which has an immediate bactericidal
oral health (Balg & He 2005). Dentifrices have evolved to action and a prolonged bacteriostatic action due to adsorb-
provide a vehicle for delivering potential cosmetic, hygienic tion. Adsorbtion occurs because the chlorhexidine mole-
and therapeutic eects to the teeth and oral mucosa (Stamm cule is strongly positively charged (cationic) and binds to
2007). ese therapeutic agents, with anti-plaque and negatively charged (anionic) surfaces such as bacterial cell
TABLE
4.1.2 Typical ingredients in toothpastes and their actions
Excipient Use Note

Sodium uoride Anti-caries
Stannous uoride
Xylitol
Triclosan Anti-plaque
Zinc chloride
Sodium hexametaphosphate
Tetrapotassium pyrophosphate Anti-calculus
Hydrogen peroxide Whitening agent
Lichen Anti-adhesive/abrasive
Silica
Carbonates & phosphates
Carrageenan, xanthan gum Thickening agents
Strontium chloride Dentine hypersensitivity All work on the hydrodynamic theory of
Arginine dentine hypersensitivity and seek to
Potassium nitrate/citrate occlude, calcify or place a protective
Novamin seal over the dentinal tubules
Sodium lauryl sulphate Surfactant/frothing agent Should be avoided by patients with
recurrent aphthous ulceration as this
surfactant can irritate the mucosa
Sodium benzoate, methyl paraben, Preservative All have been linked with mucosal irritation
and ethyl paraben
walls, the oral mucosa and tooth surface. Chlorhexidine chlorhexidine. Such an occurrence is extremely rare but,
can disrupt bacterial cell walls within 20 seconds and then nevertheless, care should be taken before prescribing
enter the cell itself to attack the cytoplasmic membrane chlorhexidine to ensure that the patient’s medical history
and cause cell death. When chlorhexidine adsorbs to teeth is reviewed and an enquiry made about possible sensitivity
and the periodontal tissues, it prevents microorganisms to chlorhexidine.
from attaching and inhibits the development of biolm. It
remains active on oral surfaces for 12 hours or more (Bri- KEY POINT 8
ner etal. 1986) and has been shown to be highly eective Chemical agents can be a useful adjunct to, but are not a
in reducing biolm accumulation and gingivitis (Jenkins replacement for, mechanical biolm control.
etal. 1993).
Chlorhexidine gluconate is produced in a variety of Conclusions
forms. It is most eective as a mouth rinse containing
0.20% or 0.12% chlorhexidine. One of the advantages of Successful treatment of periodontal diseases requires the
the mouth rinse is that it reaches areas of the mouth (interactive involvement of the patient at the outset of treatment.
dental sites and gingival crevices) which are more likely to A collaborative approach to treatment planning and long-
be missed when toothbrushing. Table 4.1.3 sets out further term supportive care fosters ownership and empowerment
uses of chlorhexidine gluconate and its disadvantages. It in the patient. e “when”, “what with” and “how” aspects
can also be used in a gel and as chlorohexidine-impreg- of self-performed biolm control should be patient-led
nated chips, which are small enough to be placed in peri- and professionally supported. e individual patient’s oral
odontal pockets where the chlorhexidine leaches out (see hygiene regimen should be monitored, modied and devel-
Chapter 5.3). oped by both patient and dental professional in what has to
In the UK, the Medicines and Healthcare Products be a mutually responsible partnership if successful clinical
Regulatory Agency (MHRA) has issued a patient safety outcomes are to be achieved.
alert on the risk of anaphylactic reactions from the use Multiple choice questions on the contents of this chapter
of medical devices and medicinal products containing are available online at Elsevier eBooks+
TABLE
4.1.3 Common mouthwash ingredients
Excipient Mode of action Indications for use Notes/disadvantages

0.12 or 0.2% Chlorhexidine Antibacterial Plaque inhibition; gingivitis; Supercial discoloration of tongue,
gluconate Cationic maintenance of oral teeth and tooth-coloured
hygiene; post-periodontal restorations, usually reversible;
surgery or treatment; transient taste disturbances and
aphthous ulceration; oral burning sensation of tongue on
Candida initial use
Less common: oral desquamation;
parotid swelling; skin reactions
Extremely rare: generalised allergic
reactions, hypersensitivity and
anaphylaxis
Triclosan Antibacterial Plaque inhibition; gingivitis; Has had some negative reports
Non-ionic maintenance of oral regarding its carcinogenic
hygiene potential in the presence of
chlorine and heat. Although there
is some evidence of hormone
damage to the immune system,

the benets for the inclusion in
oral hygiene products may well
outweigh the potential risk
Cetylpyridinium chloride Antibacterial Plaque inhibition; gingivitis Can cause supercial staining
(CPC) Cationic quaternary
ammonium
Phenolic compounds Antibacterial Gingivitis when used
in conjunction with
toothbrushing
Hydrogen peroxide Antibacterial Gingivitis; aphthous
Oxygenating agent ulceration; pericoronitis
Zinc gluconates Antibacterial Halitosis
Inhibits volatile sulphur
compound production
Fluorides Anti-caries High caries risk used Not suitable for under age 7 –
in conjunction with ingestion risk for children not able
toothbrushing to spit out
Alcohol Enhance antibacterial Suggested links with mouth cancer
activity, stabiliser for due to drying/chelating effects of
active ingredients, e.g. mucosa has led to an increased
essential oils number of alcohol-free products
Humectants Prevent drying out
Surfactant To keep ingredients in
solution
Flavourings Enhance taste
Colouring agents Point of difference for
sales
Water Vehicle for delivery
Preservatives
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4.2
Clinical Imaging in
Patient Assessment and
Motivation
UL P E E DA R B A R
CHAPTER OUTLINE
Introduction 2. Clinical Photography
Types of Imaging Systems 3. Videos
4. Digital Scanning
Factors to Consider
Clinical Imaging to Enhance Adherence
1. Radiography
Conventional Radiography
Computerised Tomography

Clinical imaging, which includes both photographic and radiographic techniques, can be used for diagnostic, educational and motivational
purposes as well as patient involvement in making decisions about their treatment. Patient-centred decision-making is the cornerstone of
managing patients with chronic diseases, including periodontal diseases, especially as behavioural change is understood to be essential in
achieving successful outcomes when treating such conditions. This chapter provides the reader with an overview of the dierent types of
imaging techniques that are available and how these can be used to help to assess periodontal conditions, to aid communication with the
patient and to improve patient compliance and motivation, as well as driving patient-centred decision-making.
• Appreciate the various systems for recording diòerent types • Types of imaging systems
of images • Applications of imaging in patient management and
• Describe how clinical imaging can be used to improve decision-making
patient understanding, motivation and adherence • Improving patient adherence and engagement using clinical
• Understand the need for consent in relation to clinical imaging
imaging • Consent for clinical imaging.
• Explain how imaging can be used to drive patient-centred care.
Introduction of clinical imaging helps patients gain a better understand-

ing of their condition and gives them the opportunity to
e successful management of periodontal diseases is largely initiate behaviour change, which is essential if treatment is
dependent on patient involvement. e role that patients to be successful.
play in the management of their conditions is crucial to
achieving a positive treatment outcome. is is particularly KEY POINT 1
true for chronic periodontal diseases for which the bacterial Successful periodontal treatment outcomes are dependent
biolm is the key initiating factor. e role of the patient in on patient involvement and acceptance of their role in disease
the management of chronic periodontitis is well established management.
(Sanz & Teughels 2008, Renz etal. 2007). Successful treat-
ment outcomes, avoiding tooth loss, are only possible with While a clinical assessment and discussion can enable
the full involvement and cooperation of the patient. e use patients to understand the disease process, it is well known
182
CHAPTER 4.2 Clinical Imaging in Patient Assessment and Motivation 183
that visual representation of a problem leads to improved

compliance and understanding (Houts et al. 2006). e Patient
visualisation of a condition and the possible outcomes of
treatment are often communicated to a patient more eec-
tively and quickly using images rather than words, par-
Treatment plan History
ticularly when before and after images are shared. Clinical
imaging can be used to explain the supporting structures
of the teeth and gums, and this enables the clinician to
discuss issues more eectively with the patient, thereby
empowering a better understanding and encouraging
improved adherence. is joint approach between patient Diagnosis Examination
and clinician enables more eective disease management
by oering the patient the opportunity to lead the con-
versation about their disease. In terms of diagnosis it is Investigations
important that clinical imaging systems are used in con- Imaging tools
junction with the clinical assessment and should never be • Figure 4.2.1 The place for imaging in patient management.
used in isolation to arrive at diagnoses (Figure 4.2.1). As
the use of video-based clinics has increased, clinical imag-
ing provides the opportunity to share information on a
virtual platform. Clinical imaging systems have the follow-
ing key benets:
• add value to the clinical assessment made by the clinician
• enable sharing of information giving more clarity and
reducing the risk of ambiguity
• underpin and strengthen the information collected as
part of the history and clinical examination
• provide additional information about the condition to
both the clinician and the patient, leading to improved
understanding and treatment outcomes
• provide documented evidence of the condition, before,
during and after treatment in the event of medico-legal A
challenge.
Imaging systems fall into two categories:
• invisible light imaging such as radiographic techniques
• visible light imaging which includes photographs and
videos.
Both types of systems have been used extensively in med-
icine; radiography has been an essential diagnostic tool since
its introduction in the early 20th century. Photography has
also been widely used in dentistry both to monitor the prog-
ress of treatment and for educational purposes. e advent B
of digital technology in both photography and radiography
has greatly broadened the scope of what can be achieved
and how patients can be involved in decision-making. Most
dental practices predominantly use digital technology as
essential tools to aid with diagnosis, as adjuncts to history
taking and physical examination and for patient engage-
ment and communication. Clinical imaging thus allows cli-
nicians to improve patient management in a variety of ways
(Figure 4.2.2), such as:
• to aid clinical assessment
• to improve patient understanding by allowing visualisa
tion of the disease C
• to improve patient motivation and adherence
• Figure 4.2.2 Images of a patient with initially poor plaque control,
• to help monitor the treatment response before and after treatment. (A) Clinical presentation; (B) radiographic
• to allow patients to see the progress and outcome of their presentation; (C) clinical response to improved oral hygiene and
treatment. treatment.
Digital photography can be particularly useful in the

management of periodontal diseases; unlike other oral con-
ditions, successful treatment outcomes are highly depen-
dent on patients’ adherence to professional advice and their
subsequent behavioural change (see Chapter 4.3). Clinical
imaging is a powerful tool in this respect. Most importantly,
untreated periodontal patients tend to display gingival
inammation which can be recorded photographically; as
inammation reduces with improved plaque control and
debridement, changes can be captured on photographs and
shared with the patient, allowing patients to engage more A
proactively in their disease management. In this way imag-
ing can be used to demonstrate to patients the eects of
improved oral hygiene on gingival inammation in the
absence of professional intervention (Figure 4.2.3), thus
emphasising the importance of self-care.
KEY POINT 2
Early understanding of periodontal diseases improves patient
compliance and ownership of the problem.
B
Several studies have reported on the strategic role patient
compliance plays in the management of patients with • Figure 4.2.3 (A) Gingival inammation in a patient with poor
oral hygiene. (B) Reduction in the inammation after oral hygiene
chronic conditions such as periodontitis (Wilson 1987,
improvement.
Soolari 2002, Ng etal. 2011, Costa etal. 2012). While writ-
ten information is valuable, imaging techniques improve
patient engagement by providing the patient with a visual
awareness of their problems both before and after treat-
ment, thus providing a means of involving patients in their
periodontal management (Figure 4.2.4).
Types of Imaging Systems

e imaging systems most often used as educational tools
in dentistry are:
1. Radiography
2. Clinical photography
3. Videos
4. Digital Scanning
Other systems, such as ultrasound and magnetic reso- • Figure 4.2.4 Patient with poor compliance. The image shows the
nance imaging, have more application in other branches severity of breakdown which can be shared with the patient during the
explanation of the problem.
of dentistry, such as oral and maxillofacial surgery and oral
medicine, and are rarely indicated or used in general den-
tistry. Laser Doppler imagining (LDI) has been used as a • What can I use to clarify the condition to the patient in
tool for monitoring blood ow in gingival tissues in research the simplest way?
studies but has only limited use in dentistry (Figure 4.2.5). • How will I ensure that the patient has understood what I
am trying to explain?
Factors to Consider Radiographs, photographs and videos can be used alone
or in combination to educate and inform the patient and
When clinical imaging is used as an educational tool, it is sometimes together with written information (such as leaf-
important to ensure that the appropriate imaging tools are lets). is visual information can also be used in combi-
used. Factors to consider include: nation with periodontal charts, which record the bleeding
• What type of disease does this patient have? scores and/or pocket depths, to enhance patients’ under
• Does this patient understand that he/she has a problem? standing of their condition. With digital technology, images
• What do I want to do for this patient? of possible treatment outcomes can be created to further
• What am I trying to explain to the patient? enhance patient understanding and to improve patient
• What do I want the patient to understand? ownership of their disease(s).
Imaging
techniques
Invisible light Visible light

imaging imaging
Others
(magnetic resonance imaging, Radiography Photography Videos
ultrasound, laser doppler)
• Figure 4.2.5 Types of imaging techniques.
1. Radiography
• Conventional radiographs (X-rays)
• Computerised tomography (CT scans).
Conventional Radiography
A. Analogue Radiographs
Conventional radiography aids diagnosis by displaying the
underlying bone support for the teeth and, as previously
mentioned, can also be used as a means of explaining dis-
ease processes to patients. In periodontology radiographic
images are used to assess bone loss and, in conjunction with
clinical data, to assess levels of disease and to aid diagno-
sis. e choice of radiographs to be taken will depend on A
the type of information needed; usually for periodontal
assessment (when bone levels need to be determined), long
cone periapical views are used. However, for patients with
minimal bone loss, vertical bitewings can be an alternative,
exposing the patient to less ionising radiation. Extra-oral
views such as orthopantomogram (OPT) can be used for
patients who cannot tolerate intra-oral lms but, although
such views provide an overview of the bone levels and are
often useful as screening tools, the denition of the image
can be inferior to the intra-oral view.
Radiography systems based on wet lm processing are
simple to use but they have the disadvantages of being slow
and prone to operator errors during processing (Figure
4.2.6). e images produced (as lms) also take up physical
storage space. B
• Figure 4.2.6 (A) Conventional wet lm long cone periapical radio-
B. Digital Radiographs graph showing elongation of the image due to incorrect positioning of
Modern radiography systems are based on digital technol- the lm. (B) Image of a correctly positioned and processed lm.
ogy and have largely superseded wet lm processing. e
main advantages of these are: • Can be more easily shared with other clinicians and
• No chemicals required patients.
• Real-time applications e main advantages and disadvantages of analogue and
• Speed of image production digital radiographs are shown in Table 4.2.1
• Ease of storage Digital radiographs are taken using a digital sensor which
• Digital image enhancement and manipulation (bright captures the image of the bone and the teeth instead of a
ness, contrast, etc.) lm and, once captured, the image is digitally transferred.
TABLE Dierences between analogue and digital

4.2.1 images
Conventional radiography
using wet films Digital radiography
More prone to processing Because of image
errors manipulation using
sensors this aspect is
eliminated
Patients nd these relatively
easy to tolerate in their be bulky
mouth
Physical handling of lms Images can be shared
necessary so can be with others easily A
cumbersome
Images are not available
immediately immediately
Storage space needed Physical storage space
not needed
Relatively low setup costs Setup costs can be high
depending on system
selected
Manipulation of images not Digital manipulation of
possible images (contrast,
brightness, etc.)
Limited training needs of staff Training of staff needed
B
e image can be enhanced using digital processing tech- • Figure 4.2.7 (A) CMOS sensor connected directly to the computer to
niques which allow manipulation of the image. Digital sen- produce the radiographic image. Note the size of the sensor. (B) PSP
sors may be direct or indirect types. being processed in a digital scanner. Note the size of the lm, which is
similar to a wet lm.
Direct sensors are solid state sensors which are either charged
coupled devices (CCD) or complementary metal oxide semi-
conductors (CMOS) (Figure 4.2.7A). Both contain silicon Computerised Tomography
crystals which covert photons to electrons, with the main Computerised tomography (CT) is an imaging technique
dierence being how the pixel conversion takes place. e that produces both two- and three-dimensional cross-sec-
CMOS devices convert at each pixel level, whereas with a tional images of an object from a at radiographic image.
CCD the pixel charges are transferred to a common output e internal structure of the object, such as the shape and
source. Both sensors tend to be thicker than indirect types severity of a bony defect, can be visualised to allow more
and some have cable connections which result in a thicker precise and detailed assessment. However, because of the
sensor. With these systems the images generated digitally are high radiation dose required, conventional CT has only
transmitted directly from the detector to the computer. limited use in periodontology. e implementation of the
Indirect sensors use photo-stimulated storage phosphor new volume-based cone beam CT scan (CBCT) (Figure
(PSP) plates as the sensors. ese are extremely thin and 4.2.9) has enabled the radiation dosages to be reduced sig-
are similar in size to conventional wet-processed intra-oral nicantly, thus making this tool more valuable in the plan-
lms. Once the plates have been exposed, they are processed ning and assessment of complex bone defects. ese images
in a digital scanner (see Figure 4.2.7B), producing a high- can be taken as sectional images exposing only the area in
quality digital image (Figure 4.2.8). Patients tend to toler- question, thus rendering their application to periodontol-
ate this type of sensor better because of the reduced bulk. ogy more appropriate (Figure 4.2.10). e images can be
e rst-generation digital sensors performed suboptimally manipulated to show the bone and other structures in three
compared to conventional lm. However, with improving dimensions, which aids both diagnosis and treatment plan-
detector technology, digital imaging is surpassing lm in ning. In the periodontally compromised patient, CBCT
terms of contrast and resolution. Images generated using aids in the assessment of intra-bony defects and furcation
the PSP detect the X-rays and capture the image, which is involvements (Misch et al. 2006). e ability to manipu-
then scanned into a PSP scanner that passes the image to late such images and show patients bone defects around
the computer through a USB cable or network connection. teeth and what could happen with treatment is useful in
B C
• Figure 4.2.8 (A) Image produced using the PSP system. The ability to manipulate the images (B, C)
enables the defects to be looked at with greater clarity and helps to explain disease to patients.
explaining the complex aetiology and treatment of such

defects. It is important to remember that CBCT should
only be used where the benets of the investigation supple-
ment the information already gathered. CBCT scans are
also useful when discussing implant treatment plans with
patients (see Chapter 7.3). e clinician should be aware of
the guidelines on the use of CBCT published by the Euro-
pean commission in 2012. Because of the lack of a robust
evidence base, the Faculty of General Dental Practitioners
claim that “CBCT is not indicated as a routine method of
imaging periodontal bone support” (2018).
2. Clinical Photography
Photographs enable the clinical manifestations of disease
to be recorded at any point during the assessment and
treatment of the disease. ey are a vital tool for patient
education, and a recent questionnaire-based study (Morse
et al. 2010) showed that 84% of the respondents used
photographs for treatment planning and 75% for patient
instruction and motivation; 55.1% reported that they
found photographs useful when giving patients instructions
and improving their motivation and 56.2% reported their
usefulness for medico-legal purposes. Prior to the use of
• Figure 4.2.9 Cone beam CT scanner. clinical photographs, it was common for clinicians to draw
B
• Figure 4.2.10 CBCT images showing the extent of information that can be seen from all angles. This
information makes it easier for patients to understand their problems.
diagrams to explain to patients aspects of their condition Clinical photography is an invaluable tool for commu-
which could not be explained verbally. Today, clinical pho- nicating information to patients and also for documenta-
tography has replaced this as a means of disease visualisation of the clinical presentation of a patient’s condition. It
tion, using images of the patient’s own condition. However, can assist in documenting the progressive changes in the
it is important to remember that: patient’s condition during a course of treatment and can be
• Photographs form part of the patient’s clinical record used to communicate to the patient changes in the condi-
• ɨe patient must have given their consent for the pho tion, especially if there are issues with compliance and moti-
tographs to be taken. An example of a consent form is vation. is visual involvement gives the patient the chance
shown in Figure 4.2.11 to directly observe what is happening in their mouth and
• Consent should include a clear explanation of why the allows the patient to become better aware of the progress
photographs are being taken, what they will be used for (or otherwise) of their treatment. In the past, photographs
and where they will be stored were taken with lms that had to be sent o to be processed,
• If the photographs are to be used for publication, the thus incurring an additional cost and inconvenience as the
patient must be informed about this, and a separate con- images could not be used immediately as part of the dis-
sent will be needed cussion. However, clinical photographs are currently taken
• If the photographs are to be used for research, the patient with either a digital camera or an intra-oral camera and are
must have consented to this as part of the process for immediately available and can be shown to the patient.
enrolling into the research project A series of photographs will help convey messages where
• If the patient is going to be identiëable in the photo complexities of advanced treatments are often dicult to
graph, they must be informed of this, and appropriate describe. Patients can thus get involved in making decisions
signed release of the photograph obtained. about the management of the problems, thereby fostering
Consent/waiver for clinical photography
Patient name: Date of birth:
I consent that photographic images (including of x-rays, models and videos) of me

(or under 16 child of which I am parent or legal guardian) may be taken and used
in perpetuity for the following purpose(s) for which I understand that it may not be
possible for me to subsequently withdraw this consent:
Level 3 (open publication)

(a) Publication in a professional journal or textbook, and/or as part of a lecture,
display and/or information/marketing leaflet and:
(b) Publication on open access website (open access means making available and
communicating to anyone worldwide, including but not limited to clinical
professionals). The publication on open access websites may, but not necessarily,
form part of a course where users will download content onto any device for their
personal and non-commercial use.
Level 2 (Restricted educational use)

Clinical teaching and/or research, and shown only to appropriate clinical
staff and students and/or displayed for use by staff and students following
a course of study on a restricted access educational institutional website.
Level 1 (Confidential record only)

Storage as part of confidential patient dental records only.
Level of consent Level 3 Level 2 Level 1
Please tick
Image types Images including face/eyes Images except face/eyes
Please tick
I confirm that I am over 16 years of age
I confirm that I am the parent/legal guardian of
(delete as applicable)
Signature: Date:
• Figure 4.2.11 An example of a photographic consent form.
patient-centred decision-making. e use of clinical pho- systems enable the information about the condition and the
tographs along with the radiological images helps the clini- clinical ndings to be shared with the patient as the assess-
cian describe diagnosis and treatment with greater clarity. ment is taking place.
Generic photographs showing the disease at the beginning Digital camera systems can vary from simple compact dig-
and after treatment are also useful tools in explaining treat- ital cameras to more complex and expensive digital single
ment proposals and possible treatment outcomes (such as lens reex (DSLR) systems with macro lens and ring ash
interdental recession). (Figure 4.2.13). Photographs taken with these systems also
ere are several dierent camera systems that are avail- allow patient communication but only after the images have
able and the choice of which to use is largely clinician driven. been uploaded to a computer.
Intra-oral cameras are essentially small television cameras e images taken, irrespective of the camera used, must
that can be connected to a hand-held device or a computer be clear and relevant, with the focus being largely on the
(Figure 4.2.12). Images are shown on the computer screen area of interest. e photographs should be standardised
in “real time” but can also be captured and stored. ese for accuracy and comparison and dated. Depending on
• Figure 4.2.12 Intra-oral camera system. These devices are small and • Figure 4.2.13 Digital SLR camera with a ring ash.
enable the patient to visualise their mouth as the examination is taking
place.
3. Videos
the sequence, the photographs can be used at the outset Videos may form part of the clinical photographic record
to communicate the issues with the patient and engage and oer the patient a real-time presentation of the condi-
them in treatment decision-making. Photographs taken tions in their mouth. Most digital camera equipment have a
during treatment will help monitor how well the situ- video-recording facility. Videos can be used to show patients
ation is improving and where there are ongoing chal- treatment as it is being carried out, or they can be shown
lenges with motivation and compliance. Monitoring recordings of procedures that they may be considering. is
photographs can be used to highlight any issues with can help the patient understand what is being proposed and
the patient, enabling the patient to better understand also gives the patient the opportunity to ask questions about
how and why the treatment may be compromised. For procedures. Videos may be used:
the photographs to be eective tools for patient educa- • To provide a realistic overview of what the patient may
tion, they must be precise and clear and also demonstrate expect
the clinical problems in question clearly. In addition to • To provide a visual representation of a procedure that
patient education, clinical photographs also have several may otherwise be dicult to describe
other uses including: • To give the patient an opportunity to ask questions about
• Monitoring the progression of disease proposed procedures
• Providing evidence to the patient of the need for certain • To demonstrate self-care such as oral hygiene.
treatments Videos can also be a good resource to use if there are
• Before and after treatment eêects postoperative complications, as they help provide an easier
• Assessment of treatment outcomes means of giving an explanation and showing the patient
• Medico-legal purposes why the complication has occurred.
• Communication with others, e.g. laboratory technicians,
clinicians
4. Digital Scanning
• Enhancing patient referrals
• Long-term monitoring of oral status (useful in patients As the digital era has evolved, dierent scanning systems
with suboptimal motivation and adherence) enable direct images to be captured and manipulated to
• Providing evidence of treatment outcomes, especially in construct restorations. ese systems can provide a means
patients who have inconsistent oral hygiene. of explaining anticipated treatment outcomes to patients.
e types of view will depend on the individual patient Furthermore, study casts that have been taken using con-
needs. e following views are standard views that should ventional impressions can also be scanned, converted
be taken at the start of treatment to form part of the clinical into digital formats and used for discussion with patients.
record (Figure 4.2.14): Depending on the software programmes, the images can be
• Smiling and at-rest view manipulated to show patients the end point of treatment,
• Intra-oral view with the teeth in occlusion and if clinical photographs are also scanned, the side-by-
• Right and left buccal views side representation gives the patient a good opportunity of
• Occlusal views of the upper and lower arches seeing the changes that can be achieved. Where the patient
• Any other views that are appropriate to the care of the is expecting a change in the appearance or where tooth posi-
patient and can include extra-oral views. tions are to be modied, digital “wax-ups” have become a
A B
C D E
F G
• Figure 4.2.14 Standard clinical views.
• Figure 4.2.15 A digital “wax-up” of proposed treatment to upper and lower anterior teeth, with the pre-
operative situation on the right.
powerful way of explaining to the patient the changes that own periodontal health and treatment planning. Patient
can be achieved (see Figure 4.2.15). adherence to professional advice is the cornerstone of
long-term success in periodontal therapy, and images can
Clinical Imaging to Enhance Adherence be used to enhance this adherence, particularly when the
patient can see that their eorts at home are having a posi-
Clinical images, such as pictures, photographs and videos, tive eect on their oral condition. Before and after images
allow the clinician to convey information more eectively can be invaluable in this respect (see Figure 4.2.3) and help
to patients about disease processes and treatment propos- patients appreciate the importance of home care. Untreated
als. ese tools are useful to help ensure that patients are periodontal diseases often present as visible gingival inam-
fully engaged in the decision-making process about their mation, which can be imaged, and changes in inammatory
status can be recorded as treatment progresses. is can be attention, comprehension, recall and adherence. Patient Educ
shown to the patient and presents the clinician with a pow- Couns. 2006;61:173–190.
erful motivational tool thus optimising patient compliance. Morse GA, Haque MS, Sharland MR, Burke FJT. e use of clini-
Written information can be useful in this respect, but imag- cal photography by UK general dental practitioners. Br Dent J.
2010;208:E1.
ing has far more impact, particularly when the images are of
Misch KA, Yi ES, Sarment DP. Accuracy of cone beam computerised
the patient themselves. tomography for periodontal defect measurements. J Periodontol.
Multiple choice questions on the contents of this chapter 2006;77:1261–1266.
are available online at Elsevier eBooks+. Ng MC, Ong MM, Lim LP, Koh CG, Chan YH. Tooth loss in compli-
ant and non-compliant periodontally treated patients: 7 years after
References active periodontal therapy. J Clin Periodontol. 2011;38:499–508.
Renz A, Ide M, Newton T, Robinson P, Smith D. Psychological
Costa FO, Cota LO, Lages EJ, Lima Oliveira AP, Cortelli SC, Cor- interventions to improve adherence to oral hygiene instructions
telli JR, et al. Periodontal risk assessment model in a sample of in adults with periodontal diseases. Cochrane Database Syst Rev.
regular and irregular compliers under maintenance therapy: a 3 2007;2:CD005097.
year prospective study. J Periodontol. 2012;83:292–300. Sanz M, Teughels W. Innovations in non-surgical periodontal ther-
European Commission. 2012. Radiation protection 172. Cone Beam apy: Consensus report of the 6th European Workshop on Peri-
CT for Dental and Maxillofacial Radiology: evidence-based guide- odontology. Group A of European Workshop on Periodontology.
lines; Luxembourg; European commission: 2012. Accessed from J Clin Periodontol. 2008;35(Suppl. 8):3–7.
https://ec.europa.eu/energy/sites/ener/ëles/documents/172. Soolari A. Compliance and its role in successful treatment of an
Faculty of General Dental Practitioners. Selection Criteria for Dental advanced periodontal case: review of the literature and a case
Radiography 2018; 2018. Recommendation 5.2. report. Quintessence Int (Berlin). 2002;33:389–396.
Houts PS, Doak C, Matthew LG, Loscalzo A. e role of pictures Wilson TG. Compliance. A review of the literature with possible
in improving health communication: a review of research on applications to periodontics. J Periodontol. 1987;58:706–714.
4.3
Patient Adherence
PH I L I P OW E R
CHAPTER OUTLINE
Importance of Adherence in Periodontal Care MI Step 3: Respond to the Patient
European Federation of Periodontology S3-Level Clinical Practice Adherence to Oral Hygiene and Other Advice
Guideline 2020 Oral Hygiene Advice
Stepwise Approach to the Management of Stages 1–3 Periodontitis Other Advice
Improving Adherence and Aecting Behaviour Change Smoking Cessation Advice
Diet Advice
Motivational Interviewing
MI Step 1: Develop a “Guiding” Style Assessing Adherence in Practice
MI Step 2: Elicit Motivation to Change Conclusion

A high standard of biolm control and self-care are essential for achieving and maintaining periodontal health. This chapter will describe the
principles of improving patients’ adherence to healthcare advice and highlight some of the diculties that are often encountered when the
clinician attempts to motivate patients to clean to a higher standard and to inuence some of the lifestyle habits that may be contributing
to their levels of periodontal breakdown. Strategies will be presented for overcoming these diculties and practical advice will be given for
improving patients’ levels of biolm and risk-factor control and assessing patients’ response to this advice.
By the end of the chapter the reader should: • Be able to motivate patients to improve their levels of self-
• Understand the need for a high level of adherence in care.
periodontal patients The chapter covers the following topics:
• Appreciate why patients can be resistant to healthcare • Importance of adherence in periodontal care
advice • Improving adherence and aòecting behaviour change
• Understand the principles of the stepwise approach to • Adherence to oral hygiene and other advice
periodontal therapy • Assessing adherence in practice.
• Be able to provide plaque control and other advice more
eòectively
Importance of Adherence in infers a collaboration between clinician and patient, in

Periodontal Care which patients develop an understanding of their condition
and the treatments required so that the patient has a collab-
Adherence to professional advice, often referred to as com- orative involvement with the clinician and reaches “concor-
pliance, has become an increasingly important feature dance” in consultations (Mullen 1997). Treatment failure
of many aspects of healthcare, as an increasing volume of is often the result of poor adherence to healthcare advice.
research has shown that the behaviour of the individual can One only has to think of heart disease and the eect of life-
have a profound eect on a range of medical conditions. style and diet on this condition to realise the importance
While a high standard of patient compliance is essential for of patient behaviour in disease management. e same is
successful periodontal therapy, absolute compliance is rare; equally true of periodontitis; there is abundant evidence
one study (Umaki etal. 2012) showed that only 32% com- that in periodontally susceptible individuals, a patient’s
pliance was achieved on average. As far as terminology is periodontal condition is aected by their own behaviour,
concerned, the term “adherence” is preferable to “compli- in particular the patient’s ability to carry out daily oral
ance” – the traditional term “compliance” denotes obedi- hygiene to a high standard; the importance of the patient’s
ence, “following doctor’s orders” – but the term “adherence” oral hygiene in periodontitis management was shown in
193
more susceptible the patient the higher their level of biolm

disruption needs to be to control disease. Failure to main-
tain a suciently high standard of plaque control results in
treatment failure in the long term (Axelsson & Lindhe 1981,
Ramord etal. 1982, Listgarten etal. 1989, Sbordone etal.
1990, Rosen etal. 1999). It is therefore essential in periodon-
tal management to adopt eective interventions to improve
patients’ adherence to oral hygiene advice (Wilson 1996).
A consensus report of the 5th European Workshop in Peri-
odontology (2005) concluded that removal of the bacterial
biolm by the patient and smoking cessation were the two
most important subject-based measures to be established in
the management of periodontitis (Ramseier 2005).
A
European Federation of Periodontology
S3-Level Clinical Practice Guideline 2020
Following the introduction of the new classication sys-
tem for periodontal and peri-implant diseases by the World
Workshop in 2017 (see Chapter 2.1 for full details), the
European Federation of Periodontology (EFP) published S3
clinical guidelines for the treatment of stages 1–3 periodon-
titis (Sanz etal. 2020), which was mapped to the new clas-
sication system. e EFP guideline combined assessment
of 15 systematic reviews with a moderated consensus process
of a group of representative stakeholders to arrive at a set of
recommendations for the treatment of stages 1–3 periodon-
titis. e term S3 refers to the highest level (or step) of guide-
B line development (see Table 4.3.1). When developing an S3
guideline the strength of consensus agreement is reported
• Figure 4.3.1 (A) A patient on presentation. (B) Patient after 1 month of (see Table 4.3.2) and a formal “evidence-to-decision” process
oral hygiene alone with no professional intervention.
is followed to arrive at a clinical recommendation (see Table
a randomised controlled trial by Preus et al. (2019). is 4.3.3). Clinical recommendations (CRs) may be evidence
study investigated the eect of a strict 3-month oral hygiene based or consensus based or both (see Figures 4.3.3–4.3.5
phase on plaque, bleeding on probing and pocket depth and for examples of CRs). For further details on the development
found that these key periodontal parameters were reduced of CRs the reader is referred to West etal. (2021) and Keb-
(by oral hygiene alone) to such an extent that therapy plan- schull & Chapple (2020). e new EFP guideline thus estab-
ning was aected. An example of how patient behaviour lished an evidence- and consensus-based stepwise approach
can have such profound eects is shown in Figure 4.3.1. In to the management of periodontitis patients (Figure 4.3.2
addition patient behaviour with respect to other risk fac- and Appendix 3), central to which was patient adherence
tors in periodontal diseases (diet, obesity, exercise, smoking, to advice on oral hygiene and risk-factor control. e Brit-
stress and diabetic status) can also have profound eects on ish Society of Periodontology and Implant Dentistry (BSP)
periodontal management. subsequently developed and published (West etal. 2021) a
UK version of this guideline using a formal process known
KEY POINT 1 as the Grade Adolopment framework (readers are referred to
Treatment failure is often the result of poor adherence to Sanz etal. [2020] and West etal. [2021] for details of this
healthcare advice. process). e BSP UK Clinical Practice Guidelines for the
Treatment of Periodontal Diseases, based on the EFP guide-
It is appropriate to try to aect behavioural change in lines, can be found at Appendix 4
patients who have periodontitis to maximise the chances
of treatment success. While advice to reduce lifestyle risk Stepwise Approach to the Management of
factors such as smoking, poor diet and lack of exercise are Stages 1–3 Periodontitis
important, treatment of periodontitis is still based largely on
reduction of the bacterial load through self-care, mainly in e main principle of the stepwise approach to periodontal
the form of eective oral hygiene. Some patients are more management (Figure 4.3.2) is that treatment is carried out
susceptible to periodontitis than others (see Chapter 1.4); the in steps and that progression to the next step does not take
CHAPTER 4.3 Patient Adherence 195
TABLE
4.3.1 Development of Clinical Guidelines
Level Guideline description Characteristics

S3 Evidence and consensus Systematic review, selection and analysis of evidence, grading of evidence
based and
representative guideline group including stakeholders from other disciplines,
moderated consensus process
S2e Evidence based Systematic review, selection and analysis of evidence, grading of evidence
S2c Consensus based Representative guideline group including stakeholders from other disciplines,
moderated consensus process
S1 Recommendation of a Informal process to reach consensus
panel of experts
TABLE TABLE
4.3.2 Strength of Consensus 4.3.3 Grades of Recommendation
Necessary agreement Recommendation

Strength of (excluding abstentions due to Grade level Wording
consensus potential conflicts of interest)
Unanimous Agreement of 100% of recommend not to ( )
consensus participants
B Recommendation We suggest ( ) / we
Strong consensus Agreement of >95% of suggest not to ( )
participants
O Open May be considered ( )
Consensus Agreement of 75–95% of
participants
Simple majority Agreement of 50–74% of
participants KEY POINT 2
No consensus Agreement of <50% of Step 1 of the stepwise approach involves:
participants 1. Supragingival biolm control (OHI)
• Adjunctive therapies to control inammation
• PMPR
• Risk-factor control (e.g. smoking cessation, improved
place until the requirements of the current step have been diabetes control, exercise, dietary control and weight loss)
met; it can be seen that patient adherence is a key compo-
nent of step 1, along with professional mechanical plaque
reduction (PMPR). is approach ensures that the foun- Improving Adherence and Affecting
dations for an optimal treatment response are in place at Behaviour Change
the start of patient management. PMPR involves not just
professional plaque removal and removal of plaque reten- ere are numerous barriers to achieving eective adher-
tion factors but also ecient and consistent plaque removal ence to professional advice in periodontal management
by the patient; PMPR should not be thought of as another including:
term for “scale and polish”, which is an outdated term that • A belief that periodontitis is a chronic, non-threatening
should not be used in clinical records. Step 1 should be disease
implemented in all periodontitis patients, regardless of the • Poor understanding of the condition by the patient
stage of their disease, and involves the following interven- • A belief that treatment is expensive
tions – the aims of which are to guide behaviour change: • Inherent dental phobias
• supragingival bioëlm control (OHI) • A perception of a lack of compassion on the part of the
• adjunctive therapies to control inìammation clinician (Wilson 1996).
• PMPR Overcoming these barriers can be dicult, and improv-
• risk-factor control (e.g. smoking cessation, improved dia ing patients’ adherence to advice may indeed be one of the
betes control, exercise, dietary control and weight loss). biggest challenges in modern dentistry. Over the years, sev-
e EFP CR (2020) on oral hygiene and patient engage- eral psychological models have been developed to try to
ment was to emphasise the importance of these aspects of understand the determinants of healthcare behaviour and to
disease control to patients (Figure 4.3.3), based on the sys- try to overcome these barriers. ese models have included
tematic review by Carra etal. (2020) social cognition models which “consider individuals to be
E
Supportive care/rehabilitation
C
Step 4 EXIT - plan longer-term care (above)
I
Step 3 CHECK - Non-responder sites: Re-RSD/surgery
R
Step 2 INTERVENE - Sub-gingival biofilm & calculus removal ± adjuncts
P
Step 1 RISK - Risk factor control, OHI, adjuncts for GI, PMPR, supra-gingival scaling
Step 0 PREREQUISITE TO THERAPY - Educate, classification, diagnosis, risk assess, care plan
• Figure 4.3.2 The European Federation of Periodontology S3-Level Clinical Practice Guideline 2020 step-
wise approach for the treatment of stages 1–3 periodontitis (Sanz etal. 2020). (Reprinted by permission
from Springer Nature: Br. Dent. J. Evidence-based, personalised and minimally invasive treatment for
periodontitis patients - the new EFP S3-level clinical treatment guidelines, Kebschull, M., Chapple, I.,
Copyright 2020.)
Expert consensus-based recommendation

We recommend emphasising the importance of oral hygiene and engaging the
periodontitis patient in behavioural change for oral hygiene improvement.
Supporting literature Carra et al.
Grade of recommendation grade A – ↑↑
Strength of consensus strong consensus (1.3% of the group abstained due to potential Col)
BSP implementation
This evidence-based recommendation is adopted.
We recommend emphasising the importance of oral hygiene and engaging the periodontitis
patient in behavioural change for oral hygiene improvement.
Strength of consensus: Strong consensus (0% abstentions due to potential Col)
• Figure 4.3.3 EFP Clinical Recommendation (BSP implementation) with respect to the importance of oral
hygiene and patient engagement in periodontal management. CoI, Conict of interest. (Reprinted from J.
Dent., 106, West, N., Chapple, I., Claydon, N., D’Aiuto, F., Donos, N., Ide, M., Needleman, I., Kebschull,
M. [2021], with permission from Elsevier.)
processors of information and vary in the extent to which 4.3.4, although the need for further research in this area was
they address the individual’s cognitions about their social acknowledged. Although to date MI has not been shown to
world” (Ogden 2000). Such models include the Health Belief improve patient adherence, there are some basic principles
Model (Rosenstock 1974), the eory of Planned Behav- of MI which can enhance a clinician’s rapport with patients
iour (Ajzen 1988), the Health Locus of Control (Wallston and thus, potentially, improve a patient’s response to pro-
& Wallston 1982), the Self-Ecacy Model (Bandura 1977) fessional advice with respect to oral hygiene and risk-factor
and motivational interviewing (MI) (Rollnick etal. 2010). control.
ere is some evidence that such models could be used to
improve oral hygiene, but there is little evidence that the use Motivational Interviewing
of such methods by clinicians would be benecial in a den-
tal practice setting. MI in particular has gained much popu- MI involves helping patients say why and how they might
larity. However a systematic review by Carra etal. (2020) change and is based on the use of a guiding style. It is a per-
which examined two randomised controlled trials (RCTs) son-centred, goal-directed method of communication for
on MI and three RCTs on psychological interventions based eliciting and strengthening patients’ intrinsic motivation for
on social cognitive theories found no signicant additional positive change. MI was developed in the 1980s by Miller
benet of implementing specic psychological interven- et al. (1988) in response to their observations regarding
tions in conjunction with oral hygiene instruction. e CR treatment of patients with alcohol-related problems. e
developed by the EFP S3 guideline (BSP implementation) standard confrontational approach to such patients often
was therefore not to recommend such approaches (Figure failed because of denial, personality defect or a failure of
Expert consensus-based recommendation

We recommend that the same guidance on oral hygiene practices to control gingival
inflammation is enforced throughout all the steps of periodontal therapy including
supportive periodontal care.
Supporting literature Van der Weijden and Slot
Strength of consensus strong consensus (3.8% of the group abstained due to potential
conflict of interest [Col])
BSP implementation
We recommend that the same oral hygiene guidance to control gingival inflammation is
practised throughout steps 1–4 of periodontal therapy including supportive periodontal
care.
Strength of consensus: Unanimous consensus (0% abstentions due to potential Col)
• Figure 4.3.4 EFP Clinical Recommendation (BSP implementation) with respect to oral hygiene practices
by the patient. (Reprinted from J. Dent., 106, West, N., Chapple, I., Claydon, N., D’Aiuto, F., Donos, N.,
Ide, M., Needleman, I., Kebschull, M. [2021], with permission from Elsevier.)
Evidence-based statement
To improve patient’s behaviour towards compliance with oral hygiene practices,
psychological methods such as motivational interviewing or cognitive behavioural therapy
have not shown a significant impact
Supporting literature Carra et al.
Quality of evidence five randomised clinical trials (RCTs) (1716 subjects) with duration ≥ 6
months in untreated periodontitis patients (4 RCTs with high and 1 RCT with low risk of
bias [RoB])
Grade of recommendation statement - unclear, additional research needed
Strength of consensus strong consensus (1.3% of the group abstained due to potential Col)
BSP implementation
Psychological methods such as motivational interviewing or cognitive behavioural therapy
have not been shown to have a significant impact on patient’s compliance with oral hygiene
practices.
Strength of consensus: Consensus (0% abstentions due to potential Col)
• Figure 4.3.5 EFP Clinical Recommendation (BSP implementation) with respect to psychological interventions
in behaviour change. CoI, Conict of interest. (Reprinted from J. Dent., 106, West, N., Chapple, I., Claydon,
N., D’Aiuto, F., Donos, N., Ide, M., Needleman, I., Kebschull, M. (2021), with permission from Elsevier.)
engagement. is study found that a confrontational style MI Step 1: Develop a “Guiding” Style
and direct persuasion were likely to increase resistance but e main communication styles that clinicians can employ
that positive change occurred more readily when the clini- to impart healthcare advice are directing, guiding and fol-
cian connected the change with what was valued by the lowing. Although each style has its own uses in dierent
patient. MI is based on the concept that patient motiva- situations and with dierent patient personalities, a guid-
tion is necessary for change to occur, that motivation resides ing style is best suited to discussions about change (Rollnick
within the individual and is achievable by eliciting personal etal. 2010). ere are three principles to follow when using
values, desire and ability to change. It allows patients to per- a guiding style:
ceive health behaviour information as being relevant to their • Engage with and work in collaboration with a patient
own situation. • Emphasise the patient’s autonomy over decision-making
ere are three steps necessary to develop an eective MI • Elicit their motivation for change.
technique: using a “guiding” communication style, elicit- e clinician can still control the direction and structure
ing motivation to change and responding to the patient’s of the consultation and provide all the information that is
language. needed, but the patient retains the responsibility for change.
It is important for such an approach to be successful that imposing one of your own. is also increases empathy with
an empathetic bond is established between clinician and your patient. is is referred to as “change talk”. It is also
patient. e three skills that a clinician needs to employ are important to remember how important body language is
asking, listening and informing: when undertaking these consultations. In the dental setting,
• Ask: open-ended questions, invite the patient to consider this means having the patient sitting upright in the dental
how and why they might change chair (or better still in an ordinary chair or in a dierent,
• Listen: to your patient’s experience and encourage them non-clinical room altogether) and facing them rather than
to elaborate; this elicits empathy and is a good way to having the patient supine, and not imposing barriers like
respond to resistance face masks and crossed arms. One set of guidelines that
• Inform: by asking permission to provide information can be used is referred to with the acronym SOLER (Egan
and asking what the implications may be for the patient. 1990):
Much of this process involves asking the patient things
Square on to the patient, not turned away, patient sitting up
rather than telling them.
Open posture, avoid crossed arms
MI Step 2: Elicit Motivation to Change Lean slightly forwards, look interested
Eye contact to establish rapport
Various strategies can be used in a guiding style to establish
Relaxed demeanour.
motivation in a patient, but this usually involves the follow-
ing, with examples in italics:
1. What would they like to change? KEY POINT 3
• What bothers you the most? Bleeding gums? Tenderness? Motivational interviewing principles:
2. Why do they want to change? • Respect patient autonomy
• Do you think it would be better if your gums didn’t bleed? • Guide rather than direct
• Activate patient desires and motivations.
What do you think will happen if they continue to bleed?
3. Assess the importance of the change
• Is it important to you that your gums stop bleeding and feel Adherence to Oral Hygiene and Other
more comfortable?
4. Assess their condence in achieving change Advice
• Do you think you would be able to spend longer on your Oral Hygiene Advice
cleaning if this reduced the bleeding and discomfort?
5. Give them the information they need – elicit understand- e EFP S3 guideline on oral hygiene practices (2020)
ing, provide information and elicit their interpretation strongly recommended the ecient use of oral hygiene
• Do you realise why your gums are bleeding? (Elicit) You are practices by the patient at all stages of periodontal therapy
right that it is common, but it does show that there is a prob- (Figure 4.3.5), based on a systematic review by Van der Wei-
lem there. (Provide) Can you see that you can do something jden and Slot (2015). In the management of periodontitis,
about this yourself? (Elicit) once you have established with the patient what they need
6. Set practical goals to do and why they need to do it, and that they are prepared
• Do you see any problems with spending longer on your to try to put your advice into action, discuss with them
cleaning? Do you see any diculties in using oss? Would when, during the day, they might be able to devote the nec-
you rather try something else? essary time to the regimen. us a “concrete plan” is made
e imparting of information to a patient is in itself a with the patient (Schüz etal. 2006). is detail should be
skill that needs to be developed, and there are a few key recorded and checked with patients at subsequent visits. If
principles that need to be followed: the patient thinks they may have diculty in establishing
• Use layman’s terms to ensure understanding the necessary routine on a daily basis, it is worth suggesting
• Remove your mask that they combine the new oral hygiene routine with a daily
• Deliver advice when the patient is upright and relaxed habit that is already established. is so-called event-based
rather than during treatment recall is more eective than “time-based recall” (Ellis 1998)
• Encourage the patient to reiterate your advice to check when patients try to carry out a particular action at a speci-
understanding ed time of day. In the case of oral hygiene, the event could
• Repeat what they say to you, so they know you are be a mealtime, the daily shower, a radio programme or any
listening established habit that could trigger recall to carry out the
• Discuss speciëc goals with which they agree to encourage oral hygiene routine.
adherence. Oral hygiene advice is traditionally given verbally, usu-
ally using a “tell–show–do” approach (tell the patient about
MI Step 3: Respond to the Patient the technique, show what is needed then get the patient to
Pay careful attention to the patient’s responses; what you do it themselves), but it has been shown that the provision
say to the patient should be in response to what they say of written information increases adherence (Ley 1988).
to you so that you are working to their agenda, rather than ɨis could be done with a locally produced leaìet, which
ORAL HYGIENE REGIME
Prepared for: Date:

. Do all once daily
. Same time each day
. Link with another event (radio or TV programme?)
. Expect bleeding and/or tenderness – this is normal and will subside
. Floss, interdental brushes, pocket brush first without toothpaste or
. water
Toothbrush last, without toothpaste or water, then have a second
toothbrush with paste
Brush Floss (+ wire interdental brush, not shown)
Pocket brush – do inside as well (not shown) – white (top) and red (bottom) – all teeth
• Figure 4.3.6 Oral hygiene regimen instruction sheet, customised for a patient.
is probably more eective than a generic, commercially their lives (Bandura 1994). Philippot etal. (2005) showed
produced document, but an alternative is to produce a cus- that patients’ sense of self-ecacy can be developed through
tomised instruction sheet utilising digital photographs of their own direct experience by observing the eects of their
the patient themselves (Figure 4.3.6). It has also been sug- behaviour on their periodontitis symptoms. In the context
gested that if a patient has a smartphone with video record- of periodontal management, this is most readily achieved by
ing capabilities (many patients have such devices) then a taking photographs before and after a period of oral hygiene
short personalised oral hygiene training video can easily be alone, usually a few weeks (Figure 4.3.7), so that patients
made for the patient to view. An individualised approach to can see that what they do, without professional interven-
oral hygiene advice, of which these are examples, has been tion, can make a visible dierence to levels of marginal
shown to improve adherence (Harnacke etal. 2012). inìammation.
Perhaps most importantly, the patient’s level of self-e- One study (Mizutani etal. 2012) investigated the asso-
cacy can be developed by withholding any form of profes- ciation between self-ecacy, oral health behaviour and gin-
sional intervention during the initial (oral hygiene) phase of gival health and found that patients with a more developed
therapy, so that they can observe that what they do them- sense of self-ecacy had better oral health behaviour and
selves can improve their condition. Self-ecacy is a patient’s less gingivitis. Self-ecacy can be improved by using the
belief about their capability to produce designated levels of techniques described above, and this will benet patients’
performance that exercise inìuence over events that aêect gingival and periodontal health.
Diet Advice
• Give appropriate advice regarding sugar and carbohy
drates and provide healthy alternatives
• ɨe motivation for change depends upon pointing out
incentives and removing disincentives to change
• Invite patients to keep a diet chart for at least 3 days and
discuss it in a non-judgemental, supportive manner, pro-
viding constructive alternatives
• Rather than directing away from “junk” food, use MI
language to elicit what they know about healthy foods
and how they could incorporate more.
Assessing Adherence in Practice

A It is important to assess patients’ oral hygiene eorts peri-
odically to ensure that the necessary levels of biolm con-
trol are being maintained. is can most conveniently be
done using digital photographs (see Chapter 4.2 and Figure
4.3.7), and this has the added advantage of providing visual
evidence to the patient of the improvement (or otherwise)
in their condition, which may further enhance their sense
of self-ecacy. Traditionally, plaque scores have been used
to assess patients’ level of oral hygiene, with or without
disclosure using plaque-staining agents, but such measures
can be unreliable because they record the plaque levels at a
single time point only, and many patients brush their teeth
especially well just before they attend a dental appoint-
ment. us a low plaque score may not be representative of
the patient’s usual level of biolm control. A more reliable
B method of oral hygiene assessment is the marginal bleed-
• Figure 4.3.7 A patient’s gingival condition before and after a few ing score (see Chapter 2.2) which records the presence (or
weeks of oral hygiene alone, with no professional intervention. (A) absence) of marginal inìammation. Since it will always take
Before plaque control advice. (B) After 1 month of plaque control. a few days for a marginal inìammatory lesion to develop
in the presence of marginal biolm (or to resolve in the
absence of the biolm), the marginal bleeding score gives
Other Advice a better indication of the patient’s usual level of cleaning. It
e dental clinician will often nd that it is necessary to is important to distinguish this measure from bleeding on
give advice with respect to other health issues, such as diet probing, which is bleeding from the base of the periodon-
and smoking, when treating a patient who has periodontal pocket and is used to assess the response to professional
titis. e principles outlined above still apply. Always try treatment.
and highlight those risk factors that are specically relevant
to the individual patient. In addition the following points Conclusion
should be observed:
Motivating patients to improve their levels of self-care can
Smoking Cessation Advice be dicult, may be met with resistance and, at times, may
• ɨe accepted method is the 5 As: ask, advise, assess, be frustrating for the clinician. In periodontics, however,
assist, arrange perhaps more so than in other dental disciplines, it is per-
• Aïrm belief in cessation, keep dialogue open, accept it haps the most crucial part of the periodontal patient’s dis-
may take time ease management. However, developing a supportive and
• Reìect back any comments which can be used to moti non-judgemental approach to oral hygiene and health-
vate, such as concerns about the cost of smoking and care advice can be highly eective, and the techniques
smelling of nicotine and in nding places to smoke in outlined in this chapter should be practiced until they
public, for example become the clinician’s routine way of communicating with
• Use positive language patients.
• Signpost the patient to smoking cessation support Multiple choice questions on the contents of this chapter
services. are available online at Elsevier eBooks+
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SECTION 5
Non-surgical Periodontal
Management
203
5.1
The Diseased Root Surface
in Periodontitis
PH I L I P OW E R
CHAPTER OUTLINE
The Clinical Presentation of Periodontitis Non-Surgical vs Surgical Treatment
Features of Periodontitis The Role of the Bioölm
The Role of Bacteria Calculus in Disease
Current Concepts of the Aetiology of Periodontitis Contaminated Cementum
Treating the Diseased Root Surface

This chapter describes the nature of the diseased root surface in periodontitis and will examine the relative roles of the bacterial biolm,
dental calculus and contaminated cementum in the disease process.
By the end of the chapter the reader should: • Be able to appreciate the importance of bioölm removal in
• Understand the nature of the diseased root surface disease control
• Appreciate the relative roles of bioölm, calculus and • Be able to select appropriate treatments for patients with
contaminated cementum in periodontitis periodontitis.
• Be able to diòerentiate between various methods for This chapter covers the following topics:
treating diseased root surfaces • Clinical presentation of periodontitis
• Treating the diseased root surface.
Periodontitis is now recognised as one of the most complex

The Clinical Presentation of Periodontitis of human diseases, and it is a major cause of tooth loss in
Features of Periodontitis all populations throughout the world. In addition, there is
also mounting evidence that periodontitis may play a sig-
Periodontitis is observed clinically as the apical migration nicant role in general health, so the eective treatment of
of the junctional epithelial attachment and progressive loss periodontitis may be even more important than was once
of the connective tissue attachment to the tooth surface, thought.
with increasing clinical pocket depth and inammatory
change in the soft tissues. Increasing levels of soft tissue The Role of Bacteria
inammation result in redness, swelling, bleeding and ten-
derness. Radiographically, alveolar bone loss is seen as the It was thought in the past that the release of bacterial tox-
bone is resorbed (by the host) to prevent its infection by ins from dental plaque caused most of the tissue damage
the encroaching bacterial biolm which colonises the root seen in periodontitis, and that only a small amount of
surface of the periodontal pocket. Although it is widely damage was caused by the host response (inammatory
accepted that periodontitis has a microbial aetiology and and immune) to these toxins. Periodontitis was then fre-
that bacteria and other microbes are essential for disease to quently, and erroneously, referred to as an infection and
occur, there is now a clearer understanding of the multiple various explanations were proposed for the bacterially
host factors that play a major part in this disease process. mediated destructive mechanisms involved; these have
205
206 SECTION 5 Non-surgical Periodontal Management
been referred to in the literature as plaque hypotheses. Ini- KEY POINT 1

tially, it was thought that it was the total plaque mass that
The ecological plaque hypothesis incorporates elements of
was responsible for disease, the non-specic plaque hypothesis both the non-specic and specic plaque hypotheses but also
(NSPH), and that the more plaque a patient had the more takes into account the role that various host factors play in the
periodontitis they would get. is clearly does not t with development and organisation of the dental biolm.
what is seen in practice, where some patients have a lot of
plaque and little periodontitis and others have little plaque e ecological plaque hypothesis was proposed (Marsh
but signicant bone and attachment loss, and is not sup- 1994) to explain how the host interacts with the microbial
ported by research ndings. For example Löe etal. (1986) biolm; this incorporates elements of both the NSPH and
investigated a population of tea workers in Sri Lanka over the SPH but also considers the role of host response fac-
a 15-year period who had no access to dental care and tors in the development of disease. us, in health, there
did not carry out any form of conventional oral hygiene. is symbiosis – a balance between the microbial composition
Despite having large deposits of both plaque and calculus, of the biolm and the host response. In disease, there is a
they did not all have periodontitis – about 10% had no dis- disturbance of this balance (think about the word “disease”
ease beyond gingivitis, about 80% had moderate progres- – a combination of “dis” and “ease”) caused by a change
sion of periodontitis and about 10% had a form of rapidly in the microbial threat or a change in the host response,
progressing periodontitis. As advances in microbiological or often a change in both (Figure 5.1.1). is is referred
investigation allowed the examination of dental plaque in to as dysbiosis. e microbial threat may increase due to an
more detail and the identication of the individual species increase in the bacterial mass – NSPH – which may result in
of bacteria that predominated in plaque, both in health and an increased host inammatory response, resulting in host-
disease, a second theory was developed – the specic plaque mediated tissue damage. Given that the host response is
hypothesis (SPH). is suggested that specic microorgan- largely genetically determined, this explains why periodon-
isms in plaque were responsible for disease and that only titis can be seen to run in families and why some patients are
plaque that contained these organisms was capable of pro- more susceptible than others to periodontal breakdown – in
ducing disease (Loesche 1976). is concept was supported these individuals, relatively small changes in biolm mass
by the fact that the microbial composition of plaque was may result in a greater, and more damaging, host response.
dierent in diseased and healthy sites (Socransky & Haf- e increased inammatory response, if sustained, results in
fajee 1992), and researchers started compiling lists of bac- increased gingival crevicular uid (GCF) ow, which con-
teria (which were colour-coded by level of pathogenicity, tains host proteins and glycoproteins that can be exploited
the “red complex” organisms being the most pathogenic) as substrates by subgingival anaerobic bacteria. is leads to
that were found in the most diseased sites (Socransky etal. a gradual shift in the microbial composition of the biolm
1998). Whether these bacteria were causative (responsible which can disrupt the natural balance of organisms within
for disease) or opportunistic (taking advantage of the liv- the biolm community – SPH – and increase the risk of dis-
ing conditions at deep sites) could not be established. is ease (Marsh etal. 2011). e host response may also change
research, which appeared to support the concept of a SPH, because of environmental factors (such as smoking, stress,
also coincided with increasing interest in and research into systemic disease or diet) which may also favour a shift in
the use of antimicrobials in periodontal treatment, spe- the microbial composition of the biolm towards greater
cically locally applied drugs, which could target certain numbers of more pathogenic (predominantly anaerobic)
bacteria as a means of disease control. However, at the bacterial species.
same time, there was a developing realisation that the host
response might have a larger role in the disease process than KEY POINT 2
was previously thought. It is thought that the majority (an estimate of 80% has been
suggested) of the damage observed in periodontitis is due to
the inammatory host response to the bacterial biolm, rather
Current Concepts of the Aetiology of than direct bacterial activity.
Periodontitis
e recognition that host factors play a major role in peri- Currently, it is thought that the majority (an estimate of
odontitis has led to the concept of the ecological plaque 80% has been suggested) of the damage observed in peri-
hypothesis which incorporates elements of both the non- odontitis is due to the inammatory host response to the
specic and specic plaque hypotheses but also takes into bacterial biolm rather than direct bacterial activity. us,
account the role that various host factors play in the devel- bacteria are necessary as a trigger for the host response, but
opment and organisation of the dental biolm. Indeed, the it is the host response that causes most of the damage. Peri-
use of the term biolm is preferable to the use of the term odontitis should therefore be thought of as an inammatory
plaque because it better reects the highly complex nature disease rather than an infection; because most of the dam-
of the growth, development and behaviour of bacteria (and age is host mediated, the bacteria involved are commensal
other microbes) on diseased root surfaces. Biolms are organisms and they do not usually invade the host tissues but
described in detail in Chapter 1.5 remain on the root surface in the biolm. Current thinking
CHAPTER 5.1 The Diseased Root Surface in Periodontitis 207
Health/Disease balance
Biofilm Host response
Inflammation
Immune system
• Figure 5.1.1 Health/disease balance.
has been encapsulated in this statement from the 2008 Work- maintenance of a healthy subgingival environment by both
shop on Inammation and Periodontal Disease: A Reappraisal: the patient and clinician. However, with the increasing
“Periodontitis is an inammatory disease initiated by the oral understanding of the inammatory nature of the periodon-
microbial biolm . . . it is the host response to the biolm titis process and the fact that the soft tissues are only rarely
that destroys the periodontium” (Van Dyke 2008). invaded by bacteria and other microbes, there has been a
So if the trigger for the damaging host response is the shift towards more conservative, non-surgically based thera-
bacterial presence on the root surface, eective treatments pies as a means of controlling inammation. at non-sur-
need to reduce this presence to a level that does not initiate gical treatment is an eective method for treating chronic
a damaging host response. periodontitis (or indeed the less common aggressive form
of disease) is not in doubt; a systematic review and meta-
Treating the Diseased Root Surface analysis published in 2005 (Heitz-Mayeld 2005) looked at
the ndings of three previous systematic reviews, published
e diseased root surface in a periodontal pocket comprises between 1993 and 2002, conrming that better treatment
several layers of potential contamination that could harbour outcomes can be achieved by non-surgical means, when
sucient microbes to trigger the disease process (Figure 5.1.2). compared to surgical treatment, for moderate pockets (up
e outermost layer of contamination will always be the to 6 mm), whereas surgical treatment is only of greater ben-
microbial biolm, but there is also the potential for contam- et for deeper pockets in excess of 6 mm. Although this
ination from subgingival calculus and from any microbes appeared to show that deep pockets should be treated surgi-
that may have invaded the cemental layer of the root. Most cally, the authors pointed out that this latter nding is only
periodontal therapies involve the removal of these sources of applicable to 12-month post-treatment results, and those
contamination, and it has been stated (Lindhe & Echeverria studies that followed patients for 5 years or more found
1993) that root surface disinfection is the primary objective that, even for deep pockets, non-surgical therapy was as
of therapy. is objective may be achieved by both non- eective as surgical treatment.
surgical and surgical means.
KEY POINT 3
Non-surgical treatment is an effective method for treating
Non-Surgical vs Surgical Treatment chronic periodontitis.
In the past, much periodontal therapy has involved the sur-
gical excision of soft tissue as a means of removing “infected” Many of the non-surgical methods commonly used
soft tissue and reducing pocket depths to facilitate the today to treat periodontal diseases have remained largely
Biofilm
Calculus
Cementum
Dentine
• Figure 5.1.2 Possible sources of contamination on a diseased root surface.
unchanged for decades. In non-surgical periodontal therapy, with any protocol of mechanical debridement” (Sanz &
for example, the process of root planing is still practised, but Teughels 2008).
it was illustrated in Egyptian hieroglyphics 4000 years ago e eects of good biolm control before starting treat-
and was described, and named, in the dental literature a ment can be dramatic (Figure 5.1.3), the goal being to estab-
century ago (Hartzell 1913). More recently, the term “root lish an optimal supragingival environment prior to starting
surface debridement” has been used to describe the instru- subgingival instrumentation. Patient self-care is considered
mentation of the diseased root surface. Some confusion has in detail in Chapter 4.1
arisen surrounding the terminology used to describe these
dierent instrumentation techniques, and denitions of the KEY POINT 4
various terms used will be considered in Chapter 5.2 on “It should be noted that the performance of optimal oral
periodontal instrumentation. e current chapter will now hygiene practices is an inseparable principle to be observed
consider the relative roles of the bacterial biolm, calculus with any protocol of mechanical debridement” (Sanz and
Teughels 2008).
and cementum in periodontitis.
As far as therapy is concerned, it is now universally

The Role of the Biofilm accepted that mechanical biolm removal forms the corner-
It may seem obvious that the biolm on the root surface stone of successful periodontal therapy (Guentsch & Pre-
needs to be removed or disrupted for treatment to be eec- shaw 2008, Chapple 2009, van der Weijden & Slot 2011)
tive. However, fundamental to the successful management and that a reduction in subgingival biolm mass is essential
of disease by non-surgical means (or indeed surgical means for successful therapy (Mombelli etal. 1995).
for that matter) is the establishment, before any treatment
is carried out, of optimal self-performed biolm (plaque) KEY POINT 5
control. Although the evidence base for an association Mechanical biolm removal forms the cornerstone of
between personal oral hygiene and the control or preven- successful periodontal therapy.
tion of chronic periodontitis is surprisingly weak (there
are no randomised controlled trials to show such an asso- Calculus in Disease
ciation; Hujoel etal. 2005), it is assumed that an adequate
level of daily plaque control is a prerequisite for successful Calculus is the result of the mineralisation of biolm by
periodontal therapy of any form. For example, the Sixth salivary mineral components (Lang et al. 2008), which is
European Workshop in Periodontology in 2008 stated that: why supragingival calculus is mostly found adjacent to the
“It should be noted that the performance of optimal oral opening of the ducts of the major salivary glands that are
hygiene practices is an inseparable principle to be observed buccal to the upper rst molars and lingual to the lower
A
• Figure 5.1.4 Exposed subgingival calculus after oral hygiene mea-
sures alone.
structure (Mombelli et al. 1995). In addition, the con-

cept of removing all subgingival calculus has been shown
to be both unrealistic and unnecessary (Cobb 2002) and
that clinical healing occurs in the presence of residual sub-
gingival calculus (Nyman etal. 1986, Blomlöf etal. 1987,
Buchanan & Robertson 1987) providing the surface of the
calculus is biolm-free (Mombelli etal. 1995, Jepsen etal.
2011). is is just as well because clinicians rarely remove
all subgingival calculus deposits even when they try to do
so, whether by non-surgical or surgical means and whether
B using hand or machine-driven instrumentation techniques
(Eaton etal. 1985, Caesse etal. 1986, Kepic etal. 1990).
• Figure 5.1.3 Effects of self-performed plaque control. (A) The patient One review (Robertson 1990) showed that, even after
on presentation. (B) The same patient after 3 months of self-performed
oral hygiene measures only with no professional intervention. 12–15 minutes of treatment per tooth, 63% of root surfaces
still harboured residual calculus. However, it is now under-
stood that calculus does not contain signicant quantities
anterior teeth. Subgingival calculus is found in periodontal of bacterial lipopolysaccharide (Chiew etal. 1991), and it
pockets and is a darker colour than supragingival calculus as has been concluded that calculus is the result of the peri-
a result of incorporation of blood products from subgingival odontal lesion and not its cause (Corbet et al. 1993, Jep-
inammation. Calculus is porous in nature; although some sen et al. 2011). Calculus is therefore another surface on
studies have identied viable organisms within the lacunae which biolm can form, but the biolm can be as easily
of supragingival calculus (Tan etal. 2004), others have sug- removed from the calculus surface as it can from other intra-
gested that most of the bacteria contained within calcu- oral surfaces. us when patients achieve high standards of
lus have been killed by the mineralisation process and are self-performed biolm control, periodontal lesions can heal,
therefore incapable of producing harmful toxins (Sidaway even in the absence of professional intervention, and previ-
1980). It is also worth remembering that individual bacteria ously subgingival calculus can become supragingival (Figure
that survive in calculus are not part of a biolm and thus 5.1.4), supporting the concept of calculus being the result
have little pathogenic potential. Traditionally, it has been of the disease process and not its cause.
thought essential to remove all such calcied deposits from
the root surface in order to achieve root surface decontami- KEY POINT 6
nation and promote resolution of periodontal inamma- The importance of biolm removal in therapy far outweighs the
tion. Indeed, in the past, treatment seems to have focused need to remove the mineralised calculus deposits or potentially
entirely on the meticulous removal of all calculus deposits, contaminated tooth structure.
and much dental hygienist training has centred on develop-
ing ecient and eective calculus-removal skills. However,
it is now understood that the importance of biolm removal KEY POINT 7
in therapy far outweighs the need to remove the miner- Calculus is the result of the periodontal lesion and not its
cause.
alised calculus deposits or potentially contaminated tooth
Calculus is sometimes described as a plaque-retention the root surface could be easily decontaminated by much
factor, but there is no evidence to support the concept of lighter and quicker instrumentation techniques than had
biolm being more adherent to the surface of the calcu- previously been thought. One invitro study (Moore etal.
lus than it is to other surfaces. However, calculus may be 1986) showed that over 99% of the bacterial contaminants
thought of as presenting an obstacle to optimal personal and could be removed by light instrumentation alone, without
professional care, as well as being unsightly, and its removal the need for cementum removal by root planing. is led
can be justied on these grounds. to the concept of “root surface debridement” that involved
ultrasonic instruments used with light and overlapping
Contaminated Cementum strokes for a limited time period (Smart etal. 1990). Often
such treatments do not require the use of local anaesthesia,
Cementum is the highly mineralised outer layer of the root and there is a much-reduced risk of iatrogenic root surface
surface and, in health, it provides a means of attachment for damage. e dierences between traditional root plan-
the collagen bres of the normal periodontal ligament. In ing and root surface debridement should therefore now be
disease, the cemental layer becomes exposed and can poten- apparent to the reader. However, following publication of
tially become a source of bacterial contamination. How- the European Federation of Periodontology (EFP) S3 clini-
ever, as has already been stated, the importance of biolm cal guideline for the treatment of stages I– III periodonti-
removal in therapy far outweighs the need to remove miner- tis (Sanz et al. 2020), and the subsequent British Society
alised deposits (calculus) or tooth structure (Mombelli etal. of Periodontology and Implant Dentistry (BSP) UK version
1995). So how important is the exposed cemental layer in of this guideline (West etal. 2021), the term “subgingival
the disease process? instrumentation” is now proposed as a universal term for
For at least the last century, it has been assumed (with non-surgical treatment of the root surface. ese issues are
no clinical evidence to support the concept) that the surface explored further in Chapter 5.2
layer of the cementum of the diseased root surface became
contaminated with both bacteria and their toxins. Invitro KEY POINT 8
research had suggested that bacteria and bacterial endotox- Bacterial contaminants are only loosely adherent to the root
ins could penetrate and be bound to root cementum (Aleo surface and do not penetrate the root cementum to any
et al. 1974, 1975, Daly et al. 1982, Adriaens et al. 1988) signicant degree.
and that this could act as a potential reservoir of toxins that
could lead to re-infection after therapy. is apparently jus- Multiple choice questions on the contents of this chapter
tied the concept of “root planing”, a treatment technique are available online at Elsevier eBooks+.
that involved the use of highly sharpened (and therefore
highly damaging) hand instruments to “plane” away the References
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5.2
Periodontal
Instrumentation
PH I L I P OW E R
CHAPTER OUTLINE
Introduction Types
Treatment Objectives Methods
Other Types of Power-Driven Instruments
Terminology and Denitions Vector
Dental Scaling Lasers
Root Planing (RP) Photodynamic Disinfection
Periodontal Debridement (PD) Subgingival Air Polishing
Subgingival Instrumentation (SI) Instrumentation Strategies
Full-Mouth Disinfection (FMD)
RP or PD – Choice of Instruments
Full-Mouth Ultrasonic Debridement (FMUD)
Hand vs Ultrasonic Instrumentation
Types of Instruments Use of Anaesthesia
Hand Instruments Full-Mouth or Quadrant Approaches?
Types
Methods Adjuncts to Periodontal Instrumentation
Machine-Driven Instruments Conclusions

This chapter will examine the methods that are available to instrument diseased root surfaces during both non-surgical and surgical therapy.
This chapter should be read in conjunction with Chapter 5.1
• Understand treatment objectives in periodontal therapy • Introduction
• Understand the terminology that is used to describe • Treatment objectives
instrumentation techniques • Terminology and deönitions
• Understand the choice of instruments that are available • Types of instruments
• Understand the eòects of diòerent types of instrumentation • Instrumentation strategies
• Be able to outline the diòerent strategies that can be • Adjuncts to periodontal instrumentation
employed to instrument diseased root surfaces • Conclusions.
• Be able to select appropriate instruments to meet treatment
objectives.
Introduction being used in current dental practice. Research has shown

that many of these treatment modalities achieve broadly
Decontamination of the teeth, and in a diseased state the similar results. e purpose of this chapter is to highlight
roots of teeth, by various methods of instrumentation has the most commonly used techniques and instruments in
been a fundamental aspect of dental treatment for hun- practice today. e use of chemicals and host-modulating
dreds, and possibly thousands, of years. Many dierent agents as adjuncts to periodontal instrumentation will also
methods, techniques and instruments to achieve a level of be examined. In 2021 the European Federation of Peri-
decontamination compatible with dental health have been odontology (EFP) published S3 clinical guidelines for the
proposed in the past, and extensive research over the last treatment of stages I–III periodontitis (Sanz et al. 2020)
century or so has resulted in a number of these techniques which introduced a series of consensus- and evidence-based
212
CHAPTER 5.2 Periodontal Instrumentation 213
Evidence-based recommendation
We recommend that sub-gingival instrumentation be employed to treat periodontitis in
order to reduce probing pocket depths, gingival inflammation and the number of diseased
sites.
Supporting literature Suvan et al.
Quality of evidence: One 3-month RCT (n = 169 patients); 11 prospective studies (n = 258)
≥6 months
Strength of consensus unanimous consensus (2.6% of the group abstained due to
potential Col)
BSP implementation
We recommend that sub-gingival instrumentation be employed to treat periodontitis in
order to reduce gingival inflammation, the number of diseased sites and probing pocket
depths.
Strength of consensus: unanimous Consensus (0% abstentions due to potential Col)
• Figure 5.2.1 EFP Clinical Recommendation (British Society of Periodontology and Implant Dentistry
(BSP) implementation) with respect to the benets of subgingival instrumentation in the treatment of peri-
odontitis. CoI, conict of interest. (image courtesy of BSP).
clinical recommendations (CRs) and included the intro- cornerstone of successful periodontal therapy (Chapple
duction of a stepwise approach to the management of peri- 2009, Guentsch & Preshaw 2008). In the past, emphasis
odontitis patients. e process is explained in more detail has been placed on the removal of all subgingival calcu-
in Chapter 4.3, and the CRs relevant to periodontal instru- lus deposits. e association of subgingival calculus with
mentation will be described in this chapter. periodontal lesions has led to the assumption that there is
a cause and eect relationship between the two; a review
Treatment Objectives of the evidence, however (Jepsen etal. 2011), has shown
that calculus is the result of disease and not its cause and
As we have seen in the previous chapter (Chapter 5.1), the that healing can occur in the presence of calculus as long
principal objective of all forms of periodontal therapy is as the overlying bacterial biolm is removed. Calculus can
the decontamination of the diseased root surface and the be thought of as an inert material and, clinically, it can
prevention of its bacterial recolonisation (Lindhe & Ech- be observed that healing of the periodontal lesion can take
everria 1993) to allow resolution of the inammatory lesion place and gingival shrinkage exposes previously subgingi-
in the soft tissues and arrest the destructive disease process. val calculus in the absence of subgingival calculus removal,
In the 2021 EFP S3 clinical guideline the second step of providing there is optimal biolm control by the patient
therapy in the stepwise approach (also referred to as “cause- during the oral hygiene phase of treatment (see Chapter
related therapy”) centres on periodontal instrumentation as 5.1). e removal of calculus then becomes necessary for
a means of reducing the bacterial load on the root surface better access to the subgingival biolm and for aesthetics.
that is responsible for triggering the periodontal disease pro- Biolm removal is therefore more important than calculus
cess. e EFP S3 clinical guideline considered a systematic removal (Kocher etal. 2001).
review carried out by Suvan etal. (2020) which had exam-
ined whether subgingival instrumentation (SI) was bene- KEY POINT 2
cial for the treatment of periodontitis, and this resulted in Biolm removal is more important than calculus removal.
a CR which strongly recommended the use of SI to reduce
gingival inammation, the number of diseased sites and Similarly, the original concept of the need to remove
probing pocket depths (see Figure 5.2.1). the outer layer of root cementum, which was assumed to
retain bacteria and their toxins, by means of planing the
KEY POINT 1 root surface with highly sharpened hand instruments, as was
The principal objective of all forms of periodontal therapy is the advocated in the dental literature in 1913 (Hartzell 1913)
decontamination of the diseased root surface. and has remained largely unchanged over the last century,
has been shown by more recent evidence to be both harm-
e main source of bacterial contaminants on the ful and unnecessary. e World Workshop in Periodontol-
root surface is the bacterial biolm. It is therefore ogy (Cobb 1996) stated: “Aggressive root planing to remove
widely accepted that mechanical biolm removal is the cementum does not seem to be warranted”.
Although such techniques have persisted, largely because Root Planing (RP)
they have been found to be eective because the biolm
is also removed during these procedures, there has been an Root planing is “a procedure for smoothing of the rough-
increasing acceptance over recent years, in light of new evi- ened surface or cementum of a tooth after subgingival
dence, that such treatment is overly destructive to the dental curettage or scaling, as part of periodontal therapy” (MeSH,
tissues, is excessively time consuming and causes unneces- introduced 1992). It is a technique of instrumentation by
sary discomfort for the patient. us it has been found that which cementum is removed and the root surface is made
equally eective clinical outcomes can be achieved by less hard and smooth. is is usually done by hand instrumenta-
invasive approaches in a shorter time by using dierent tion using sharpened blades. Because of the length of time
forms of instrumentation which are less technically demand- involved in achieving the goal of a hard and smooth root
ing than traditional hand instrumentation techniques. surface, the treatment is usually carried out by quadrant,
From the early 1980s onwards, studies have shown that typically 45–60 minutes per quadrant (Palmer & Floyd
bacterial toxins were only loosely adherent to the root sur- 2006), using local anaesthesia. It is sometimes referred to as
face and could be removed by much lighter instrumentation scaling and root planing (SRP) or quadrant scaling and root
which did not damage the root surface to the same extent as planing (QSRP).
root planing (Nakib etal. 1982, Ito etal. 1985, Hughes &
Smales 1986, 1990, Moore etal. 1986, Nyman etal. 1988). Periodontal Debridement (PD)
One in vitro study (Moore et al. 1986) showed that over
99% of the bacterial contaminants could be removed by Periodontal debridement (PD) is the term that has now
light instrumentation alone without the need for cemen- replaced the original term root surface debridement (RSD),
tum removal by root planing. is led to the concept of and it is dened as “the removal or disruption of dental
root surface debridement (RSD) (Cheetham et al. 1988, deposits and plaque-retentive dental calculus from tooth
Smart etal. 1990) as an alternative to root planing, the goal surfaces and within the periodontal pocket space without
being the achievement of a biocompatible root surface with- deliberate removal of cementum as done in RP and often in
out the removal of tooth structure. It was shown that RSD dental scaling. e goal is to conserve dental cementum to
had the potential to achieve the same level of root surface help maintain or re-establish a healthy periodontal environ-
decontamination as root planing but with the advantages of ment and eliminate periodontitis by using light instrumen-
conservation of tooth structure, shorter treatment time and tation strokes and non-surgical techniques (e.g. ultrasonic,
greater patient comfort. e study by Smart et al. (1990) laser instruments)” (MeSH, introduced 2011).
showed that less than 1 second per mm2 of debridement
of the root surface, using ultrasonics alone, was required to KEY POINT 3
render the root surface entirely toxin free. is amounted Periodontal debridement (PD) is the removal or disruption of
to a mean of 17 seconds instrumentation per diseased root dental deposits and plaque-retentive dental calculus from tooth
surface. In addition, the concept of RSD allowed for the surfaces and within the periodontal pocket space without
exclusive use of ultrasonic instrumentation, because there deliberate removal of cementum.
was no need to remove cementum by hand planing.
However there is some confusion about the meaning
of the terminology used to describe dierent non-surgical
Subgingival Instrumentation (SI)
treatment techniques, and this will be addressed in the next
section. In view of the confusion that was inevitably caused using so
many dierent terms in the scientic literature to describe
Terminology and Definitions decontamination of the root surface, the 2021 EFP S3 clini-
cal guideline agreed to use the term subgingival instrumen-
e following terms will be found in the dental literature tation (SI) for all non-surgical procedures performed by
and they have dierent meanings, so they should not be hand (i.e. curettes) or power-driven (i.e. sonic/ultrasonic
used synonymously. Where appropriate, the denitions devices) instruments that are specically designed to gain
given here have been taken from the Medical Subject Head- access to the root surfaces in the subgingival environment.
ings (MeSH) pages of the National Library of Medicine
website.
Full-Mouth Disinfection (FMD)
Dental Scaling Full-mouth disinfection (FMD) is a specic technique that
was proposed by a group of researchers who compared full-
Dental scaling is instrumentation to “remove dental plaque mouth instrumentation (all diseased root surfaces treated
and dental calculus from the surface of a tooth, from the within a 24-hour period) and quadrant-by-quadrant instru-
surface of a tooth apical to the gingival margin accumulated mentation, using chlorhexidine gluconate extensively in
in periodontal pockets, or from the surface coronal to the the full-mouth test groups (Bollen etal. 1998, Mongardini
gingival margin” (MeSH, introduced 1991). etal. 1999, Quirynen etal. 1999).
Blade
Shank
Handle
• Figure 5.2.2 Hand instrument – handle, shank, blade. • Figure 5.2.3 Curette, hoe, scaler from left to right.
Full-Mouth Ultrasonic Debridement (FMUD) carpenter’s wood plane. us, the blade is maintained at
an approximately 45-degree angle to the root surface and
Full-mouth ultrasonic debridement (FMUD) is a full- drawn along the root surface using pressure against the root
mouth treatment carried out in one session, using ultrasonic surface to remove the surface layer, along with calcied
instrumentation alone and a debridement (conserving tooth (calculus) and uncalcied (biolm) dental deposits (Figure
structure) technique. 5.2.4). A pen grip and nger rest should be used.
is is a technically demanding process which requires
a high degree of clinical skill in order to be eective, and
Types of Instruments the instruments need to be repeatedly sharpened (using a
Hand Instruments sterilised sharpening stone chairside) during the treatment
because of the rapid blunting of the blades. Repeated over-
Hand instruments usually take the form of scalers, curettes lapping strokes are performed to cover the entire root sur-
and hoes which have sharpened blades that permit the face of the periodontal pocket, starting at the base of the
removal of the root surface. All hand instruments consist of pocket and proceeding coronally with each stroke. Local
a handle, shank and blade (Figure 5.2.2). anaesthesia is usually required for such procedures, hence
the need to treat the mouth quadrant by quadrant in most
Types cases.
Scalers
Scalers, sometimes referred to as sickle scalers, have a curved
Machine-Driven Instruments
or straight blade with a triangular cross-section and two cut-
ting edges. ey are usually used for supragingival instru- Machine-driven instruments take the form of a metal tip
mentation or instrumentation in shallow pockets (Figure vibrating at sonic or ultrasonic frequencies, thereby disrupt-
5.2.3). ing both hard (calculus) and soft (biolm) deposits from the
root surface, if used correctly, without causing any loss of
Curettes tooth structure. In all forms of machine-driven instrumen-
Curettes have a curved blade with curved cutting edges. tation, the vibrating tip is cooled by a water supply. Ultra-
ey are usually double-ended with mirrored angles to the sonic devices for non-surgical periodontal therapy were
blades and come in a variety of shank lengths and angles and introduced in the 1950s.
a variety of blade sizes. ey are mostly used for subgingival
root instrumentation (see Figure 5.2.3). Types
Sonic Scalers
Hoes Sonic scalers (Figure 5.2.5) use air pressure to create a
e hoe has only one cutting edge, which is angled at over mechanically vibrating tip at 2–6 kHz (Gankerseer &
90 degrees to the shank. It is used mostly for supragingival Walmsley 1987) which disrupts biolm and removes calcu-
scaling (see Figure 5.2.3). lus deposits from the tooth surface.
Methods Ultrasonic Scalers

e methods used to hand instrument the root surface are Ultrasonic scalers (Figure 5.2.6) have vibrating tips which
analogous to those used to plane a piece of wood using a operate at frequencies of between 18 and 45 kHz by using
• Figure 5.2.6 Magnetostrictive ultrasonic scaler.

• Figure 5.2.4 Curette against a root surface.
• Figure 5.2.7 Piezo-electric ultrasonic scaler.

• Figure 5.2.5 Sonic scaler.
Methods
the conversion of electrical energy to mechanical energy. All forms of machine-driven instruments should be used in
ere are two main types of ultrasonic scalers – magneto- the same way, with the metal tip of the instrument used par-
strictive and piezo-electric. As the physical action of the tip allel to the root surface and the entire root surface debrided
on the biolm and calculus deposits on the root surface, using a series of light, overlapping strokes, usually in a
ultrasonic instrumentation may also have cavitational and “cross-hatching” form. e objective is to disrupt the entire
acoustic microstreaming eects that may also cause disrup- biolm and remove as much subgingival calculus as possible
tion of surface deposits. but without causing any damage to the root surface.
Other Types of Power-Driven Instruments
Magnetostrictive
In this type of ultrasonic scaler, the electrical current pro- Vector
duces a magnetic eld in the handpiece that causes the e Vector ultrasonic instrumentation system is a unique
insert to expand and contract and thus lead to vibration of form of ultrasonic instrument that uses a resonating ring
the metal tip. e movement of the vibrating tip has an around a ne tip to deect the horizontal oscillations verti-
elliptical pattern. cally, producing a linear oscillating movement of the tip.
e frequency used is 25 kHz. e system must be used in
Piezo-Electric conjunction with a suspension of hydroxyapatite particles in
In piezo-electric scalers (Figure 5.2.7), the electric current water. is is capable of removing or disrupting the biolm
leads to a dimensional change in the hand piece which is and removing subgingival calculus and causes no damage to
translated into vibration of the metal tip of the instrument. the root surface. e main advantages are little heat develop-
e tip movement is also elliptical (Lea etal. 2009). ment at the tip, no pathogenic aerosol and improved tactile
sensation (Sculean etal. 2004). A review of studies that have

investigated this system has shown that it is an eective
method of treatment for periodontitis and results in similar
clinical improvements to those achieved by other methods
of periodontal therapy (Guentsch & Preshaw 2008).
Lasers
Dental laser systems are available in a number of forms (car-
bon dioxide, Er:YAG, Nd:YAG) and are used in a variety
of clinical situations for treating both hard and soft tissues.
Soft tissue lasers can be used for simple forms of periodontal
surgery where the bone is not exposed. In non-surgical peri-
odontal therapy, the system with the most promising poten-
tial use is the Er:YAG system which is a hard tissue laser, the
goal being biolm and calculus removal. However, there is
the potential for damage to the root surface using this type • Figure 5.2.8 PerioWave system.
of system. A review of the literature on lasers in periodontal
therapy (Cobb 2006) concluded that there was insucient
evidence to suggest that lasers were superior to conventional Subgingival Air Polishing
therapy, either alone or as an adjunct. A statement issued by Subgingival air polishing has been developed from the
the American Academy of Periodontology in 2011, on the concept of supragingival stain removal using sodium bicar-
ecacy of lasers in the non-surgical treatment of chronic bonate powder sprayed under pressure. In subgingival use,
inammatory periodontal diseases, concluded: “Current such systems would damage the root surface so a much
evidence shows lasers, as a group, to be unpredictable and ner glycine powder (20 μm particles) has replaced sodium
inconsistent in their ability to reduce subgingival microbial bicarbonate and the pressure reduced by a disposable nozzle
loads beyond that achieved by SRP alone.” design (Figure 5.2.9). is system is not capable of remov-
Furthermore, the statement highlighted the potential ing calculus, simply of disrupting the bacterial biolm
for root surface damage because the root surface is being and, to date, it has not been evaluated as a means of initial
debrided without being visualised. A prospective randomised therapy but as an alternative to supportive therapy using
controlled trial in 2012 that compared the Er:YAG laser and conventional forms of instrumentation. In this context, it
mechanical debridement found better clinical outcomes for has been shown to be safe, more acceptable to patients and
the conventional mechanical debridement approach (Soo more time ecient (Moëne etal. 2010) and as eective as
etal. 2012). A systematic review by Salvi etal. (2020) found ultrasonic debridement (Wennström etal. 2011).
insucient evidence to recommend adjunctive application
of lasers to SI, and the EFP S3 guideline CR (Sanz et al. Instrumentation Strategies
2020) was to suggest not to use lasers as adjuncts to SI.
Several decisions about the instrumentation strategy need to
Photodynamic Disinfection be made before commencing treatment:
Photodynamic disinfection therapy (PDT) is a laser-based 1. Whether a PD or RP technique is to be used
treatment that involves the sensitisation of subgingival bac- 2. Which is the most suitable instrument to use
teria with a variety of dyes (for example methylene blue). 3. Whether local anaesthesia is required
e dye is taken up by the bacterial cell walls and when the 4. Whether a full-mouth or quadrant-by-quadrant approach
sensitised bacteria are exposed to low energy laser light the is to be taken.
dye molecules are dissociated with the subsequent release of
oxygen-free radicals that destroy the bacterial cell walls and RP or PD – Choice of Instruments
thus destroy the bacteria (Figure 5.2.8). Although such sys-
tems have been shown to be eective invitro, results from e clinician needs to decide at the outset exactly what the
clinical studies have been less convincing. A 2010 systematic therapeutic objectives are; if it is the intention to debride
review of the studies that have investigated the use of such the root surface but preserve tooth structure, then a suit-
systems, both as a stand-alone treatment or as an adjunct able debridement instrument should be chosen, but if it is
to conventional instrumentation, found that there was no intended to remove the outer layer of cementum, then a
evidence of the ecacy of PDT in periodontal therapy and planing instrument should be chosen. Used correctly the
concluded that the routine use of such systems could not ultrasonic tip is the most suitable debridement instrument
be recommended (Azarpazhooh etal. 2010). A systematic because it does not damage or remove any root surface. If
review by Salvi etal. (2020) found insucient evidence to RP is the goal, then a variety of sharpened hand instruments
recommend the use of PDT as an adjunct to SI, and the should be used. It is not logical to attempt debridement with
EFP S3 guideline CR (Sanz etal. 2020) suggested not to use a sharpened hand instrument because removal of some tooth
PDT as adjuncts to SI. structure is inevitable, nor is it possible to plane roots with
evidence that a smooth surface is necessarily a clean surface

or that a smooth surface is a necessary end point for success-
ful therapy (Cobb 2002). It has therefore been stated that:
“When one considers the demands of clinical skill, time and
stamina, the instrument of choice for universal application
would appear to be either a sonic or ultrasonic scaler” (Cobb
2002).
KEY POINT 5
“When one considers the demands of clinical skill, time and
stamina, the instrument of choice for universal application
would appear to be either a sonic or ultrasonic scaler” (Cobb
2002).
Use of Anaesthesia
• Figure 5.2.9 PerioFlow tip in use. Traditionally, local anaesthesia has been used to carry out
root surface instrumentation, but this has been based on the
an ultrasonic tip. An analogy would be to attempt to clean traditional use of sharpened hand instruments to carry out
a wood surface with a wood plane but without removing a RP technique which, being an invasive and tooth-destruc-
any of the wood surface. e choice of instrumentation for tive procedure, has necessitated some form of anaesthesia.
non-surgical therapy is therefore determined by the choice Although the use of local anaesthesia improves patient com-
of RP or PD as a treatment strategy. Given that the main fort, under these circumstances there are a number of disad-
objective of therapy is biolm disruption, with calculus vantages relating to its use: rst, the use of local anaesthesia
removal where possible and conservation of tooth structure, has forced clinicians into partial mouth treatment strategies
the instrument of choice would appear to be the ultrasonic (since it is impractical to anaesthetise the entire mouth in a
tip, and it is dicult, if not impossible, to justify the use of single session) which has resulted in the traditional QSRP
hand instruments in modern non-surgical periodontal ther- approach. us the mouth is treated by quadrant over four
apy. However, it is worth considering whether any clinical visits, under local anaesthesia, with 45–60 minutes treat-
studies have shown any benets of hand instrumentation. ment time per visit. Second, there is a risk of greater iatro-
genic damage to the root surface and soft tissues if the area
KEY POINT 4 is anaesthetised. As a result, patients often experience pain
Used correctly, the ultrasonic tip is the most suitable of signicant duration and magnitude following scaling
debridement instrument because it does not damage the root and RP (Pihlstrom etal. 1999). However, machine-driven
surface. instrumentation is non-invasive, as tooth structure is pre-
served, and local anaesthesia is usually not needed. Some
patients may have individual teeth where there is some
Hand vs Ultrasonic Instrumentation dentinal sensitivity, but this can usually be alleviated with
Several studies have directly compared hand and machine- desensitising agents and dietary control and by using the
driven instruments in non-surgical periodontal therapy. In instrument at lower power and with a reduced water sup-
all such studies, ultrasonic or sonic instrumentation has been ply. e shorter treatment time needed for machine-driven
shown to produce equal or superior clinical outcomes (e.g. Lie instrumentation and the reduced need for anaesthesia also
& Meyer 1977, Iouanniou etal. 2009). Several studies have permits the use of full-mouth treatment strategies, where all
reported on the increased time savings and therefore cost- diseased sites are treated at a single clinical session.
eectiveness of ultrasonic instrumentation, showing 20–50%
time savings (Checchi & Pelliconi 1988, Dragoo 1992, Full-Mouth or Quadrant Approaches?
Copulos etal. 1993, Drisko 1995). A systematic review of the
literature in 2002 (Tunkel etal. 2002) found no dierence in A series of studies carried out in the late 1990s questioned the
the ecacy of subgingival debridement whether using hand biological rationale of the quadrant approach to non-surgical
or machine-driven instruments, a nding that was repeated in periodontal therapy, suggesting that there was a risk of reinfec-
the systematic review by Suvan etal. (2020). Greater comfort tion of treated sites by microorganisms from untreated sites,
of ultrasonic devices for patients, with less postoperative pain, and proposed a “full-mouth approach” as an alternative, the
has also been noted (Iouanniou etal. 2009). One of the argu- object being to instrument all pathological pockets at a single
ments for using hand instruments has been the production of session, or within a 24-hour period (Quirynen etal. 1995,
greater root surface smoothness; although hand instruments 1999, Bollen etal. 1996, 1998, Vandekerckhove etal. 1996,
have been shown to produce smoother root surfaces than Mongardini etal. 1999). e results of these studies showed
ultrasonic instruments (Schmidlin et al. 2001), there is no that the full-mouth-treated patients achieved better clinical
and microbiological treatment outcomes. e patients in (CHX) in various formulations, none of these putative
these studies were treated using a RP instrumentation tech- adjuncts to SI oered any benets as adjuncts to SI and
nique, and the full-mouth-treated groups also received exten- none was recommended as such by the EFP S3 clinical
sive chlorhexidine gluconate application as an adjunct, both guideline (Sanz et al. 2020). With respect to CHX, the
during and after treatment. e test treatment was referred EFP S3 clinical guideline considered that CHX mouth
to as FMD. Later studies showed that the benets of the test rinse, used for a limited time period, could be consid-
treatments were because of the full-mouth approach and ered as an adjunct to SI in specic cases (da Costa et al.
not because of the use of chemical adjuncts (Quirynen etal. 2017). An example of such a case might be a patient who
2000). Subsequent studies (Koshy et al. 2005) used a full- presented with extensive marginal inammation that pre-
mouth debridement technique with ultrasonics exclusively for vented them from carrying out adequate self-care at home.
both test and control groups (FMUD vs QUD) and achieved e EFP guideline also found that locally delivered sus-
the same results. e ecacy of the full-mouth approach was tained-release CHX could be considered in patients with
conrmed in a 2008 Cochrane systematic review (Eberhard periodontitis (Herrera et al. 2020), although the clinical
etal. 2008). Several studies have directly compared FMUD benets remained small, amounting to a pocket reduction
with QSRP (Wennström etal. 2005, Zanatta etal. 2006, Del eect of only about 10%.
Peloso Ribiero etal. 2008) and have found that an hour (or
less) of the FMUD treatment is as eective (clinically, micro- Conclusions
biologically and immunologically) as 4 hours of QSRP and
“oers tangible benets for the chronic periodontitis patient” e principal objective of non-surgical therapy (or surgical
(Wennstrom etal. 2005). However in terms of clinical treat- therapy for that matter) is the disinfection of the periodon-
ment outcomes (reduction in inammation, pocket depth tally involved root surface (Lindhe & Echeverria 1993).
and number of diseased sites) there would appear to be little e main source of microbial contamination on the root
or no dierence between quadrant or full-mouth approaches, surface is the bacterial biolm, and it is biolm disrup-
and the EFP S3 clinical guideline (Sanz et al. 2020, West tion/removal that is the treatment goal. Removal of root
etal. 2021) suggested that SI can be carried out with either surface calculus can enhance biolm removal, but subgin-
approach, based on the systematic review by Suvan et al. gival calculus does not per se have pathogenic potential.
(2020). One argument against the full-mouth approach has It is no longer justied to remove root surface cementum.
been the possibility that this treatment strategy may produce e choice of instrumentation should reect these treat-
a systemic acute-phase inammatory response that may have ment objectives, and there is a strong case for not treating
the potential to be harmful to patients, especially those with root surfaces with potentially damaging hand instruments
vascular co-morbidities. One study (Graziani etal. 2015) has but instead to use lighter forms of instrumentation such as
shown that full-mouth treatment may trigger a moderate ultrasonic devices.
acute-phase response compared to a quadrant approach. e
signicance of this nding is unclear at this time. KEY POINT 7
The main source of microbial contamination on the root
surface is the bacterial biolm, and it is biolm disruption/
KEY POINT 6 removal that is the treatment goal.
An hour (or less) of FMUD treatment is as effective (clinically,
microbiologically and immunologically) as 4 hours of QSRP.
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5.3
ANTIBIOTICS IN THE
MANAGEMENT OF
AN D R E W WA L K E R
CHAPTER OUTLINE
The Rationale for Antibiotic use Evaluating Studies which use Antibiotics as Adjuncts to RSD
Which Periodontal Conditions can be Treated with The Evidence for Antibiotic use in Periodontal Therapy
Antibiotics? Local Delivery Antibiotics
Reasons for the Failure of Root Surface Debridement Systemic Delivery Antibiotics
Antibiotics as an Alternative Monotherapy to RSD Recommendations on the use of Systemic Antibiotics in
Periodontal Therapy
Comparison of Local or Systemic Delivery of Antibiotics

This chapter will explore the rationale for antibiotic use and indicate which periodontal conditions can be treated with antibiotics. It will
examine the reasons for failure of root surface debridement (RSD) and assess the role of antibiotics as an alternative monotherapy to
RSD. Local and systemic delivery of antibiotics will be compared, with reference to current evidence, and evaluation of such studies will be
discussed. Current evidence to support or refute antibiotic use in daily practice will then be examined.
By the end of the chapter the reader should: • The rationale for antibiotic use
• Understand why RSD sometimes fails • Which periodontal conditions can be treated with antibiotics
• Recognise when it might be appropriate to use antibiotics in • Reasons for the failure of RSD
periodontal therapy • Antibiotics as an alternative monotherapy to RSD
• Be able to evaluate studies which investigate antibiotic use • Comparison of local or systemic delivery of antibiotics
in periodontal therapy. • Evaluating studies which use antibiotics as adjuncts to RSD
The chapter covers the following topics: • The evidence for antibiotic use in periodontal therapy
• Recommendations on the use of antibiotics.
The Rationale for Antibiotic use not succeed, we may employ chemicals in the form of anti-
septics or antibiotics. Failure of these procedures to resolve
If it is believed that periodontal diseases are infections the problem might result in the need for surgical excision to
(which is in fact debatable – see Chapter 1.2), then we need remove infected tissue. e wound can then be closed with
to focus on controlling the infection in much the same way healthy margins being opposed. If infection of the wound has
as we would control infection elsewhere in the body. become advanced, then more radical excision may need to be
It is helpful to think of periodontitis as having parallels considered, which could include amputation of the limb. e
with an open wound on the forearm. Basic concepts of man- parallels with periodontal management are clear:
aging the forearm wound would involve debridement to 1. wound debridement = root surface debridement
remove foreign bodies and reduce bacterial load. If this does 2. antiseptics or antibiotics = antiseptics or antibiotics
222
CHAPTER 5.3 Antibiotics in the Management of Periodontal Diseases 223
3. excision of wound margins = periodontal surgery management of infections in general. is focuses on remov-
4. limb amputation = tooth extraction. ing the source of infection and establishing drainage when
e sites which most commonly fail to respond to RSD possible. Depending upon the clinical circumstances, this
are usually dicult to instrument, and this may be because may be achieved through incision of the mucosa, debride-
the pocket depth is deep, there are multiple roots or there are ment of the pocket or a pulpal access cavity. ese actions
infra-bony defects. is may result in an inability to reach along with mechanical debridement reduce the bacterial
and disrupt the biolm in these areas. ere may be a need load and allow wound healing to occur in most instances.
for chemical agents, such as antibiotics, to act as an adjunct e presence of pyrexia, lymph node involvement and
to the mechanical debridement at such sites. An alternative swelling in the fascial spaces may require the use of antibiot-
form of treatment would be periodontal surgery, which needs ics, but this should be the exception rather than the norm.
a higher level of training and skill, is more costly and more
invasive. erefore, if the eects of non-surgical periodontal KEY POINT 4
therapy could be improved by the use of adjunctive antimi- The presence of pyrexia, lymph node involvement and swelling
crobial therapies, it might be possible to achieve healthy tis- in the fascial spaces may require the use of antibiotics, but this
sues without the need for invasive surgical techniques. should be the exception rather than the norm.
Most periodontal treatment is focused on mild, moderate,
Since bacteria are the initiating agents of periodontal dis- or severe periodontitis (stages I–III), with a small but important
eases, systemically or locally administered antibiotics are con- percentage having very severe periodontitis (stage IV). Hospital
sidered as possible adjuncts for their control. However, studies and specialist practices may also encounter patients who
on the ecacy of these agents show inconsistent results. have periodontitis as a manifestation of systemic disease. The
use of antibiotics has been considered a possibility for the
management of most types of periodontitis, apart from the
KEY POINT 1 most mild forms.
Sites which most commonly fail to respond to root surface
debridement are usually difcult to instrument.
KEY POINT 2 Reasons for the Failure of Root Surface

There may be a need for chemical agents such as antibiotics Debridement
to act as an adjunct to mechanical debridement at non-
responding sites. e conventional treatment of periodontal diseases involves
cause-related therapy, directed at reducing the bacterial
load. e objective is to cause a shift in the microora of
KEY POINT 3 the gingival sulcus/pocket to one that is compatible with
Because bacteria are the initiating agents of periodontal
gingival health, allowing inammatory resolution. Non-sur-
diseases, systemically or locally administered antibiotics are
considered as possible adjuncts for their control. However, gical periodontal therapy includes oral hygiene advice and
studies on the efcacy of these agents show inconsistent professional debridement of the gum pocket (see Chapter
results. 5.2). For most patients, this approach is eective, but the
outcome varies depending upon the original pocket depth.
If the poor response is widespread then operator and
Which Periodontal Conditions can be patient-based factors should be considered. If sites have
Treated with Antibiotics? responded and others are refractory to treatment, then more
local factors should be considered. Common causes for a
Several classication systems have been used over the years, poor response to RSD include:
and in 2017 a new worldwide classication system was intro- 1. Operator factors
duced. Under the new classication (Tonetti & Sanz 2019, a. poor-quality RSD performed
Dietrich etal. 2019), the rst part of diagnosis involves stag- b. inexperienced operator
ing the periodontitis by assessing the degree of bone loss. is c. not enough time allocated to instrument adequately all
allows the periodontitis to be classied as either initial (I), the sites
moderate (II), severe (III) or very severe (IV). e speed of pro- 2. Patient factors
gression is then estimated by comparing the bone loss against a. poor oral hygiene
the age of the patient. e speed of progression is graded as b. smoking
c. systemic diseases such as diabetes giving a poor response
slow (A), moderate (B), or rapid (C). For further information
to treatment
about the most recent classication, see Chapter 2.1
3. Site factors
Within the latest classication system, more acute con- a. very deep pockets, where the operator fails to instru-
ditions exist, such as necrotising periodontal diseases, ment to the base
abscesses of the periodontium and periodontitis associated b. intra-bony defects where the base is inaccessible without
with endodontic lesions. Although it may be tempting for surgical access
the clinician to prescribe antibiotics immediately for these c. tooth and root morphology, such as furcation defects,
conditions, it is important to adhere to the principles for the grooves and hollows
4. Bacterial invasion of the tissues TABLE Comparison of local and systemic

a. gingiva 5.3.1 antibiotic use
b. dentinal tubules.
Systemic Local
If response has been poor, then further treatment options
should be considered, including: Sites treated All sites including Only treated
1. a second cycle of RSD tongue, tonsillar pockets
tissues, etc.
2. a second cycle of RSD with adjunctive antimicrobials
3. periodontal surgery Concentration Spread all over High in treated
4. supportive periodontal care body, lower at sites
sites of interest
5. extraction.
Periodontal therapy often results in pocket reduction, Limitations Relies on patient Re-infection from
but it is common to nd residual pockets of 4–5 mm compliance, non-treated
adverse side
post-treatment. At this stage, if the oral hygiene is good
effects of GCF
and there is no bleeding on probing, such pockets can washing
be maintained with appropriate supportive periodontal
care. It has been suggested that sites with pockets ≥6 GCF: gingival crevicular uid
mm have an increased risk of disease progression and

an increased risk of tooth loss. As a consequence, this
should be “viewed as incomplete periodontal treatment”
(Matuliene etal. 2010) and further treatment should be COMPARISON OF LOCAL OR SYSTEMIC
provided. DELIVERY OF ANTIBIOTICS
Since bacteria have a causative role in periodontal dis-
ease aetiology, the use of antibiotics in therapy can be e antibiotic agent needs to be in the right location, with
considered. Extensive research has investigated a wide a high enough concentration, for a long enough period of
range of drugs, at varying dosages, for dierent time peri- time, to be eective. ere are dierent ways of delivering
ods, using dierent routes of administration, to patients antimicrobial agents and, in periodontology, there is the
with dierent forms of periodontal diseases. ese have choice of either systemic or local delivery. Systemic antibi-
been evaluated both as adjuncts to non-surgical and sur- otics are usually administered orally, and local antibiotics
gical treatments and as monotherapies in the absence of are placed directly into the periodontal pocket by means of
RSD. a carrier. Comparisons of both delivery systems follow and
are summarised in Table 5.3.1
Systemic antibiotics have the advantage that all sites
Antibiotics as an Alternative Monotherapy are treated, including areas such as the tongue and ton-
to RSD sillar crypts, which are areas thought to be implicated in
the recolonisation of pockets. e disadvantages are more
ere has been some research that shows antibiotics as a widespread adverse side eects, achieving high enough drug
monotherapy may impact the bacteria and improve peri- levels in periodontal pockets and the reliance on patient
odontal health equivalent to that achieved with RSD in compliance.
the short term (López et al. 2006). is is a controversial Advantages of local delivery include assured compliance,
issue, and whilst it does pose an interesting question, a high minimal systemic exposure and drug levels which far exceed
level of caution must be used when interpreting the results the mean inhibitory concentration for key periodontal
of this study and applying it to clinical practice. ere are pathogens. e time that therapeutic drug levels are main-
several aws in the study by López et al., and for a more tained often depends on the delivery vehicle. Preparations
in-depth review of the paper the reader is directed to the such as gels are washed away from the pocket by gingival
online content. crevicular uid, hence protocols usually recommend a sec-
Such an approach would ow against the drive for medi- ond or third application. More solid vehicles, such as bres
cal professionals to reduce the amount of antibiotics pre- or chips, are retained longer, but then have the problem of
scribed because of concerns surrounding hypersensitivity adequate and consistent drug release from the vehicle.
and development of resistant strains. Furthermore, using A wide range of systemic antibiotics have been evaluated
antibiotics as a monotherapy would be contrary to one of the in the management of chronic or aggressive periodontitis,
paradigms of clinical periodontology: that RSD is the key and Table 5.3.2 lists some of the more widely used and
intervention to treat periodontal diseases. Indeed, the Euro- investigated.
pean Federation of Periodontology S3 level clinical practice Local delivery systems include a range of dierent drugs
guideline (Sanz et.al. 2020), adopted by the British Society and vehicles. Gel systems, applied by syringe, include 25%
of Periodontology and Implant Dentistry (BSP) (West etal. metronidazole and 2% minocycline. ese are quickly and
2021), recommends all periodontitis patients undergo oral easily applied to pockets and can readily be used at multiple
hygiene instruction and professional debridement. sites. However, their substantivity is less assured as they are
TABLE Systemic antibiotics in the management

5.3.2 of periodontal diseases
Commonly used single

therapies Combination therapies
Metronidazole Amoxicillin and
Tetracycline group metronidazole
Penicillin group
Azithromycin
• Figure 5.3.2 25% tetracycline hydrochloride.
• Figure 5.3.1 2% minocycline gel.
washed out of the pocket by crevicular uid. Consequently,

the protocols recommend that the dosage is repeated on sev- • Figure 5.3.3 Chlorhexidine chip.
eral occasions. Chlorhexidine (2.5 mg) can be applied in
a degradable gelatin chip, 25% tetracycline hydrochloride
in a non-resorbable bre and doxycycline hyclate in a gel/ for any professional to be able to critically appraise the lit-
sol carrier. Examples of local delivery devices are shown in erature so that they can provide the most clinically eective,
Figures 5.3.1–5.3.4 and the most cost-eective, treatment for their patients.
e literature can be confusing, and similar studies
KEY POINT 5 undertaken by dierent research groups can often produce
Locally applied systems for antibiotics are quickly and easily conicting results. A few key skills in critical appraisal can
applied to pockets and can readily be used at multiple sites.
However, their substantivity is less assured as they are washed
equip the reader in analysing published papers. ese are
out of the pocket by crevicular uid. summarised below, but the reader is encouraged to use the
online content for more in-depth guidance.
Carefully examine the research methods presented:
Evaluating Studies which use Antibiotics 1. Is there a clear objective, asking a question that you are
as Adjuncts to RSD interested in?
a. “Do antibiotics provide additional benet when used as
As resistant strains of bacteria emerge, and new antibiotics an adjunct to RSD?”
are produced, it is impossible to provide specic protocols b. “What degree of improvement do antibiotics give over
and regimens for clinical practice. Research into both local RSD alone and is it clinically relevant?”
and systemic antibiotics is constantly published (more than 2. Are the outcomes clearly dened?
2000 papers on the subject), and this information is often 3. Is there a control group and is it appropriate? Was there
distributed to the dental profession by manufacturers aim- adequate randomisation between the control and test
ing to support a particular product. It is therefore important groups?
The Evidence for Antibiotic use in

Periodontal Therapy
Local Delivery Antibiotics
A systematic review (Matesanz-Pérez etal. 2013) reported
on studies that tested one or more chemical antimicrobial
agents as an adjunct to RSD alone or in comparison with
placebo. Fifty-two studies were reported in 56 publications
(some tested more than one antimicrobial agent). Over-
all, it was found that adjunctive local antibiotic therapy
reduced pocket depth levels with a weighted mean dier-
ence (WMD) of 0.41 mm. However, the authors indicated
that even when the dierences were statistically signicant,
eects were modest in some studies. Data were reported
separately for the dierent antimicrobials, but these dif-
ferences were described as marginal and a fraction of the
improvement achieved by RSD alone. e review suggested
that these results should be interpreted with caution because
such improvements, even if statistically signicant, had
• Figure 5.3.4 25% metronidazole gel.
questionable clinical relevance.
e key outcome variable described in this systematic
review is additional reduction in “weighted mean pocket
4. Were researchers blinded as to who was in the control depth” achieved by the adjunctive therapy. As discussed in
and test groups? the critical appraisal section, we never measure a patient’s
5. Has a “power calculation” been performed to help deter- mean probing pocket depth, and hence the improved out-
mine appropriate sample size? come of 0.18–0.73 mm is not something we can readily
a. Many studies have inadequate sample sizes translate to our patients. In one study from this systematic
b. Underpowered studies are misleading review (Griths etal. 2000), RSD alone resulted in a 1.0
c. Systematic reviews and meta-analysis can to some extent mm mean pocket probing depth (PPD) reduction, whereas
compensate for small sample sizes. with RSD plus metronidazole gel, the mean pocket depth
Critical analysis of data: reduction was 1.5 mm. Because this means of reporting the
1. Did the control group achieve the outcomes you would data is not ideal, the study by Griths et al. (2000) and
expect? other more recent studies have tended to present the results
a. Are results comparable to the Cobb (2002) review? using information that clinicians often use in practice. Table
2. What is the magnitude of the dierence between the test 5.3.3 shows the results as a percentage of the sites represent-
and control group? ing “successful treatment” or sites showing improvement by
a. Described as a collective mean pocket depth reduction
more than 2 mm.
b. Subdivided into outcomes for shallow, moderate and
deep pockets A more recent systematic review of local antimicrobials
3. Can I translate the outcomes to patients in my practice? (Herrera et al. 2020) reviewed 50 independent investiga-
a. e dierence between treatment groups is usually tions and found that there was a range of study designs.
described as the mean change in mm, yet we never cal- e ndings of this review were that in short-term studies
culate this for patients of 6–9 months, local antimicrobials reduced pocket depth
b. e percentage of sites that needed treatment initially levels with a WMD of 0.37 mm. For longer-term studies
and are then deemed healthy after treatment is a better (12–60 months) a statistically signicant WMD in pocket
measure of success: depth reduction of 0.19 mm was found. Again, the data for
i. All sites >3 mm are treated so studies report the individual antimicrobials were presented, as were changes
change in the number or % of such sites in clinical attachment loss (CAL), and interestingly the
ii. Sites <6 mm are considered maintainable (Matu- data from the long-term studies did not show signicant
liene etal. 2010); the number or % of sites con- improvement in CAL for any of the antimicrobials.
verting to this depth post-treatment would be Overall, the evidence suggests that most of the local
another clinically relevant outcome. adjuncts could confer an additional clinical benet, and the
European S3 level clinical practice guideline advises that
KEY POINT 6 they may be considered. However, it should be remembered
As resistant strains of bacteria emerge, and new antibiotics that the results and conclusions drawn from a systematic
are produced, it is impossible to provide specic protocols and review are only as good as the original studies. is was
regimens for clinical practice.
highlighted in the discussion of the 2020 review which also
concluded that the high risk of bias and the heterogeneity Systemic Delivery Antibiotics
of the studies makes it very dicult to dene when and
where such products would be of use. Another aspect the Two systematic reviews, Herrera et al. (2002) and Haajee
clinician must consider in relation to using a local antimi- etal. (2003), summarised the literature relating to the role of
crobial is careful analysis of the cost of this gain in nancial systemic antibiotics in the management of periodontal diseases
(Heasman etal. 2011) and environmental (Needleman and dened by the 1999 classication. ese reviews revealed that
Wilson 2006) terms. systemic antibiotics were consistently benecial in providing
an improvement in the clinical outcomes of gain in attachment
and pocket depth reduction when used as adjuncts to RSD.
TABLE “Clinically relevant measures of successful Chronic periodontitis (as dened by the 1999 classica-
5.3.3 treatment” as alternatives to mean tion): Systemic antibiotics used as an adjunct to RSD were
pocket reduction in studies examining found to oer additional benets over RSD alone, especially
the adjunctive eect of local delivery in deep pockets.
antibiotics Aggressive periodontitis (as dened by the 1999 classica-
tion): e limited information available showed that the
RSD RSD + gel Difference adjunctive eect of some antimicrobials might be greater
Mean 1.0 1.5 0.5 in aggressive forms of periodontitis. Figure 5.3.5 shows a
reduction in patient with aggressive periodontitis who has been treated
PPD (mm) with systemic antibiotics as an adjunct to RSD.
% Improved to 18.0 30.0 12.0 ese conclusions were based on mean change in PPD or
≤3 mm mean gain in attachment. e mean gain in attachment was
% Improved by 32.0 47.0 15.0
0.3–0.4 mm at 6 months, but this was based on whole-mouth
≥2 mm data and was diluted by the inclusion of healthy sites which
would not be expected to change. ese mean clinical val-
Adapted from data presented in Grifths et al. 2000. PPD: pocket prob-
ues may have little clinical relevance, although Haajee etal.
ing depth; RSD: root surface debridement; RSD + gel: RSD with adjunc-
tive metronidazole gel. (2003) put it into some clinical context when she described it
as “equivalent to reversing 4–7 years of disease progression”.
B C
• Figure 5.3.5 A patient diagnosed at the time with aggressive periodontitis treated with adjunctive sys-
temic antibiotics. (A) Radiographic appearance on presentation. (B) Clinical appearance on presentation.
(C) Clinical appearance after treatment.
TABLE “Clinically relevant measures of successful recruited patients with periodontitis stages III and IV. As such,
5.3.4 treatment” as alternatives to mean pocket it remains the case that systemic antibiotics may be considered
reduction in studies examining the for the management of periodontitis, but their use should be
adjunctive eect of systemic antibiotics. restricted to certain groups, such as those with severe and pro-
gressing forms of periodontitis. e S3 level clinical guideline
RSD + further advises that systemic antibiotics should not be used
adjunctive Difference routinely but may be considered for specic patient catego-
RSD antimicrobials (mm) ries, such as generalised periodontitis stage III in young adults
Mean reduction 0.7 1.2 0.5 where a high rate of progression is documented.
in PPD (mm)
% Improved to 37 55 18 Recommendations on the Use of Systemic
≤3 mm
Antibiotics in Periodontal Therapy
% Improved by 21 30 9
≥2 mm Despite the large number of research investigations in this
Clinically relevant data adapted from Guerrero et al. (2005) and area, it is still dicult to provide clear guidance on antibi-
et al. (2011). PPD: pocket probing depth; RSD: root surface debride- otic use in periodontics because of small sample sizes and
ment; RSD + Adj: RSD plus adjunctive amoxicillin and metronidazole.
study heterogeneity. It seems clear that antibiotics con-
fer therapeutic advantage, but questions still remain as to
whether they should be part of routine use or restricted to
As illustrated previously with local delivery antibiotics, individuals with “severe periodontal breakdown”.
more clinically relevant methods of data presentation have Further research needs to be undertaken to show ecacy
been used. is is illustrated in Table 5.3.4, which shows in terms of patient-centred outcomes and cost-eectiveness.
results adapted from Guerrero etal. (2005) and Griths etal. e timing of delivery of antibiotics is also important as
(2011), which was a study comparing RSD alone with RSD shown by Griths et al. (2011), and this needs further
plus adjunctive amoxicillin and metronidazole in patients with investigation.
aggressive periodontal disease. e dierence in the mean full- Side eects of antibiotic use should be considered,
mouth PPD before and after RSD was 0.7 mm and, with which, on an individual basis, can range from the relatively
adjunctive antimicrobials, it was 1.2 mm. It is dicult when common nausea/vomiting to anaphylaxis. On a population
using these mean data derived from the mean of all sites in basis, there are concerns over resistant strains (Feres et al.
all subjects to decide whether this has clinical relevance to an 2002, Needleman & Wilson 2006).
individual patient, particularly as these are not data that we Appropriate antibiotic stewardship is a prominent issue
usually record for our patients. Data presentation using infor- for dental professionals, and so careful thought must be
mation we use in the clinic showed that adjunctive systemic given to weighing up the risks and benets of any prescrip-
antimicrobials resulted in an additional 18% of sites convert- tion. Numerous professional guidelines are available to help
ing from needing treatment to not needing treatment. ey with the decision-making process in clinical practice. In
also resulted in an additional 9% of sites improving by ≥2 mm. particular, the Faculty of General Dental Practice UK pub-
A further review (Teughels etal. 2020) again found that lication Antimicrobial Prescribing in Dentistry: Good Practice
systemic antibiotics result in statistically signicant improve- Guidelines, 3rd Edition (2020) is a useful resource. Alter-
ments in periodontal parameters. is review identied 28 native treatment options to antimicrobials should always
randomised controlled trials and found that the adjunctive be considered, and for those in general practice, that may
use of systemic antibiotics in the active phase of periodontal include consideration as to whether referral for specialist
treatment resulted in a WMD full-mouth pocket reduction opinion and/or treatment is warranted.
of 0.45 mm and CAL gain of 0.39 mm at 6 months. It
further found that these benets were present for at least
a year (PPD WMD 0.49 mm, CAL WMD 0.23). Specic KEY POINT 7
data was reported for dierent antibiotic regimens, but the Current recommendations are as follows:
• antibiotics should be considered in periodontal
strongest evidence was found for the use of a combination treatment planning
of amoxicillin and metronidazole, and this was more pro- • antibiotics should not be used in all cases of
nounced in initially deep pockets. Interestingly, this review periodontitis
was unable to show any statistically signicant dierence in  • if antibiotics may be required, consider seeking a
the benet of using systemic antimicrobials for aggressive specialist opinion
• antibiotics may be considered in the following
periodontitis over chronic periodontitis. circumstances:
Similar to previous reviews, Teughels et al. (2020) con-  • severe periodontal disease (multiple deep sites with
cluded that it remained debatable whether the improvements pus discharge)
found were clinically relevant, and it highlighted the lack of  • patients who failed to respond to conventional
conclusive evidence for the long-term benet of systemic anti- periodontal therapy
 • young patients with severe disease
microbials. It was also noted that the vast majority of studies
Multiple choice questions on the contents of this chapter scaling and root planing in periodontitis patients. J Clin Periodon-
are available online at Elsevier eBooks+. tol. 2002;29(Suppl. 3):136–159.
Herrera D, Matesanz M, Conchita M, Oud V, Feres M, Teughels W.
Adjunctive eect of locally delivered antimicrobials in periodonti-
References tis therapy: a systematic review and meta-analysis. J Clin Periodon-
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Cobb CM. Clinical signicance of non-surgical periodontal therapy: López NJ, Socransky SS, Da Silva I, Japlit MR, Haajee AD. Eects
an evidence-based perspective of scaling and root planing. J Clin of metronidazole plus amoxicillin as the only therapy on the
Periodontol. 2002;29(Suppl. 2):6–16. microbiological and clinical parameters of untreated chronic peri-
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Griths GS, Smart GJ, Bulman JS, Weiss G, Shrowder J, Newman Needleman I, Wilson M. Antimicrobial resistance in the subgin-
HN. Comparison of clinical outcomes following treatment of gival microora in patients with adult periodontitis. A com-
chronic adult periodontitis with subgingival scaling or subgingival parison between e Netherlands and Spain. J Clin Periodontol.
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917. Palmer, N. (Ed). Antimicrobial Prescribing in Dentistry: Good Prac-
Griths GS, Ayob R, Guerrero A, Nibali L, Suvan J, Moles DR, tice Guidelines. 3rd Edition. London, UK: Faculty of General
Tonetti MS. Amoxicillin and metronidazole as an adjunctive treat- Dental Practice (UK) and Faculty of Dental Surgery; 2020.
ment in generalized aggressive periodontitis at initial therapy or Sanz M, Herrera D, Kebschull M, Chapple I, Jepsen S, Beglundh T,
re-treatment: a randomized controlled clinical trial. J Clin Peri- Sculean A, Tonetti MS. Treatment of stage I–III periodontitis—
odontol. 2011;38:43–49. e EFP S3 level clinical practice guideline. J Clin Periodontol.
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Tonetti MS. Adjunctive benets of systemic amoxicillin and met- Teughels W, Feres M, Oud V, Martín C, Matesanz P, Herrera D.
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5.4
Assessment of Treatment
Outcomes and Supportive
Periodontal Therapy
VA L E R I E C L E R E H U G H
CHAPTER OUTLINE
Introduction SPT Frequency
What is Supportive Periodontal Therapy? SPT Appointment
Examination, Re-Evaluation, Re-Diagnosis
Gingival Inammation Oral Hygiene Motivation and Re-Instruction
Value of SPT Risk Assessment
Assessment of Treatment Outcomes Assessing Risk during SPT
When and How to Provide SPT
SPT Plan

This chapter explains the meaning of supportive periodontal therapy (SPT). The role of gingival inammation in disease pathogenesis is
explored. This leads into a discussion of the value of SPT in maintaining periodontal health and preventing tooth loss. Consideration is given
to the assessment of treatment outcomes following SPT and when and how best to provide SPT, including the importance of plaque biolm
control and patient motivation in the context of the stepwise approach to periodontal therapy and the S3 clinical treatment guidelines.
Various models of periodontal risk assessment during SPT are covered.
By the end of the chapter the reader should be able to: The chapter covers the following topics:
• Explain what is meant by supportive periodontal therapy • Introduction
(SPT) • What is SPT?
• Understand the role of SPT in managing patients with • Gingival inøammation
periodontal diseases • Value of SPT
• Understand how SPT öts into the stepwise approach to • Assessment of treatment outcomes
periodontal therapy • When and how to provide SPT
• Outline the assessment of treatment outcomes following SPT • Risk assessment
• Outline key aspects of SPT.
230
CHAPTER 5.4 Assessment of Treatment Outcomes and Supportive Periodontal Therapy 231

SPT consists of “therapeutic measures to support the patient’s
Periodontal therapy has traditionally been undertaken in own efforts to control periodontal infections and avoid
three phases: initial, corrective and supportive, each with a re-infections” (Lang etal. 2008).
number of stages. However, this approach has been super-
seded by a four-step stepwise approach to periodontal treat-
ment which evolved following the 2017 World Workshop KEY POINT 2
on Classication of Periodontal and Peri-implant Diseases Although the dental professional is responsible for providing
and Conditions (Caton etal. 2018), and the development the necessary therapeutic measures to achieve the best
possible outcome, the patient has a key role in maintaining
by the European Federation of Periodontology (EFP) of their periodontal health.
a set of stringent S3-level, evidence-based guidelines and
clinical recommendations (CRs) for the management of Other important goals are to:
stages I–III periodontitis (Sanz et al. 2020). e reader is • prevent or minimise any disease recurrence or progression
directed to Chapter 4.3 and Appendix 3 for further details • prevent or reduce the incidence of tooth loss or implant
of the stepwise approach and an explanation of the devel- loss by monitoring the dentition, prosthetic replace-
opment of the EFP S3 guidelines. e British Society of ments and implants
Periodontology and Implant Dentistry (BSP) adapted these • treat any diseases found during the examination
EFP S3-level guidelines and produced UK Clinical Prac- • ensure adequate control of supragingival plaque bioëlm
tice Guidelines for the Treatment of Periodontal Diseases by the patient.
illustrating the four-step sequence for the practitioner to To achieve these goals, it is necessary to ensure:
follow for the treatment of periodontal diseases in the UK • regular clinical assessments and recall periodontal main
healthcare system, covering the spectrum from periodontal tenance visits tailored to each patient
health to gingivitis and periodontitis (West etal. 2021; see • appropriate interceptive periodontal therapy
Appendices 3 and 4), with SPT forming the basis of step 4. • continued psychological support, encouragement and
motivation for the patient
What is Supportive Periodontal Therapy? • life-long commitment by the patient
• life-long commitment by the dental professionals sup
SPT (AAP 1998, Lang etal. 2008) embraces the philosophy porting the patient.
that both the patient and dental professional are involved in e biological basis of SPT takes into account several
maintaining the patient’s periodontal health. factors. ese are shown in Box 5.4.1
SPT is directed at supporting the patient in maintain-
ing their periodontal health and preventing recurrence or Gingival Inflammation
progression of the disease. Although the dentist, hygienist
or therapist is responsible for the provision of the profes- Although the microbial aetiology of periodontal diseases
sional periodontal treatments, the patient must be proactive is well-documented, the role of gingival inammation in
if they are successfully to maintain periodontal stability. e disease pathogenesis has been increasingly recognised. In
maintenance of successful periodontal outcome is weighted a classic longitudinal study of the natural history of peri-
heavily towards the contribution of the patient (Figures odontal diseases in 565 middle-class, dentally aware Nor-
5.4.1 and 5.4.2). wegian males, it was reported that teeth with consistently
e main objective of SPT is to preserve the gingival and inamed gingiva showed greater clinical loss of attach-
periodontal health achieved following the previous active ment over 26-years observation (Schatzle et al. 2003,
phases of periodontal therapy. It is important to prevent or Lang etal. 2009). Sites with consistent bleeding (Gingival
minimise the recurrence of disease progression in all patients Index (GI) = 2) had 70% more clinical loss of attachment
treated for gingivitis, periodontitis and peri-implantitis and than sites that were consistently non-inamed (GI = 0)
take account of their level of periodontal risk. (Figure 5.4.3).
Professional
Patient
• Figure 5.4.1 Balance of professional versus patient.

Patient’s
sites that do not progress have less gingival inammation
contribution over time (Löe et al. 1986, Ismail et al. 1990, Clerehugh
etal. 1995, Albandar etal. 1998, Schatzle etal. 2004, Tan-
ner etal. 2007, Ramseier etal. 2017, Chapple etal. 2018).
For the rst time, the 2017 World Workshop on classi-
Professional cation gave clear denitions of periodontal health and gingi-
contribution vitis on an intact periodontium, on a reduced periodontium
due to causes other than periodontitis and on a reduced
• Figure 5.4.2 Patient’s and professional’s contribution to maintaining periodontium due to periodontitis (Chapple etal. 2018).
oral health.
KEY POINT 3
• BOX 5.4.1 Biological Basis of SPT Gingival inammation is a precursor of periodontitis and a
clinically relevant risk factor for periodontal clinical attachment
Plaque biolm aetiology of periodontal diseases loss and tooth loss.
Balance between microbial challenge, patient’s host defences,
conducive environment/plaque biolm ecology
Individual patient risk assessment
Role of inammation
KEY POINT 4
Less clinical attachment loss (CAL) and tooth loss occur with Clinically healthy gingivae are a prognostic indicator of tooth
regular SPT longevity.
Tooth loss is inversely proportional to SPT frequency
Recurrent periodontitis can be limited or prevented by optimal
oral hygiene Overall these studies emphasise the importance of:
SPT provides for monitoring following periodontal treatment or • the prevention and treatment of periodontal diseases
implant provision • maintaining periodontal health and avoiding recurrence
of disease and inammation
• the role of SPT.
Subgingival calculus formation increased the odds ratio Value of SPT

of progressing from gingivitis to periodontitis (attachment
loss) from 3.22 to 4.22 for the GI = 2 group compared to Many studies have been published since the 1970s that
the GI = 0 group. Furthermore, there was signicantly more have demonstrated the value of SPT (including Suomi etal.
cumulative tooth loss for those with the highest severity rat- 1971, Axelsson and Lindhe 1981, Becker et al. 1984a, b,
ing (GI severity group III) for teeth which consistently had Axelsson etal. 2004).
bleeding on probing (GI = 2) in all sites and at all observa- Compared to patients without SPT or with less SPT,
tions compared with GI severity group I, who never had patients receiving regular SPT have:
bleeding on probing over the 26-year study period (Figure • reduced risk of tooth loss
5.4.4). • reduced risk of clinical attachment loss (CAL)
“Tooth age” was calculated in order to determine cumu- • decreased probing pocket depth (PPD).
lative tooth survival data for the dierent levels of gingival Recurrence of periodontitis can be prevented, or limited,
inammation – this was based on published national data by optimal personal plaque control and through periodic
on permanent tooth eruption dates and depended on the professional SPT.
survey dates of when the tooth was last present and then A systematic review (Chambrone etal. 2010) assessed
subsequently lost (see Schatzle etal. [2004] for more infor- factors inuencing tooth loss during periodontal mainte-
mation). Teeth with gingival tissues that always bled on nance. Of 527 potentially eligible publications, 13 retro-
probing (GI severity group III) had a 46 times higher likeli- spective case series were scientically robust enough and
hood to be lost than teeth always surrounded by healthy met the study criteria to include in the review. Most of
gingivae (GI severity group I). e data showed that well- the studies monitored patients for over 10 years. Of the
maintained teeth with healthy gingivae were practically 41,404 teeth present after active periodontal therapy, 3904
maintained for half a century (see Figure 5.4.4), which sug- were lost during periodontal maintenance. Age, smoking
gests that clinically healthy gingivae are an important prog- habit and initial tooth prognosis aected tooth loss out-
nostic indicator of tooth longevity. come and, overall, there were low rates of tooth loss for
is 26-year longitudinal observational study supported periodontal reasons. e ndings demonstrated that long-
the widely held view that gingival inammation is a precur- term periodontal supportive therapy was able to maintain
sor of periodontitis and a clinically relevant risk factor for periodontal health and prevent tooth loss in most patients
periodontal attachment loss and tooth loss. Other longitudi- and further emphasised the importance of regular peri-
nal studies have also conrmed that sites that progress have odontal maintenance and smoking cessation in preventing
persistently greater levels of gingival inammation whereas further tooth loss.
3.5
Mean loss of attachment

2.5
1.5
0.5
0
< 20 20–24 25–29 30–34 35–39 40–44 45–49 50–54 55–59
Age group
Key
GI = 0 Normal gingiva. Healthy
GI = 1 Mild inflammation; slight change of colour; slight oedema.

No bleeding on probing
GI = 2 Moderate inflammation; redness, oedema and glazing.

Bleeding on probing
• Figure 5.4.3 Effect of different gingivitis levels on attachment loss. From: Reprinted from Journal of
Clinical Periodontology, 30(10):15, Niklaus P. Lang, Hans Boysen, Åge Ånerud et al. (2003), with permis-
sion from John Wiley & Sons.
1.00 99.5%
93.8%
Survival distribution function
0.75
63.4%
0.50
0.25
0.00
0 10 20 30 40 50 60
Tooth age in years

Key
GI severity group I = sites always scoring GI=0, ie healthy
GI severity group II = sites always scoring GI=1, ie slightly inflamed
GI severity group III = sites always scoring GI=2, ie inflamed with

bleeding on probing
• Figure 5.4.4 Effect of different gingivitis levels on tooth loss. Survival distribution function for different
Gingival Index severity groups. After 50 years of tooth age, the cumulative survival for teeth with health
gingivae is 99.5%. Teeth with always bleeding gingivae demonstrate a cumulative survival of 63.4% after
48 years of tooth age. From: Reprinted from Journal of Clinical Periodontology, 31(12):6, Hans Boysen,
Åge Ånerud, Walter Bürgin, et al. (2004), with permission from John Wiley & Sons.
Based on the literature and biological plausibility, peri- SPT needs to be undertaken in all patients who have
odontitis patients with a low proportion of residual peri- been treated for periodontitis. However, it is fundamentally
odontal pockets and little inammation have been deemed important to acknowledge that because of their inherent
to be more likely to have periodontal stability and less tooth periodontal susceptibility, a periodontitis patient can never
loss over time (Loos & Needleman 2020). be deemed to be permanently “healed”. Rather, albeit they
can become periodontally “stable" (see Appendix 2), they stage, it is pertinent to wait 8 to 12 weeks to re-evaluate
will require ongoing periodontal maintenance for life, via probing depths and measure the clinical attachment level
SPT, to achieve tooth retention for life (Chapple etal. 2018, in order to monitor the success of the treatment outcome.
Kebschull & Chapple 2020, Sanz et al. 2020, West et al. As subgingival microbial recolonisation can occur within 4
2021). to 8 weeks of subgingival instrumentation in the absence
of improved plaque biolm control, an essential aspect of
SPT is the maintenance of optimal oral hygiene and eec-
KEY POINT 5 tive plaque biolm control (Segelnick & Weinberg 2006,
Although a periodontitis patient can become periodontally
stable after successful periodontal treatment, remember that
Sanz etal. 2020, West etal. 2021).
“once a periodontitis patient, always a periodontitis patient”, e position paper by Loos & Needleman (2020)
and ongoing SPT and periodontal maintenance are required addressed the question of which commonly applied peri-
for life. odontal probing measures recorded after completion of
active periodontal therapy related to: stability of the clini-
cal attachment level, tooth survival, need for re-treatment
Assessment of Treatment Outcomes and oral health-related quality of life. From their extensive
literature review, they concluded that: periodontitis patients
An evidence-based review of the clinical signicance of non- with a low proportion of residual pockets are likely to have
surgical periodontal therapy has been conducted (Cobb stability of clinical attachment levels and less tooth loss over
2002), and a systematic review on the eectiveness of time; probing pocket depths >6 mm and bleeding on prob-
mechanical non-surgical therapy performed (Suvan 2005). ing (BOP) score >30% are a risk for tooth loss; there were
At all stages of provision of periodontal therapy, it is no studies found that investigated the use of various peri-
important to recognise that the ability to remove all depos- odontal probing measures on the need for re-treatment; and
its is limited by the depth of the pocket, and this inuences nally, there was a lack of evidence that periodontal probing
the amount of pocket reduction and attachment level gain measures after completion of active treatment were tangible
ultimately achieved. to the patient.
e removal of all subgingival calculus has been shown
to be dicult to achieve in clinical practice, and it seems
that clinically acceptable healing occurs in spite of micro- When and How to Provide SPT
scopic aggregates of residual subgingival calculus. e criti- SPT Plan
cal mass of plaque biolm does need reducing to a threshold
where there is a balance between the microbial deposits and Each SPT plan must be individually tailored for patients
the patient’s host response which is conducive to periodon- following completion of steps 1–3 of periodontal therapy as
tal stability. Following successful treatment of periodontal per the stepwise approach (Sanz etal. 2020, West etal. 2021;
pockets, healing takes the form of a long junctional epithe- Appendices 3 and 4). e stepwise approach is described
lium, replacing the ulcerated pocket epithelium lining the in detail in Chapters 3.1, 3.3 and 4.3 and is illustrated in
pocket. Clinically: Appendices 3 and 4. Step 4 aims to maintain periodontal
• probing pocket depths should decrease stability through supportive periodontal care in all treated
• bleeding on probing from the base of the pocket should periodontitis patients by combining preventive/therapeutic
reduce or resolve interventions from steps 1 and 2. Regular recall intervals
• there should be a gain in the clinical connective tissue are needed, tailored to patient’s individual needs. Recurrent
attachment disease should be managed with an updated treatment plan.
• there may be gingival recession as the inìammation sub Integral to SPT is patient compliance with optimal plaque
sides and normally less redness and swelling along with a biolm control and a healthy lifestyle.
reduction or elimination of suppuration
• tooth mobility may decrease and there may be less furca KEY POINT 6
tion involvement in some cases. Each SPT plan must be individually tailored for patients
Radiographically, in due course, there may also be some following completion of active periodontal therapy.
bony inll at the base of angular defects where vertical bone
loss had previously occurred. Following the development of the EFP S3-level treat-
After professional mechanical plaque removal (PMPR) ment guidelines (Sanz etal. 2020) and the BSP implemen-
and thorough subgingival instrumentation, junctional epi- tation protocol (West etal. 2021), a number of CRs were
thelium re-establishes quite quickly, within 2 weeks, but produced for the UK healthcare system (see Chapter 4.3 for
the granulation tissue is not yet mature and not replaced more information on this process). In respect to SPT in step
by collagen bres. In fact, repair of connective tissue con- 4 of the stairway, a total of 20 CRs were formulated (West
tinues for 4 to 8 weeks after subgingival instrumentation etal. 2021). e following section describes those key CRs
and, therefore, although monitoring could be done at this (reproduced from West etal. 2021) applicable to SPT.
TABLE • BOX 5.4.2 What Constitutes the SPT

5.4.1 Frequency of SPT
Appointment?
SPT frequency Examination, re-evaluation, diagnosis
(months) Study Motivation, re-instruction (oral hygiene, smoking cessation/
modiable risk-factor management)
3–4 Most Treatment of re-infected sites, may need further
4–6 14 years (Lindhe and Nyman 1984) appointment(s)
• Non-surgical periodontal therapy
6–12, some tailored 15 years (Axelsson etal. 1991)  • Supragingival +/- subgingival PMPR with local analgesia
as required
30 years (Axelsson etal. 2004)
 • Adjunctive local antimicrobials if indicated
3, 6, 12, 18 5 years (Rosen etal. 1999) • Small surgicals
Polishing, uorides
Determine future recall visit
SPT Frequency
e frequency of SPT should be based on the patient’s risk suggested not to replace PMPR with alternative methods,
of disease progression. Studies ranging from 5 to 30 years e.g. Er: YAG laser treatment in SPT, nor to use adjunctive
(Table 5.4.1) have investigated dierent SPT intervals; the methods to PMPR (sub-antimicrobial dose doxycycline or
risk of insucient SPT visits or excessively long intervals photodynamic therapy) in SPT (Trombelli etal. 2020, West
between visits may constitute under-treatment with the etal. 2021).
potential for disease recurrence and a lack of support to help
the patient maintain adherence to oral hygiene procedures. Examination, Re-Evaluation, Re-Diagnosis
KEY POINT 7 During the SPT appointment the clinician should:
The frequency of SPT should be based on the patient’s risk of • update medical and dental history
disease progression. • assess smoking status and other risk factor assessments
including diabetes control if applicable
Although dierences were not statistically signicant, the • assess oral hygiene/plaque score
5-year study by Rosen etal. (1999) showed some rebound • carry out a clinical examination and diagnosis
in the 18-month SPT group compared with those on more  • soft tissue evaluation
frequent SPT intervals.  • dental examination including fremitus and occlusal
assessment
KEY POINT 8  • periodontal assessment – probing depths, BOP, plaque
• Start with three monthly recalls biolm score, level of calculus, furcation involvement,
• Maximum SPT interval should be 1 year suppuration, recession, mobility
 • radiographs if clinically justiëed
CR 4.1 (West etal. 2021) recommended that SPT visits • reassess the patient’s periodontal health status compared
should be scheduled at intervals of 3 to a maximum of 12 to baseline.
months and should be tailored to a patient’s risk prole and
periodontal conditions after active therapy. CR 4.2 recom- Oral Hygiene Motivation and Re-Instruction
mended that adherence to SPT should be strongly promoted
because it is crucial for long-term periodontal stability and Excellent plaque biolm control is an essential feature of
potential further improvements in periodontal status. successful SPT in step 4 and throughout all steps of peri-
odontal therapy, and patients need to be re-instructed and
SPT Appointment re-motivated if their plaque biolm control is not opti-
mal. CR 4.3 recommended repeated individually tailored
It is likely that up to an hour will be required for the SPT instruction in mechanical oral hygiene, including inter-
appointment, but this will depend on individual patient dental cleaning, in order to control inammation (see also
requirements. Such treatment can be carried out by a den- Figure 4.3.4 in Chapter 4.3). In respect of what additional
tist, hygienist or therapist. A typical SPT appointment is strategies for motivation are useful, CR 4.9 recommended
illustrated in Box 5.4.2. It is suggested by the EFP and BSP using step 1 of the stepwise approach.
in CR 4.14 that routine PMPR be part of an SPT care plan
in order to limit the rate of tooth loss and provide periodon- KEY POINT 9
tal stability/improvement, as part of a supportive periodon- Excellent plaque biolm control is an essential feature of
tal care programme, based on the systematic review and successful SPT, and patients need to be re-instructed and
meta-analysis by Trombelli etal. (2020). However, the CRs re-motivated if their plaque biolm control is not optimal.
Various methods of plaque biolm control are avail- Risk-factor control interventions have been recom-
able and should be tailored to each patient individually. A mended in periodontitis patients in SPT by the EFP and
choice can be made between powered or manual brushes in BSP (CR 4.17) to improve the maintenance of periodontal
conjunction with interdental cleaning aids, and where ana- stability (Ramseier etal. 2020) – implementation of smok-
tomically possible, interdental brushes are recommended in ing cessation interventions was recommended (CR 4.18)
preference to oss (Slot etal. 2020), as reected in the CRs and promotion of diabetes control interventions was sug-
of both the EFP and BSP (West etal. 2021). CR 4.10 stated gested (CR 4.19); however, it was not known if physical
that the basis of the management of gingival inammation exercise, dietary counselling or lifestyle modications aimed
is self-performed mechanical removal of plaque biolm, but at weight loss are relevant to SPT (CR 4.20) (Ramseier etal.
adjunctive measures can be considered on an individual 2020, West etal. 2021).
basis as part of a personalised plan (Figuero et al. 2020).
e BSP were unable to make a clinical recommendation Assessing Risk during SPT
in respect of adjunctive use of antiseptics in dentifrices (CR
4.12) without further research but was able to suggest con- Numerous risk models have been introduced in which BOP
sideration of adjunctive use of mouthwashes containing is a key parameter for risk of future periodontal breakdown.
chlorhexidine, essential oils and cetylpyridinium chloride ese are largely based on the presence or absence of BOP
in periodontitis patients undergoing SPT (CR 4.13). Based and have shown the following.
on the systematic review and meta-analysis by Figuero etal. Absence of bleeding on probing (Lang etal. 1986)
(2020), it was stated by both EFP and BSP that it is not Low risk for disease progression
known if other adjunctive agents such as probiotics, pre- • Almost 100% predictable for periodontal health. Sites
biotics, anti-inammatory agents and antioxidant micro- which do not exhibit BOP should not be instrumented dur-
nutrients are eective in controlling gingival inammation ing recall visits, the exception being in a smoker in whom
during SPT (West etal. 2021). the cigarette smoke may be associated with less bleeding.
Patients need to understand the value of eective
oral hygiene, but it is equally important to translate this Persistent bleeding on probing at successive recall visits (4/4)
understanding into action and behavioural change and • 30% of sites progress to develop CAL (but 70% do not!).
for patients subsequently to adopt and maintain any oral • Reinstrumentation of deep sites ≥5 mm may have a ben-
hygiene changes (see Chapter 4.3 for more information and ecial eect by altering the microbiota in the pocket to
Figure 4.3.5 for the EFP/BSP CR on this). be less pathogenic.

Patients need to understand the value of effective oral hygiene, Absence of BOP is a better indicator of health than presence is
but it is equally important to translate this understanding into of disease (Lang etal. 1990).
action and behavioural change and for patients subsequently
to adopt and maintain any oral hygiene changes. Dierent risk assessment models exist which share sev-
eral common attributes. In general, they can evaluate future
e rationale and evidence base for oral hygiene mea- risk of disease based on current and past ndings. Each nd-
sures and behavioural change are covered in Chapter 4.3 ing provides a relative risk value and, taken collectively, they
can assign a patient to a particular risk category indicating
Risk Assessment specic therapeutic approaches. Some models have been
validated for new (untreated) patients, such as the Previser
Susceptibility to periodontitis varies from patient to patient system (see Chapter 1.6), whereas others have been vali-
and depends on several acquired and inherent risk factors dated for SPT patients only. Examples of systems which are
(see Chapter 1.6). Risk assessment is dierent from diag- suitable for SPT patients include:
nosis, because risk assessment predicts disease at some time • Periodontal risk assessment (PRA) – six factors (Lang
in the future whereas diagnosis is an expression of current and Tonetti 2003):
disease status (Kye etal. 2012).  • % BOP, probing depth (PD) ≥5 mm, tooth loss, sys-
Risk can be dened as “the probability that an event will temic and/or genetic conditions, ratio of radiographic
occur in the future or the probability that an individual bone loss to age, smoking
develops a given disease or experiences a change in health • Modiëed PRA – eight factors (Chandra 2007):
status during a specied interval of time” (Albandar 2002).  • as above plus CAL-to-age ratio, diabetes, psychoso-
Risk factor is a “characteristic, aspect of behaviour or envi- cial factors; omitted radiographic bone loss-to-age
ronmental exposure associated with destructive periodonti- ratio
tis not necessarily causal” (Genco 1996). Local risk factors • UniFe – ëve factors (Trombelli etal. 2009):
include subgingival calculus, furcations and restoration  • smoking, diabetes, PD ≥5 mm, BOP, bone loss/age
overhangs; systemic risk factors include smoking, poorly • DentoRisk – 20 factors (Lindskog etal. 2010):
controlled diabetes, poor nutrition and stress.  • various systemic and local predictors.
Table 5.4.2 and Figures 5.4.5A, B and C show the PRA TABLE
model and how it can be used (Lang and Tonetti 2003). 5.4.2 Periodontal risk assessment (PRA) model
A low PRA patient has all parameters in the low-risk
PRA parameter Risk of further breakdown
categories, or maximum of one in the moderate risk
category. 1. Bleeding on probing % <10% low risk; >25% high
In the worked example, all parameters are in the low-risk sites risk
category. 2. Residual pockets of ≤4 low risk; >8 high risk
In Figure 5.4.5A, the patient: (1) has 5% sites with BOP; 5 mm or more
(2) has two sites with residual pockets of 5 mm or more; 3. Loss of teeth (from ≤4 low risk; >8 high risk
(3) has lost three teeth; (4) has a bone loss/age ratio of 0.25 total of 28 teeth,
excluding third molars)
derived from 10% bone loss at age 40 years (bone loss is
calculated from the worst posterior site measured either 4. Loss of support <0.5 low risk; loss of higher
related to age (%
on a periapical radiograph as % of root length, or from a
bone loss at worst site risk
bitewing, where 1 mm is considered to represent 10% bone posteriorly/age)
loss); (5) has no systemic or genetic risk factors; and (6) is
5. Systemic and genetic ↑ Risk, if any of risk factors
a non-smoker. factors, e.g. diabetes present
An online web tool is available to allow clinicians to cal-
6. Environmental factors, Former smoker, low risk;
culate and complete the PRA template and also to access a e.g. smoking occasional smoker
link to a newly developed tool by Ramseier of the University (<10 cigarettes per day)
of Bern for a personalised SPT interval (https://www.perio- and moderate smoker
tools.com/pra/en/index.php, accessed 09/08/21; see Figure (10–19 cigarettes per day),
5.4.5A showing the previously mentioned low-risk example). moderate risk; ≥20 high risk
BOP
>50
36
25
Envir. PD≥5mm
16 >12
S>20 10
S<20 9 8
S>10 6
IS 4 4
NS
0.25 4
6
0.5 8
10
0.75 >12
Syst./Gen. Tooth loss
1.0
1.25
>1.5
A
BL/Age
• Figure 5.4.5 Periodontal risk assessment (PRA). (A) PRA low risk, worked example online tool for PRA
available at https://www.perio-tools.com/pra/en/index.php, accessed 09/08/21. PRA low risk example in
(A) shown.(B) PRA moderate risk, worked example.(C) PRA high risk, worked example. Source: Figures
A–C are based on Functional Diagram Figure 1 from Lang and Tonetti (2003).
BOP
>50
36
25
Envir. PD≥5mm
16 >12
S>20 10
S<20 9 8
IS 4 4
NS 2
0.25 4
6
0.5 8
10
0.75 >12
1.0
1.25
>1.5
B
BL/Age
Figure 5.4.5 cont’d

BOP
>50
36
25
Envir. PD≥5mm
16 >12
10
S<20 9 8
S>10 6
IS 4 4
NS 2
0.25 4
6
0.5 8
10
0.75 >12
1.0
1.25
>1.5
C
BL/Age
Figure 5.4.5 cont’d
A moderate PRA patient has at least two parameters in Multiple choice questions on the contents of this chapter
the moderate category, but at most one parameter in the are available online at Elsevier eBooks+
high-risk category.
In the worked example, only one parameter (category 5)
is high risk, and the rest are moderate risk. References
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SECTION 6
Surgical Periodontal Therapy
241
6.1
Rationale for Periodontal
Surgery
JOS É Z U R D O
CHAPTER OUTLINE
Introduction Outcomes
When is Periodontal Surgery Appropriate? Apically Repositioned Flap (ARF)
Objective
Control of Disease
Technique
General Objectives
Outcomes
Periodontal Plastic Surgery
Osseous surgery
Case Selection for All Forms of Periodontal Surgery Objective
Subject Factors Techniques
Tooth Factors Surgical Treatment of Furcation-Involved, Multi-Rooted Teeth
Site Factors
Surgical Treatment Options
Medical Contraindications
Furcation Plasty
Surgical Approaches Objective
Pocket Production Procedures Technique
Pocket Elimination Procedures Outcomes
Regenerative Procedures Root Resection or Amputation
Open Flap Debridement (OFD) Objective
Objectives Technique
Technique Outcomes
Outcomes Regenerative Techniques
Modiöed Widman Flap (MWF)
Objective
Objective
Techniques
Technique
Guided Tissue Regeneration (Gtr)
Outcomes
Biological Root Modiers
Gingivectomy
Grafting and Combined Therapies
Objective
Technique Summary

This chapter explains the basis to considering periodontal surgery as an additional therapeutic measure in the management of periodontitis.
It outlines the most common surgical approaches, describing the specic objectives, techniques and expected outcomes.
• Understand the principles of periodontal surgery • Introduction
• Be able to describe the objectives of the most common • When is periodontal surgery appropriate?
surgical approaches • Surgical approaches
• Recognise the potential beneöts and risks associated with • Surgical treatment of furcation-involved, multi-rooted teeth
periodontal surgery • Regenerative techniques
• Appreciate the importance of case selection. • Summary
243
244 SECTION 6 Surgical Periodontal Therapy
Introduction ere are standardised surgical protocols with support-

ive research evidence about their potential advantages, but
e ultimate goal of all forms of periodontal therapy is com- a special eort should be made to consider all the risk fac-
monly considered to be the prevention of tooth loss (true tors on a case-by-case basis, keeping in mind that the main
end point). For the clinician, surrogate end points of success objective is to provide a signicant clinical improvement
may be dened as no bleeding on probing (BoP) and prob- with tangible benets for the patient. In terms of overall
ing pocket depths (PPD) of ≤4 mm. treatment planning and the scheduling of periodontal sur-
Following periodontal therapy, an increased resistance of gery, the European Federation of Periodontology (EFP)
the gingival tissues to probing and the absence of BoP are S3-level clinical treatment guideline (Kebschull & Chapple
signs of resolution of the inammatory lesion and useful 2020, Sanz etal. 2020) should be followed; details of this
indicators that the risk of further attachment and tooth loss guideline, and the British Society of Periodontology and
is minimised. Implant Dentistry (BSP) implementation of this guideline
ere is evidence that non-surgical therapy, with a (West et al. 2021), can be found in Chapter 4.3 and in
combination of root instrumentation and optimal supra- Appendices 3 and 4. us it can be seen that usually peri-
gingival plaque-control measures, is an eective treat- odontal surgery should only be considered during step 3
ment modality in reducing PPD and BoP in the majority of the stepwise approach – that is, when interventions to
of the cases and sites (Figure 6.1.1). Nevertheless, some control poorly or non-responding sites need to be employed
patients and/or sites can show persistent disease that is and after adequate execution of steps 1 and 2. e guideline
dicult to control and may be considered for more com- suggests that residual 4–5 mm pockets should receive repeat
plex corrective treatment (Heitz-Mayeld et al. 2002). subgingival instrumentation whereas pockets of 6 mm or
Because periodontitis is a plaque-induced disorder, sur- greater may benet from surgical procedures (Sanz-Sanchez
gical therapy should be considered on the basis of its etal. 2020).
potential to facilitate the removal of subgingival deposits Surgical management requires adequate planning and
and to enhance the long-term preservation of the peri- specic skills in tissue handling that are critical to the suc-
odontal tissues. cess of the treatment; therefore, the operator should antici-
pate the level of diculty and evaluate their own skills to
undertake cases within their own limits of competence. e
When is Periodontal Surgery EFP S3-level guideline recommends, based on expert opin-
Appropriate? ion rather than evidence, that surgical periodontal treat-
ment should only be carried out by specialists or dentists
Control of Disease with appropriate training (consensus-based clinical recom-
Periodontal surgery is elective; therefore a careful assessment mendation 3.4).
should be made to identify the potential benets and risks
involved.
General Objectives
e main objective of periodontal surgery is to improve the
prognosis of the tooth by one or more of the following means:
• Creating accessibility for eêective root surface debride
ment (Figure 6.1.2)
• Improving the gingival or tooth morphology to facilitate
the patient’s self-care
• Regenerating lost periodontal attachment.
Traditionally, persistent increased PPD following initial
A therapy has been the main parameter used to assess the indi-
cation for periodontal surgery and the classic main objective
was “pocket elimination”.
Evidence suggests that pocket depth does not nec-
essarily correlate with active disease and that clinical
signs of inflammation (BoP) should be considered.
Although the presence of inflammation has a poor posi-
tive predictive value for disease progression (Joss etal.
1994), the lack of it may be a more reliable indication
of disease control/stability. The emphasis is now less
B on pocket elimination and more on control of inflam-
• Figure 6.1.1 Gingival tissues (A) before and (B) after a course of non- mation. Thus deeper sites of pocketing with persistent
surgical treatment.
CHAPTER 6.1 Rationale for Periodontal Surgery 245
B
• Figure 6.1.3 (A) An example of a “gummy smile” with short clinical
crowns and diastemas. (B) This patient received crown-lengthening
surgery and cosmetic rehabilitation with porcelain veneers.
• Figure 6.1.2 Examples of intra-osseous defects. These types of and site-specic factors have to be considered, and patients
defects often limit access for root surface debridement. may need to be referred to a specialist for this.
Subject Factors
inflammation (BoP) may be candidates for additional
treatment (Tomasi etal. 2006). • Compliance: a patient with poor plaque control and
who has shown a poor response to initial therapy is not
a good candidate for surgical treatment. Periodontal
KEY POINT 1 surgery without appropriate plaque control and main-
Periodontal surgery is only appropriate when it is used as part tenance care may result in a sub-optimal treatment
of a well-formulated treatment plan and the objectives are
outcome.
clearly dened and reasonable.
• Patient coping skills and operator skills: periodon
tal surgery is technically demanding for the opera-
Periodontal Plastic Surgery tor and requires high levels of cooperation from the
patient.
Additional objectives of periodontal surgery unrelated to • Wound-healing potential: general factors such as poorly
the treatment of periodontal diseases are: controlled diabetes, smoking or stress may inuence the
• Correction of gingiva–alveolar mucosal problems (Figure response to the treatment.
6.1.3)
• Preparation of adequate periodontal architecture prior to
restorative treatment Tooth Factors
• Aesthetic improvement (Figure 6.1.4).
• Anatomic factors such as furcation anatomy and loca
tion, malposition or root proximity to adjacent teeth,
Case Selection for All Forms of position of the tooth in the dental arch, tooth mobility
Periodontal Surgery and occlusal factors may have a signicant impact in the
response to treatment.
e selection of patients for surgical periodontal therapy is • Restorative, cosmetic and endodontic considerations will
a delicate decision-making process in which subject, tooth inuence the treatment approach and outcome.
• Medication with immunosuppressive drugs (e.g. cyclo

sporine A).
KEY POINT 3
Periodontal surgery should be regarded as a potential tool to
improve the prognosis of specic teeth with lesions that are
realistically manageable and as long as the technique to be
used is within the technical capability of the operator.
Surgical Approaches
e choice of a conservative approach (preserving tissue),
a resective approach (removing tissues) or reconstructive
approach (regenerating tissue) will vary according to various
factors. e following factors should be considered:
• ɨe anatomy of the residual pocket (e.g. supra-bony or
infra-bony lesion, amount of keratinised gingiva)
• ɨe anatomy of the tooth (e.g. single-rooted or multi-
rooted tooth with or without furcation involvement)
• ɨe position of the tooth in the dental arch (e.g. cos
metic area)
• ɨe complexity and predictability of the technique in dif
ferent case scenarios (e.g. patient and operator factors).
Historically, periodontal surgery has comprised several
techniques and multiple variations within each technique, giv-
ing a confusing picture of the appropriate surgical approach
• Figure 6.1.4 Surgical correction of gingival recession at LR1 with a
laterally repositioned ap.
in individual cases. Evidence suggests that the choice of tech-
nique is not a determinant in successful treatment outcomes.
Pocket Production Procedures

• Poor-quality, non-surgical root debridement is not an
• Open ìap debridement
indication for surgical debridement; it is an indication
 • Papillae preservation technique, simpliëed papilla
for improved instrumentation.
preservation technique
KEY POINT 2 • Modiëed Widman ìap
Periodontal surgery should not be used to compensate for Pocket Elimination Procedures
inadequate non-surgical debridement.
• Soft tissue
Site Factors  • Gingivectomy
 • Apically repositioned ìap
• Adverse root morphology, pocket depth, bone and soft • Hard tissue
tissue anatomy will also inuence the healing potential  • Osseous surgery
and the technique of choice.  • Osteoplasty
 • Ostectomy
Medical Contraindications • Resective procedures of furcation-involved teeth
 • Furcation plasty
ere are some conditions that may require further investi-  • Root separation and resection
gation or advice from the patient’s physician prior to surgery
being undertaken. ese conditions include: Regenerative Procedures
• Bleeding predisposition • Guided tissue regeneration (GTR)
 • Blood disorders (e.g. haemophilia) • Root surface modiëcation
 • Medication with anticoagulant treatment (e.g. warfa • Other grafting biomaterials
rin resulting in a high INR)
• Poorly controlled diabetes Open Flap Debridement (OFD)
• Uncontrolled hypertension Objectives
• Immunocompromised patients
• Blood disorders (e.g. leukaemia) e main goal of the “replaced ap”, “access ap” or “open ap
debridement” is to obtain improved visibility and accessibility for
subgingival instrumentation of both soft and hard root surface Modified Widman Flap (MWF)
deposits which have not been removed by non-surgical means. Objective
Technique e modied Widman ap was historically designed as an
e technique for this procedure is as follows: access ap with removal of the inamed pocket epithelium
(Ramɦord & Nissle 1974). is technique aims to excise a
• Intrasulcular incisions and full-thickness mucoperiosteal marginal tissue cu to facilitate direct postoperative pocket
aps (buccal and lingual/palatal) preserving the inter- depth reduction (Figure 6.1.5).
dental soft tissue (“papilla preservation”) in the aps
(Cortellini etal. 1995) Technique
• Removal of granulation tissue e technique for this procedure is as follows:
• ɨorough root surface debridement
• Initial scalloped inverse bevel incision 1 mm from the
• Replacement of the ìap margins to their original posi
gingival margin and parallel to the long axis of the
tion and held with sutures.
tooth
Note: e ap should be of sucient size to expose the • Muco-periosteal ìaps within the attached gingiva
area that requires instrumentation. • Second intrasulcular incision to the bone crest to sepa
Vertical relieving incisions can facilitate the access and rate the tissue collar from the root surface
reduce the tension of the ap, but such incisions should be • Removal of the soft tissue collar
used with caution as they can reduce blood supply and sta- • As described with OFD, removal of granulation tissue,
bility of the ap. mechanical instrumentation of the root surface and
Complete soft tissue coverage of the alveolar bone should replacement of the ap.
be achieved at the termination of the surgery.
Outcomes
Outcomes MWF may result in greater pocket reduction than OFD
Although pocket reduction is not the intention of this because of the greater potential for gingival recession post-
technique, some pocket reduction may result from postoperatively. It is technically more demanding than OFD.
operative gingival recession. is will depend on soft tissue
biotype (thick or thin) and the morphology of any underly-
Gingivectomy
ing bone lesions (supra- or infra-bony). Gingival recession Objective
can be minimised by using microsurgical techniques and a is procedure involves the excision of the soft tissue wall
minimally invasive surgical approach. of the periodontal pocket aiming for pocket elimination
(Goldman 1951). Currently, it is commonly used for the
KEY POINT 4 surgical management of gingival overgrowth (hyperplasia)
OFD is the most reasonable surgical approach when the characterised by enlargement of the gingival tissues with-
objective is to carry out effective root surface debridement in out apical migration of the junctional epithelial attachment
areas with difcult access.
(“false pocketing”) (Figure 6.1.6).
Control of the causative factors should be completed
before surgical treatment is considered.
(d)
(c)
(a)
(a)
(b)
(b)
pre-surgical post-surgical post-healing

• Figure 6.1.5 Stages in a modied Widman ap procedure. Lines: (a) gingival margin; (b) bottom of
pocket; (c) scalloped inversed bevel incision; (d) intrasulcular incision.
external
bevel
incision
pre-surgical post-surgical post-healing

• Figure 6.1.6 Stages in a gingivectomy.
Technique • Mucoperiosteal ìap and crevicular incision removing a

e technique for this procedure is as follows: collar of gingival tissue
• Exposure of the bone margins and possible bone reshap
• Identiëcation of the bottom of the pocket with the probe ing, avoiding removal of tooth-supporting bone
• Marking the outer aspect of the gingiva creating a bleed • Repositioning of the ìaps at the level of alveolar bone
ing point crest, securing them in this position with adequate
• First scalloped external bevel incision (45 degrees to the suturing.
long axis of the roots) apical to the bleeding points to termi-
nate at a level slightly apical to the “bottom” of the pocket Outcomes
• Removal of the detached gingiva
• Gingivoplasty to create a better aesthetic contour. Pocket reduction should result where the soft tissues have
been apically displaced, although there may be residual
Outcomes pocketing in areas of greater bone loss.
e exposed tissue will heal by secondary intention. Peri- Osseous Surgery
odontal dressing should be used to cover the wounded Objective
area and reduce postoperative discomfort and bleeding. If
there is limited attached gingiva, a modied Widman ap e most signicant factor in the nal position of the gin-
approach may be more appropriate. gival margin following any periodontal surgical technique is
the anatomy of the underlying bone. erefore, the objec-
Apically Repositioned Flap (ARF) tive of bone surgery is to establish a “physiological” anatomy
Objective of the alveolar bone but at a more apical level. However, the
removal of tooth-supporting bone should be avoided.
e objective of this technique is to reduce the pocket, Osseous surgery is commonly used in conjunction with
maintaining an adequate zone of attached gingiva by dis- an apically repositioned ap (see Figure 6.1.7) and resective
placing the ap with the whole complex of the soft tissue surgery (pocket elimination procedures), but it can be used
(gingiva and mucosa) in an apical direction, as described by with other ap techniques involving pocket reduction.
Friedman (1962) (Figure 6.1.7).
In the palatal surfaces of the upper jaw, where the lack Techniques
of mucosa impedes any apical displacement of the ap, or • Osteoplasty or “bone recontouring” is the removal of
where there is sucient attached gingiva, a purely resective non-supporting bone to facilitate ap adaptation
technique (inverse bevel incision) can be used. • Common clinical situations
 • Elimination or reduction of shallow intra-bony defects
Technique  • Reduction of the thickness of the buccal/lingual bone
e technique for this procedure is as follows: at interdental areas
• Create horizontal relief one tooth either side of the surgi Ostectomy is the intentional removal of supporting bone
cal eld by means of crevicular incisions to correct osseous defects when signicant discrepancies in
• Scalloped inverse bevel incision connecting the releasing bone height remain following osteoplasty around teeth with
incisions sucient periodontal support.
(a)
(a)
(b) (b)
• Figure 6.1.7 Stages during an apically repositioned ap procedure. Lines: (a) gingival margin; (b) bottom
of pocket.
Common clinical situations in which osseous surgery is Furcation Plasty

indicated:
Signicant variations in the morphology of multi-rooted
• Elimination of small peaks of bone that often remain in teeth explain the diculties in diagnosing, treating and
the line angles managing furcation areas and in predicting their prognosis.
• Correction of reversed osseous architecture.
Objective
KEY POINT 5 e periodontal pocket in a furcation lesion is inuenced
Resective surgical therapies are destructive to the tissues and by the anatomy of the soft tissue (thick or thin), the bone
should be undertaken with restraint. The most common clinical
(horizontal or angular loss) and the inter-radicular anat-
indications involve the management of molars with furcation
lesions and cosmetic or restorative crown lengthening. omy of the tooth. Odontoplasty (reshaping the tooth),
osteoplasty (reshaping bone) or gingivoplasty (reshap-
ing gingiva) may be used to enhance the probability of
pocket and furcation closure following open debride-
Surgical Treatment of Furcation-Involved, ment (Figure 6.1.8).
Multi-Rooted Teeth Technique
Molars with periodontal breakdown aecting the furcation e technique for this procedure is as follows:
area tend to respond less favourably to non-surgical peri- • OFD to access the inter-radicular area
odontal therapy and, although earlier evidence suggested • Odontoplasty to reduce the horizontal component of the
that they have reduced prognosis (Hirschfeld & Wasserman defect and widen the furcation entrance
1978), more recent studies suggest that, properly managed • Osteoplasty to reduce the vertical component of the
and maintained, furcation-involved molars may survive for defect (e.g. eliminating the intra-bony lesion) and the
long periods (Huynh-Ba et al. 2009). e EFP S3-level horizontal component (e.g. decreasing the thickness of
treatment guideline recommends the retention and treat- the bone)
ment of teeth with class II and III furcation involvement • Positioning the ìap at the level of the alveolar bone crest.
and that furcation involvement is not a reason for extrac-
tion (clinical recommendation 3.10, based on Jepsen etal. Outcomes
[2020] and Dommisch etal. [2020]). However, if non-sur- Improved access for self-care and professional support-
gical treatment of furcation lesions has not been successful, ive care should result. Aggressive odontoplasty should be
various surgical options may be considered. avoided on vital teeth due to the risk of hypersensitivity.
Surgical Treatment Options Root Resection or Amputation

ese are as follows: Objective
• Resective surgery: Complete elimination of the furcation defect is frequently
 • Furcation plasty only possible if the roots are sectioned. Root separation
 • Root separation or root resection involves keeping all the roots, and root resection involves
• Regenerative surgery. the removal of one or more of the roots (Figure 6.1.9).
A B
C
• Figures 6.1.8 Result after periodontal ap surgery with osteoplasty and odontoplasty to reduce the verti-
cal and horizontal components of the pocket.
A B C D
E F
• Figures 6.1.9 Disto-buccal (DB) root resection and mesio-distal tunnelling case. The patient presented
with a class 3 furcation involvement. The DB root was sectioned and removed and the mesio-distal furca-
tion entrance exposed to facilitate oral hygiene. A four-unit bridge has stabilised the remaining roots.
is treatment requires a multidisciplinary approach before surgery; occasionally, the decision to resect a root is
(endodontic and restorative treatment) and aims to reserve made during surgery, in which case, the endodontic treat-
the tooth or part of it when no other alternative is eective ment is carried out as soon as possible after surgery.
and the tooth has a high strategic value.
Methodical treatment planning is critical in the suc- Technique
cess of this therapy. Endodontic treatment should be done e technique for this procedure is as follows:
• Figure 6.1.10 Use of a barrier membrane. The membrane (in blue) acts as a barrier to the down growth
of epithelial cells, the “sprinter” cells in wound healing. It also helps protect and stabilise the blood clot
within the defect area.
• Mucoperiosteal ìap to expose the furcation area Techniques

• Root sectioning with straight line cut and preparation of Guided Tissue Regeneration (Gtr)
the roots avoiding undercuts or ledges
• Careful removal of the root selected for extraction with Following open debridement of a periodontal lesion, barrier
out damaging the adjacent roots membranes can prevent the epithelium and connective tis-
• Repositioning of the ìaps at the level of the bone crest. sue from contacting the root surface during the periodon-
tal wound healing, allowing the undierentiated cells from
the periodontal ligament and bone to populate the area and
Outcomes
promote new attachment formation (Figure 6.1.10). Cor-
e remaining root(s) should have adequate bone sup- tellini etal. (2017) compared GTR with access ìap (OFD)
port. Failures are usually related to non-periodontal alone in 45 patients over a 20-year follow-up period and
complications, so care should be taken to ensure sound found that regeneration provided better long-term benets
endodontic therapy and a balanced occlusion (Carnevale than OFD alone.
etal. 1998).
Biological Root Modifiers
Biologic root modiers, such as enamel matrix proteins
Regenerative Techniques (EMPs) obtained from porcine tooth follicles, have been
Objective shown to induce proliferation of periodontal ligament cells,
gingival broblasts and osteoblasts; increase the rate of peri-
e ultimate and realistic goal of periodontal therapy is to odontal ligament cell attachment; and inhibit epithelial
stop the progression of the disease. down growth when applied to a treated root surface fol-
Although conventional non-surgical and surgical tech- lowing open debridement (Figure 6.1.11). e biological
niques can lead to predictable pocket reduction and decrease eects also include upregulation of markers of bone forma-
risk of disease progression, they are characterised by repair, tion (Bosshardt 2008).
often associated with recession and formation of long-junc- e clinical cases in Figures 6.1.12 and 6.1.13 illustrate
tional epithelium (the majority of the repaired soft tissue the regenerative capacity of these biological root surface
in contact with the treated root surface being epithelium). modiers.
A more idealistic goal is to restore completely the struc-
ture and function of the lost periodontal tissues (root Grafting and Combined Therapies
cementum, periodontal ligament, alveolar bone and con- A huge number of materials, techniques and combined
nective tissue attachment). therapies claim to promote periodontal regeneration, which
Although there is histological evidence demonstrating makes it very dicult for the clinician to choose the most
that partial periodontal regeneration is possible, complete appropriate therapy (Figures 6.1.14 and 6.1.15).
periodontal restoration is an elusive goal (Needleman etal. Only a few techniques, namely GTR and EMPs (the most
2002). Regeneration can only be attempted in vertical bone documented), are supported by sound scientic evidence.
defects. e EFP S3-level guideline recommends treating
teeth with residual deep pockets associated with intra-bony KEY POINT 6
defects of 3 mm or more with periodontal regenerative sur- Regenerative therapy is demanding and in general has low
gery (clinical recommendation 3.7, based on Nibali et al. cost-effectiveness. Case selection is important.
2020).
• Figure 6.1.11 Use of enamel matrix protein (EMP). The blue zone on the root surface represents the
EMP.
A B C
D E F
G H I
• Figure 6.1.12 A case treated with EMP (alone). The blue line in the diagram represents the incision line
and borders of the ap (intrasulcular incisions on both teeth connected by a semilunar incision). At the
root surface of UR3 there was 13+ mm of attachment loss on the mesial surface and UR1 palatally. The
ap involved a papilla preservation technique, as there was enough space to bring the whole tissue to the
palatal side. EMP was used according to manufacturer’s instructions. The three radiographs show the
situation before surgery, at 6 months follow-up and 1 year. Note the bone ll at 1 year.
A B
• Figure 6.1.13 Another case (intra-bony defect involving only the distal aspect of a vital LR6) where root
surface modiers were used. (A) The preoperative radiograph and (B) the 1-year postoperative control
radiograph.
• Figure 6.1.14 Combined regenerative approach using a barrier membrane and a bone “ller”, intended
to keep space for the blood clot and prevent membrane collapse into the defect.
A B
• Figure 6.1.15 Intra-bony defect at LR6 distally with involvement of the furcation, treated with GTR com-
bined with a xenographic bone substitute. Preoperative radiograph and healing control after 6 months.
Summary only be considered when non-surgical therapy has failed to

produce adequate healing because of identiable local fac-
e aim of non-surgical periodontal therapy (NST) is to tors and in spite of a high standard of care.
control the cause-related factors, allow resolution of the Multiple choice questions on the contents of this chapter
inammation and establish a clinical condition that can be are available online at Elsevier eBooks+.
easily maintained by the patient. Periodontal surgery should
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Regenerative surgical treatment of furcation defects: a system-
Bosshardt DD. Biological mediators and periodontal regeneration: a atic review and Bayesian network meta-analysis of randomized
review of enamel matrix proteins at the cellular and molecular lev- clinical trials. J Clin Periodontol. 2020;47(suppl 22):352–374.
els. J Clin Periodontol. 2008;35:87–105. Joss A, Adler R, Lang NP. Bleeding on probing. A parameter for
Carnevale GG, Pontoriero RR, di Febo GG. Long-term eects of monitoring periodontal conditions in clinical practice. J Clin Peri-
root-resective therapy in furcation-involved molars. A 10-year lon- odontol. 1994;21:402–408.
gitudinal study. J Clin Periodontol. 1998;25:209–214. Kebschull M, Chapple I. Evidence-based, personalised and minimally
Cortellini PP, Prato GPG, Tonetti MSM. e modied papilla pres- invasive treatment for periodontitis patients - the new EFP S3-level
ervation technique. A new surgical approach for interproximal clinical treatment guidelines. Br Dent J. 2020;229(7):443–449.
regenerative procedures. J Periodontol. 1995;66:261–266. Needleman I, Tucker R, Giedrys-Leeper E, Worthington H. A system-
Cortellini PP, Buti J, Pini Prato G, Tonetti MS. Periodontal regen- atic review of guided tissue regeneration for periodontal infrabony
eration compared with access ap surgery in human intra-bony defects. J Periodontal Res. 2002;37:380–388.
defects 20-year follow-up of a randomised clinical trial: tooth Nibali L, Koidou VP, Nieri M, Barbato L, Pagliaro U, Cairo F. Regen-
retention, periodontitis recurrence and costs. J Clin Periodontol. erative surgery versus access ap for the treatment of intrabony
2017;44:58–66. periodontal defects. A systematic review and meta- analysis. J Clin
Dommisch H, Walter C, Dannewitz B, Eickholz P. Resective surgery Periodontol. 2020;47(suppl 22):320–351.
for the treatment of furcation involvement - a systematic review. J Ramɦord SP, Nissle RR. e modied Widman ap. J Periodontol.
Clin Periodontol. 2020;47(suppl 22):375–391. 1974;45:601–607.
Goldman HMH. Gingivectomy. Oral Surg Oral Med Oral Pathol. Sanz M, Herrera D, Kebschull M, Chapple I, Jepsen S, Beglundh
1951;4:1136–1157. T, Sculean A, Tonetti M. Treatment of stage I-III periodontitis-
Friedman N. Mucogingival surgery. e apically repositioned ap. J e EFP S3 level clinical practice guideline. J Clin Periodontol.
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Heitz-Mayfield LJA, Trombelli F, Needleman I, Moles D. A Sanz-Sanchez I, Montero E, Citterio F, Romano F, Molina A, Aimetti
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SECTION 7
Interaction with Other Dental

Disciplines
255
7.1
The Periodontal–
Restorative Interface
EW E N M CCO L L
CHAPTER OUTLINE
General Restorative Considerations Partial Dentures
Patient Engagement Occlusion
Engaging Patient Mobility
Non-Engaging Patient
Periodontitis and Implant Dentistry
Crown and Bridge Construction
Endodontic/Periodontal Relationships
Supracrestal Tissue Attachment
Summary

This chapter examines the relationship and interactions between the periodontium and a range of aspects of restorative dentistry.
• Understand the importance of a healthy periodontium and • General restorative considerations
meticulous oral hygiene in restorative dentistry • Crown and bridge construction
• Be able to describe the key phases of restorative treatment • Supracrestal tissue attachment
planning • Partial dentures
• Recognise the practical and aesthetic challenges of • Occlusion
restorative dentistry in treated periodontal patients • Mobility
• Understand the importance of a structured periodontal • Implant dentistry
maintenance regimen in successful restorative dentistry. • Pulpal tissues
• Summary and conclusions.
General Restorative Considerations treatment-planning approach in restorative dentistry cannot

be over-emphasised. ese phases are often categorised as:
Periodontal health is the foundation for successful restor- 1. Emergency treatment
ative dentistry whether the treatment involves a single occlu- 2. Cause-related therapy
sal amalgam restoration or full-mouth rehabilitation. Often, 3. Re-evaluation
in the rush to proceed to the corrective phase of treatment, 4. Corrective therapy
insucient attention is paid to the control of active disease. 5. Maintenance/supportive therapy.
is may be due to lack of clinical awareness, lack of clini-
cal time, patient impatience, or nancial imperatives. How-
ever, if the cause-related phase of disease management is KEY POINT 1
Periodontal health is the foundation stone for successful
ignored, this may risk treatment failure and the potential for
restorative dentistry.
litigation. us the importance of a structured and phased
257
258 SECTION 7 Interaction with Other Dental Disciplines
KEY POINT 2
Phases of treatment:
1. Emergency treatment
2. Cause-related therapy
3. Re-evaluation
4. Corrective therapy
5. Maintenance/supportive therapy.
One of the most important elements of cause-related

therapy is the control of gingivitis and periodontitis.
e most important aspect of regaining and retaining
periodontal health is improving levels of self-performed oral • Figure 7.1.1 “Black triangle” effect at lower anteriors.
hygiene. Behavioural change can take time, whether improv-
ing oral hygiene or altering lifestyle habits. It is crucial that
patients, with guidance from their clinician, establish these e periodontal tissues should be suciently healthy to
changes prior to embarking on complex restorative treatment facilitate soft tissue management, allowing better moisture
plans. is concept is now referred to as “patient engagement”. control during restorative procedures. is will help with
long-term restoration marginal stability.
KEY POINT 3
The British Society of Periodontology and Implant Dentistry Crown and Bridge Construction
has dened patients as being engaging or non-engaging
depending on their compliance or ability to comply with While the control of active disease (gingivitis, periodonti-
recommended oral hygiene regimens.
tis and caries) is the key to successful restorative dentistry,
the importance and relevance of the periodontal condition
Patient Engagement in more advanced restorative dentistry will be discussed
here.
e British Society of Periodontology and Implant Den- Fixed prosthodontics can be a challenge at the best of
tistry have dened patients as being engaging or non-engag- times, but it can become even more demanding in the
ing depending on their compliance or ability to comply with treated periodontal patient. In a successfully treated peri-
recommended oral hygiene regimens (https://www.bsperio odontal patient, gingival recession may be an unavoidable
.org.uk/assets/downloads/Delivering_phased_Care_Final_6 result of the reduction in inammation and loss of clini-
th_May_2021_1.pdf ). cal attachment. Apart from the obvious aesthetic concerns
that patients may have, the appearance of triangular spaces
Engaging Patient between the teeth (the “black triangle” eect) may mean
crowns need to have longer contact points to mask this
e average engaging patient demonstrates a favourable eect (Figure 7.1.1).
response to self-care advice and sucient improvement in However, these long contact points may make oral
oral hygiene as indicated by a 50% or greater improvement hygiene measures more challenging interdentally, and close
in plaque (disclosing is required) and marginal bleeding liaison with the laboratory will be necessary to ensure that
scores OR: patients are able to carry out eective oral hygiene measures.
• Indicative bleeding levels <30% e production of high-quality temporary crowns is
• Indicative plaque levels <20% essential to allow optimal oral hygiene practices and avoid
• AND a stated preference to achieving periodontal health. inammation of the marginal periodontal tissues. e reso-
lution of any inammation that is present at the provisional
Non-Engaging Patient stage may result in some recession when the nal restora-
tions are cemented, as this may lead in turn to exposure of
e non-engaging patient demonstrates an unfavourable restorative margins.
response to self-care advice and insucient improvement in From an operative dentistry perspective, it is also impor-
oral hygiene as indicated by less than a 50% improvement tant to remember that in teeth with conical roots where
in plaque and marginal bleeding scores OR: recession has occurred, the circumference of the root
• Indicative bleeding levels >30% decreases the more apically you prepare, and this may mean
• Indicative plaque levels >20% there is an increased risk of pulpal exposure if margins are
• OR a stated preference to a palliative approach to peri cut too heavily. Where recession has occurred around furca-
odontal care. tions, the anatomy of the exposed cement–enamel junction
Most restorative treatment will occur in the corrective may also increase the diculties of marginal preparation
phase of treatment, and it is essential that, prior to this, patient around the curvature of this margin, so careful pretreatment
engagement and periodontal stability has been achieved. planning is of paramount importance.
CHAPTER 7.1 The Periodontal–Restorative Interface 259
A B
• Figure 7.1.2 Poor pontic design making patient oral hygiene more difcult.
Bridges should be designed to ensure that gingival papillae Supracrestal Tissue Attachment
are not traumatised, and pontic design should allow adequate
oral hygiene to be performed by the patient (Figure 7.1.2). Although margins of crowns and bridges need to be slightly
subgingival in aesthetic zones, i.e. where the gingival margins
KEY POINT 4 are visible when a patient smiles, it is crucial that these do
Abutment preparations may be more complex where not impinge on the supracrestal tissue attachment. Gargiulo
periodontal attachment loss has occurred. etal. (1961) established the concept of biological width (now
referred to as supracrestal tissue attachment) by looking at
Pontic design in bridgework (Figure 7.1.3) can be cat- the dento-gingival complex in cadavers. ey established that
egorised as follows: the supracrestal tissue attachment (Figure 7.1.4) in humans is
1. Hygienic approximately 2 mm, extending from the base of the gingi-
2. Ridge lap/saddle val sulcus to the alveolar crest. is was found to comprise an
3. Modied ridge lap epithelial attachment of about 1 mm and a connective tissue
4. Ovate pontic. component of about 1 mm. Although this study established
Although the hygienic pontic does not contact the eden these dimensions, it is dicult to measure this clinically when
tulous ridge and is in eect self-cleansing, it will not provide preparing crown margins, so a gure of 3 mm is used, taking
adequate aesthetics and, for many patients, is unacceptable. into account possible measurement error (Figure 7.1.5). Sub-
e ridge lap/saddle design can limit oral hygiene mea- gingival margins of crowns or restorations can impinge on the
sures, and the modied ridge lap or ovate pontic tend to be supracrestal tissue attachment causing inammatory change
favoured to allow for adequate aesthetics and oral hygiene and the risk of alveolar bone resorption. Impinging on the
measures. e crucial element of pontic design is that the supracrestal tissue attachment can result in recession in patients
patient can use interdental aids to access abutments and with a thin gingival tissue biotype and inammation and peri-
associated margins so that the risk of bacterial recolonisa- odontal pocketing where there is a thick gingival biotype.
tion and disease recurrence is kept to a minimum. At the
t appointment, it is essential to ensure that the patient KEY POINT 6
can still reach all areas of potential bacterial accumulation Supracrestal tissue attachment
for oral hygiene to prevent the recurrence of inammation. • Approximately 2 mm, consisting of epithelial (junctional)
Close liaison with the laboratory is necessary to minimise and connective tissue attachment
this risk. At the cementation stage of crown and bridge • Impinging on the supracrestal tissue attachment may
lead to inammation (in thick biotypes) or recession (in
work, it is important to ensure that excess cement is not left thin biotypes)
as a long-term irritant to the periodontal tissues.
KEY POINT 5 e concept of supracrestal tissue attachment is impor-

Pontic design tant when planning for the location of crown margins. In
Ensure pontic design does not compromise patient’s ability to wear cases, or where the crown margins are likely to impinge
carry out oral hygiene measures. upon the supracrestal tissue attachment, crown lengthening
surgery may be necessary. e basic principle is that, in order Poorly designed dentures in poorly maintained patients
to avoid impinging on the supracrestal tissue attachment, 3 may lead to increased mobility of abutment teeth and
mm of space is needed between the restoration margin and breakdown of the periodontium. However, if consideration
the alveolar bone. is given to the periodontium in designing dentures, and
the patient maintains the highest standards of oral hygiene,
Partial Dentures then this can be avoided. e classic “gum stripper” style
of denture can be damaging to the periodontal tissues and
With any prosthesis, whether xed or removable, it is should be avoided.
important to ensure that the prosthesis does not have any
negative impact on the periodontal tissues. KEY POINT 7
Denture design
• Minimise gingival coverage
• Passivity of clasps
• Avoid lateral forces
• Patient needs carefully monitored maintenance regimen
Where an acrylic denture is indicated, the “Every” design

A of denture, rst described by Every in 1949, incorporates
features in an acrylic denture conducive to maintaining
periodontal health. Key to this design is that coverage of the
gingival margin is kept to a minimum to prevent gingival
damage, and lateral interdental forces are kept to a mini-
mum (Figure 7.1.6).
Bates & Addy (1978) established that removable partial
dentures performed best when given to patients with good
B oral hygiene, where tissue coverage was kept to a minimum
and the dentures were kept out at night.
Similar principles apply to chrome cobalt dentures where
the design should be such that gingival coverage is kept to
Floss
a minimum, clasps are passive and rest seats are designed so
that forces are axial rather than lateral in order to reduce the
Floss
C D likelihood of tooth mobility.
Where the clinician is faced with a Kennedy class 1 situ-
• Figure 7.1.3 (A) Bullet pontic: makes point contact with tip of ridge;
(B) hygienic pontic: easy to clean molars only; (C) saddle pontic: dif
ation with bilateral free end saddles, the risk of overload-
cult to clean; (D) ridge lap: minimal contact with buccal aspect of ridge. ing the last standing tooth is increased and denture design
Connective 1.0 mm
Biologic tissue
width
2.0mm Junctional
1.0 mm
epithelium
Sulcus 1.0 mm
• Figure 7.1.4 Diagram of the biologic width.

KEY POINT 8
Occlusal overload does not cause periodontal breakdown and
there is no human evidence that it exacerbates periodontitis.
Further animal studies by Lindhe & Ericson (1982)

suggested that, in the presence of uncontrolled periodon-
titis, greater attachment loss could occur in the presence of
occlusal trauma. is suggested that occlusal trauma may
exacerbate periodontitis. However, this eect has only been
shown in some animal studies, and the evidence for this
so-called co-destructive eect is weak. Such eects have
not been shown in human studies, and there is a lack of
evidence from such human studies to implicate occlusal
• Figure 7.1.5 3 mm of clearance between predicted crown margin trauma in the progression of attachment loss in periodonti-
and alveolar bone. tis. Whereas some clinicians advocate occlusal intervention
to reduce occlusal trauma in periodontitis patients, a recent
Cochrane systematic review showed that there was insuf-
cient evidence to justify such treatment in periodontitis
cases (Weston et al. 2008). e World Workshop on the
Classication of Periodontal and Peri-implant Diseases and
Conditions (2018) has stated that there is no evidence that
traumatic occlusal forces cause periodontal attachment loss
in humans.
Mobility
From a clinical relevance perspective, where treatment has
been completed and attachment loss has occurred, occlusal
overload may contribute to the mobility of teeth. It should
be remembered that mobility is not just the result of occlu-
• Figure 7.1.6 Every style denture. sal loading of teeth but that the level of bone support and
the inammatory status of the soft tissues are also contribu-
becomes more challenging. is emphasises the importance tory factors. In patients for whom the mobility is a prob-
of retaining molar teeth wherever possible to allow some lem, occlusal analysis to eliminate premature contacts may
posterior support. In many cases, the shortened dental arch, help to reduce the extent of tooth mobility. Splinting such
as suggested by Kayser (1989), may be preferable to over- problematic teeth where the mobility is causing the patient
loading the remaining teeth. discomfort may also be an option. In these patients, occlusal
analysis to eliminate premature contacts may address this
Occlusion problem.
Numerous types of splint design have been suggested over
It was initially suggested by Glickman (1965) that angular the years. Direct types involve splinting the teeth directly
bony defects and increasing tooth mobility were caused by with composite material. In addition, orthodontic wire can
trauma from occlusion. However, further studies by Waer- be used to run between the teeth which allows some ex-
haug & Randers-Hansen (1966) established the presence ion on occlusion. Additionally, composite ëbre mesh has
of such bone defects in teeth unaected by trauma from become available which may also be used for direct splinting
occlusion. A study by Ericsson & Lindhe (1977) established (Figure 7.1.7).
that occlusal overload does not cause periodontal break- Indirect methods of splinting may involve the use of
down. Periodontitis was caused in dogs by allowing the ani- orthodontic wire with composite. e bending of the wire
mals to accumulate plaque and calculus around the teeth. in the laboratory may allow a more accurate t, although
When almost 50% of bone loss occurred, the animals were diculties may be encountered when taking impressions
brought back to periodontal health by undergoing a metic- of very mobile teeth which may also aect the accuracy of
ulous oral hygiene regimen including scaling, root planing any laboratory work. Another method of indirect splinting
and pocket elimination. Certain teeth were then exposed is to use an adhesive bridge-style, nickel-chromium back-
to jiggling forces and, although the teeth became mobile, ing. However, there may be aesthetic issues as, normally, in
there was no increase in attachment loss or development of mobile periodontally involved teeth there is spacing and the
periodontitis. metal will show. e same can be said for orthodontic wire
A B
C D
• Figure 7.1.7 Use of composite mesh in immediate adhesive bridge. Photos courtesy of Dr Neil Macbeth.
palatally. is means the most practical and aesthetic solu-

tion is often directly applied composite.
e key component of splint design is that it does not
impede the patient’s oral hygiene measures and careful
monitoring and maintenance are essential.
e splint should be designed in such a manner that
interdental brushes can still easily access interdental spaces
so that oral hygiene is not compromised in any way.
When hopeless periodontally involved teeth are extracted
in the short term, they can be splinted back in place to pro-
vide the patient with an aesthetic xed tooth replacement • Figure 7.1.8Implant placement in a treated periodontal patient with
(Figure 7.1.7). is will allow healing to take place prior to meticulous oral hygiene.
construction of a denitive restoration.

Splints may be indicated where mobility is causing patient Implants may suffer peri-implant mucositis or peri-implantitis.
discomfort. Supportive care, maintenance and monitoring are essential for
implants, especially in patients with a history of periodontitis.
Periodontitis and Implant Dentistry

Risk indicators for peri-implant disease are essentially the
As periodontitis may result in the loss of teeth, patients with same as those for periodontitis. In implant cases that are
a history of periodontitis will sometimes seek implant treat- managed in a general practice, a strict periodontal and peri-
ment to replace these missing teeth. implant maintenance and monitoring regimen is essential
However, many patients do not realise that implants may (Figure 7.1.8).
themselves be exposed to disease processes similar to gin- Periodontally susceptible patients should be warned that
givitis and periodontitis (peri-implant mucositis and peri- they may be at higher risk of implant complications and
implantitis), particularly in those patients who have a history also that implant treatment should not be carried out unless
of periodontitis. is is not surprising given that the micro- there is no uncontrolled disease present and an optimal level
ora around implants is similar to that around teeth, and of plaque control is maintained (Lindhe & Meyle 2008).
many of the host factors involved in periodontitis remain e management of implants and their complications is dis-
the same. cussed in detail in Chapter 7.3
probing depth and mobility should be assessed before

embarking on complex treatment of this sort.
KEY POINT 11
When managing a tooth with a suspected endo-periodontal
lesion, always test pulp vitality of suspect tooth and, if vitality
is lost, always carry out endodontic treatment rst, followed by
periodontal therapy if required.
Summary
e key element in the provision of restorative treatment for
periodontally susceptible patients is control of active disease
prior to denitive restorative treatment and maintenance of
a healthy periodontium. It is important to ensure that there
are regular periodontal reviews and that self-performed
plaque control is maintained at an optimal level.
• Figure 7.1.9 Radiographic appearance of an endo-periodontal lesion
at tooth 21. are available online at Elsevier eBooks+
References
Endodontic/Periodontal Relationships Bates JF, Addy M. Partial dentures and plaque accumulation. J Dent.
1978;6:285–293.
e close relationship between the pulpal complex and the
Ericcson I, Lindhe J. Lack of eect of trauma from occlusion on
periodontium via the apical foramina and lateral canals the recurrence of experimental periodontitis. J Clin Periodontol.
means that infection in one may result in infection in the 1977;9:497–503.
other. ese lesions have been classied by the World Work- Gargiulo AW, Wentz FM, Orban B. Dimensions and relations of the
shop on the Classication of Periodontal and Peri-implant dentogingival junction in humans. J Periodontol. 1961;39:261–267.
Diseases and Conditions (2018) as endo-periodontal lesions Glickman I. Clinical signicance of trauma from occlusion. J Am
(Herrera etal. 2018). Where periodontal infection has led to Dent Assoc. 1965;70:607–618.
pulpal necrosis, this is classed as a primary periodontal lesion. Herrera D, Retamal-Valdes B, Alonso B, Feres M. Acute periodon
Where pulp necrosis has occurred and the infection drains tal lesion (periodontal abscesses and necrotizing periodontal dis-
through the periodontal ligament, this often presents as an eases) and endo-periodontal lesions. J Periodontol. 2018;89(Suppl
isolated narrow pocket (often in the absence of periodontal 1):S85–S102.
Kayser AF. Shortened dental arch a therapeutic concept in reduced
lesions elsewhere), and the lesion is classed as primarily end-
dentitions and certain high risk groups. Int J Periodontics Restor-
odontic in origin. Where both a periodontal infection and ative Dent. 1989;9:426–449.
endodontic infection are present together, this is classed as Lindhe J, Ericcson I. e eect of elimination of jiggling forces
a true combined lesion and such lesions can be dicult to on periodontally exposed teeth in the dog. J Periodontol.
diagnose (Figure 7.1.9). 1982;53:562–567.
In all cases, pulp vitality should be established, and if Lindhe J, Meyle J. Peri implant diseases: Consensus report of the
the pulp is found to be non-vital then endodontic treat- sixth European Workshop on periodontology. J Clin Periodontol.
ment should be carried out ërst. No periodontal treatment 2008;35(Suppl. 8):282–285.
should be carried out until the endodontic lesion has had an Papaspyridakos P, Chen CJ, Singh M, Galluci GO. Success criteria in
opportunity to resolve. In those cases where the lesion is of implant dentistry: a systematic review. J Dent Res. 2012;91:242–248.
primary endodontic origin, the periodontal component of Proceedings of the World Workshop on the Classication of Peri-
odontal and Peri-implant Diseases and Conditions. J Clin Peri-
the lesion may resolve completely.
odontol. 2018;45(Suppl 20):S1–S291.
Where the lesion is suspected to be primarily periodontal Waerhaug J, Randers-Hansen E. e infrabony pocket and its rela-
in origin, providing the tooth has a reasonable prognosis, tionship to trauma from occlusion and subgingival plaque. J Peri-
endodontic treatment should still be carried out rst and odontol. 1966;50:355–365.
again periodontal treatment delayed until the endodontic Weston P, Yaziz YA, Moles DR, Needleman I. Occlusal interven-
infection has been resolved. Careful assessment of prognos- tions for periodontitis in adults. Cochrane Database Syst Rev. 2008:
tic indicators such as bone volume, furcation involvement, CD004968.
7.2
The Periodontal–
Orthodontic Interface
IA N D U N N
CHAPTER OUTLINE
Introduction 3. Reduced Bone Support
The Role of Orthodontics in Periodontal Therapy Inuence on Treatment
4. Missing Teeth and Poor Anchorage
1. Crowded Teeth, Anterior Splaying or over Eruption
Inuence on Treatment
Orthodontic Treatment
5. Relapse and Retention
2. Infra-Bony Defects
6. Gingival Biotype and Gingival Recession
3. Gingival Asymmetry
7. Minor Soft Tissue Surgery to Assist with Orthodontic
4. Loss of Interdental Papillae
Treatment
8. Frenotomy or Frenectomy
The Role of Periodontics in Orthodontic Therapy 9. Gingival Invaginations
1. Oral Hygiene Preparing Periodontal Patients for Orthodontic Treatment
Periodontal Treatment
2. Tooth Crowding
Monitoring and Maintenance
Medico-Legal Issues

This chapter describes the interactions between periodontal and orthodontic treatment. It explains the need for a stable and healthy
periodontium before, during and after orthodontic treatment and how orthodontically moving teeth can reposition them such that they and
the associated gingivae are easier to maintain.
• Understand how orthodontics can beneöt a periodontal • Introduction
patient (a patient who has suòered from periodontal • The role of the orthodontics in periodontal therapy
attachment loss) • The role of periodontics in orthodontic therapy
• Understand how periodontitis aòects orthodontic treatment • Preparing periodontal patients for orthodontic treatment.
planning
• Know how to prepare a periodontal patient for orthodontic
treatment
• Understand how periodontics can help orthodontics.
Introduction has been stabilised, orthodontic therapy can be benecial in

improving the appearance and function of a periodontally com-
Adult orthodontic treatment is a growing area of orthodontic promised dentition. is chapter will look at the ways in which
practice because of the increased desire by patients to improve orthodontic treatment can complement periodontal therapy;
the appearance of their teeth. As already discussed in previ- the potential issues that may arise; how the reduced periodon-
ous chapters, periodontal diseases can have devastating eects tium aects orthodontic treatment planning; how to prepare a
on both the appearance and function of a dentition. As such, patient for, and maintain a patient during, orthodontic treat-
for many periodontal patients, as long as their periodontium ment; and look at how periodontics can assist orthodontics.
264
CHAPTER 7.2 The Periodontal–Orthodontic Interface 265
The Role of Orthodontics in Periodontal can be aligned, de-rotated, extruded or intruded to improve
Therapy the appearance. Intrusion, in particular, is not without its
risks, as this often leads to some apical resorption of the
In the following section, a series of clinical problems and how intruded tooth without any additional gain in periodontal
orthodontic treatment may solve them will be described. support eectively leading to reduced periodontal support.
It should be stressed that, in all cases, the patient should A study by Melsen etal. (1989) showed that when intruding
be displaying optimal oral hygiene before any orthodontic teeth, apical resorption could be as much as 3 mm (Figure
treatment commences and that, although the periodontal 7.2.2). Whereas the primary goal in these cases is improved
support for the teeth may be reduced, there should be no aesthetics, improved alignment may make cleaning and
evidence of ongoing periodontal breakdown, such as bleed- periodontal maintenance easier.
ing on probing or pus from periodontal pockets.
KEY POINT 1
1. Crowded Teeth, Anterior Splaying Intruding teeth may lead to up to 3 mm of apical resorption.
or Over Eruption
2. Infra-Bony Defects
Periodontal patients may suer from the same malocclu-
sions as non-periodontal patients, i.e. crowding, over-jets Although the majority of patients exhibit horizontal bone
and cross-bites. In addition, because of the reduced peri- loss, it is not unusual for vertical bone defects to occur,
odontal support and inammatory status of the tissues, resulting in infra-bony defects. As discussed in previous
teeth can also drift or splay and over-erupt. chapters, it is possible to regenerate this type of defect using
biomaterials and surgical techniques. However, patients
Orthodontic Treatment planning to undergo orthodontics with infra-bony defects
Correction of tooth position through routine orthodontics may benet from having any surgical periodontal treat-
is achievable in periodontal patients (Figure 7.2.1). Teeth ment well in advance of any orthodontic intervention(s),
A B
C
• Figure 7.2.1 A 30-year-old patient who presented with an aggressive form of periodontitis that was suc-
cessfully treated. (A) clinical appearance on presentation. (B) Fixed orthodontic appliances in place. (C)
Final post-orthodontic result.
A C
B D
• Figure 7.2.2 Apical resorption in a periodontally susceptible, orthodontically treated patient. (A) The
patient before orthodontic treatment; (B) the UL1 before orthodontic treatment; (C) the patient after orth-
odontic treatment; (D) the UL1 after orthodontic treatment.
highlighting the need for multidisciplinary treatment plan- techniques such as crown lengthening, this usually results
ning for these complex cases. in the need to restore the exposed crown or root structure,
possibly with veneers. However, the need for restorative
Orthodontic Treatment intervention for aesthetic gain must be balanced against the
In one cohort study (Corrente et al. 2003), 10 patients desirability of retaining tooth structure.
were treated initially non-surgically and then surgically at
the infra-bony defect sites followed by constant, light force Orthodontic Treatment
orthodontic treatment started within 2 weeks. is resulted Patients undergoing orthodontic treatment to correct malpo-
in signicant gains in all the usual parameters when moving sitioned teeth or for pre-restorative purposes should have their
the teeth into the defect sites. It should be noted that, as a gingival margin positions assessed. Combinations of intrusive
cohort study, there was no control group to allow for assess- and extrusive tooth movements can lead to a more favourable
ment of the additional eect of the orthodontic treatment. gingival margin symmetry. It should be noted that teeth requir-
ing extrusion, where the gingival margin is already in the cor-
KEY POINT 2 rect position, may also require pericision to prevent the alveolar
Patients planning to undergo orthodontics with infra-bony and gingival architecture from being brought down with the
defects may benet from having any surgical periodontal extruded tooth. Pericision or breotomy involves anaesthetis-
treatment well in advance of any orthodontic intervention(s). ing the soft tissues and, with a blade held in the long axis of the
tooth concerned, cutting through the gingival epithelium and
connective tissue attachment down to the crest of the alveolar
3. Gingival Asymmetry
bone with the aim of severing the soft tissue attachment. is
Some patients have asymmetrical teeth or gingival anatomy. eliminates the “pull” on the root from these tissues and makes
While gingival anatomy can be altered surgically using it easier to move the tooth vertically out of the bone.
KEY POINT 3 the opposite side. Patients who are susceptible to periodon-
titis have dentitions with reduced bone levels around some,
Pericision involves cutting through the gingival epithelium and
connective tissue attachment down to the crest of the alveolar or sometimes all, of their teeth. ey require regular pro-
bone with the aim of severing the soft tissue attachment. fessional maintenance (supportive periodontal care) by the
dental team and self-performed plaque removal. As such,
these factors may inuence the orthodontic management.
4. Loss of Interdental Papillae
Periodontal problems which inuence orthodontic treat-
Patients undergoing periodontal treatment will often expe- ment will now be considered.
rience gingival recession and loss of the interdental papillae
as a result of the bone loss and resolution of the inamma- 1. Oral Hygiene
tion within the periodontal tissues. e loss of interdental
papillae is often, unkindly, referred to as “black triangle dis- Oral hygiene and supportive periodontal care can become
ease” because of the resulting interdental spacing. Surgical more dicult when orthodontic appliances are present.
attempts at regenerating lost interdental papillae have gen-
erally been unsuccessful around teeth and most techniques Influence on Treatment
involve masking the spaces with either xed or removable Wherever possible, orthodontists should avoid using bands
prostheses such as porcelain veneers with longer contact on molar teeth, as Boyd & Baumrind (1992) have shown an
points or removable silicone gingival veneers. increase in plaque retention around such bands. Anything
that encourages plaque accumulation can be detrimental to
Orthodontic Treatment periodontal health. Patients should also be taught how to
In cases where there is minimal labial recession but loss of clean around any appliance so that plaque accumulation is
interdental tissue, it may be possible to improve the appear- minimised.
ance with orthodontics. is involves interproximal “strip-
ping”, another term for reduction of the interproximal KEY POINT 5
enamel, to create small spaces between the teeth, allowing Orthodontic bands on molar teeth may increase plaque
the orthodontist to move the teeth together. is in turn (biolm) retention.
lengthens the contact points and reduces the interdental
papilla space. e technique is particularly useful in patients 2. Tooth Crowding
with triangular-shaped incisors, where the contact point
between adjacent teeth is often small and towards the inci- Many dentitions suer from crowding, which can be aes-
sal edge. In these cases, when the reduction and space clo- thetically displeasing and can also create diculties in oral
sure is complete, a more rectangular tooth shape is achieved, hygiene for patients. A common solution for crowding is
and the interdental space is reduced. Tarnow etal. (1992) extraction, and this is usually done through loss of a num-
investigated the distance between the contact point and the ber of premolars in certain combinations depending on the
alveolar crest and found that if this distance was 5 mm or desired tooth movement.
less, then an interdental papilla was present nearly 100%
of the time. When this distance was only 1 mm more, i.e. Influence on Treatment
6 mm, there was only a papilla approximately 56% of the Periodontitis can aect dierent teeth to a dierent extent in
time. Although orthodontics cannot predictably produce a the same mouth. As such, the orthodontist may want to alter
contact point to bone distance and hence a papilla, reducing the usual extraction pattern and remove a more compromised
the size of the “black triangles” usually leads to a signicant tooth to create the required space and leave the remaining
aesthetic improvement. teeth, which may have a more predictable prognosis.
KEY POINT 4 3. Reduced Bone Support

The loss of interdental papillae is often, unkindly, referred to
as “black triangle disease” because of the resulting interdental Although reduced bone support may mean that there is less
spacing.
bone to resist orthodontic tooth movement, it also means
that the teeth are more susceptible to tipping rather than
bodily movement, as the centre of rotation is lower. Under
The Role of Periodontics in Orthodontic these circumstances, using a force that would be suitable
Therapy for a healthy periodontium may result in “hyalinisation”
within the periodontal ligament. Hyalinisation describes
Orthodontic treatment involves applying a force to a tooth the cellular changes that occur if an excessive force is placed
that in turn induces osteoclastic and osteoblastic activity, on the periodontal ligament for a prolonged period. Blood
allowing the tooth to be moved within the alveolar bone. supply is compromised, and areas of sterile necrosis occur
As the tooth is moved, bone resorption takes place in the within the ligament. is in turn can result in a slowing or,
direction of the movement and bone deposition occurs on in extreme cases, prevention of tooth movement.
Influence on Treatment have orthodontic treatment (Melsen 1991). is dierence

Periodontal–orthodontic patients are usually treated with means that adult retention periods are usually signicantly
xed, as opposed to removable, appliances, allowing greater longer than those of children. It should be noted that xed
control of the force and the direction of the force. Practi- retainers should be inspected at every dental examination
cally, the orthodontist applies a signicantly lighter force for signs of debond or damage. ere are documented cases
to the teeth to avoid potential tipping problems and still where the retainer wire appears to have been “activated”,
achieve the desired tooth movement. possibly by trauma to the wire, leading to unwanted orth-
odontic tooth movement (Figure 7.2.3).
KEY POINT 6
Teeth with reduced bone support are more susceptible to Influence on Treatment
tipping rather than bodily movement. Adult orthodontic retention, in cases where there has been
periodontal destruction, usually requires permanent reten-
tion. It is preferable that this retention is of the palatal/lin-
4. Missing Teeth and Poor Anchorage
gual bonded arch wire variety. e patient’s consent must be
Tooth loss due to periodontitis is relatively common, and obtained prior to starting treatment, and permanent reten-
this can cause problems for the orthodontist who requires tion is something that a patient will need to accept and get
anchorage for orthodontic appliances. used to if they are to maintain a successful orthodontic out-
come in the long term. ese bonded retainers will have an
Influence on Treatment impact on self-performed plaque control, particularly with
In a stabilised periodontal patient where there may be miss- respect to interdental cleaning.
ing teeth, anchorage can be obtained using dental implants
or, more recently, temporary anchorage devices (TADs). KEY POINT 7
TADs are narrow diameter mini-implants, often placed After active orthodontic appliance therapy, adult retention
horizontally between teeth or in edentulous areas, that allow periods are usually signicantly longer than those of children
and, in adults where there has been periodontal destruction,
an anchor point from which forces can be applied. Con- retention may have to be permanent.
ventional implants can be restored on completion of the
orthodontic treatment, whereas TADs are removed when
no longer needed.
6. Gingival Biotype and Gingival Recession
5. Relapse and Retention Localised or generalised gingival recession is relatively com-
mon, especially in thinner periodontal biotypes where there
Post-orthodontic retention is a well-documented require- may be bone dehiscences and thin gingival tissues with little
ment for all patients to prevent orthodontic relapse which or no attached gingiva.
leads to extraction sites reopening or realigned teeth drift-
ing. Retention can be xed by way of bonded retainers or Influence on Treatment
using removable retainers such as Essix retainers. Sometimes e risk of post-operative recession in orthodontics relates
a combination of the two systems may be used. Studies have to the periodontal biotype and the desired tooth movement.
shown that there are biological and anatomical dierences Historically, in the UK, orthodontic treatment has centred
in the tissue reaction between adults and children who around an extraction-based approach in crowded dentitions.
A B
• Figure 7.2.3 Unplanned orthodontic tooth movement in an adult at the retention stage post-orthodon-
tics, possibly as a result of “activation” of the xed retention wire. (A) Incisal view, (B) labial view.
Routinely, a number of premolars are removed and the Sometimes, a prominent labial frenum has been thought
remaining teeth moved around in the spaces created. More responsible for a midline diastema, especially when the
recently, there has been an increasing trend towards non- maxillary labial frenum is thick and extends into the pala-
extraction, arch-expansion techniques, increasing the radius tal tissues. In these cases, a frenotomy may be considered
of the arch to create space for tooth movement. is results to remove this tissue. is is a more involved procedure
in a broader arch that is regarded by many patients as more compared to a frenectomy and it has been suggested that if
aesthetically pleasing, but evidence suggests that this result provided towards the end of the diastema closure, the scar-
is less stable and will require a longer period of retention. In ring and contracting of the healing tissue helps to main-
addition, labial tooth movement may move teeth outside tain the diastema closure. However, this assertion is not
the alveolar bone envelope, creating a bone dehiscence or evidence-based.
dehiscences. If the overlying soft tissue is thin, then there
may well be an increased chance of developing gingival 9. Gingival Invaginations
recession. Although this may not compromise the health of
the dentition, it can be aesthetically displeasing in a patient Occasionally, as teeth are brought together with orthodon-
undergoing an aesthetic procedure, such as orthodontics. tic appliances, there is an element of soft tissue bunching
Careful pretreatment assessment of the gingival health, peri- inter-proximally. Whereas this usually remodels over time,
odontal biotype and desired tooth movement is essential if occasionally, small soft tissue clefts or invaginations occur
post-treatment recessions are to be avoided. that can appear and look unsightly. Simple periodontal
Interestingly, Wennström etal. (1987) have shown that surgical techniques can eliminate such defects, producing a
it is not the apical–coronal measurement of the attached more favourable appearance.
gingiva that is important in determining the chances of
developing recession, but the bucco-labial “thickness” of the
tissues. Preparing Periodontal Patients for
Although some clinicians advocate pre-orthodontic aug- Orthodontic Treatment
mentation of thin biotypes in an attempt to prevent reces-
sion, the general consensus is that this is over-treatment Periodontitis is a destructive inammatory condition that
and the defects can be treated with free gingival grafts or results in bone loss around aected teeth. When an orth-
coronally advanced aps with subepithelial connective tis- odontic force is applied to a tooth, areas of both tension
sue grafts should they occur. and compression are established within the periodontal
ligament. On the side of the tooth under compression,
KEY POINT 8 osteoclasts resorb bone, and on the side of the tooth under
When dental arches are expanded during orthodontic tension, osteoblasts deposit bone, allowing a tooth to be
treatment, labial tooth movement may move teeth outside the moved within the alveolus. Orthodontic tooth movement
alveolar bone, creating a bone dehiscence or dehiscences. can be thought of as primarily a periodontal ligament phe-
nomenon that results in bone remodelling.
7. Minor Soft Tissue Surgery to Assist with Studies have shown that if periodontitis is not controlled
then orthodontic treatment may have an exacerbating eect
on the rate of bone loss (Kessler 1976, Bollen etal. 2008)
ere are several simple soft tissue procedures that can com- and, as such, careful preparation of a periodontal patient
plement orthodontic procedures, including pericision or is essential to prevent further bone loss during the active
berotomy, as discussed previously. is procedure involves orthodontic phase.
severing the periodontal bres under local anaesthetic. It
needs to be repeated every 4–6 weeks and has been advo- KEY POINT 9
cated for preventing the alveolar bone being moved down If periodontal diseases are not controlled, then orthodontic
when extruding a tooth and occasionally in preventing orth- treatment may have an exacerbating effect on the rate of bone
loss.
odontic relapse in de-rotated teeth.
8. Frenotomy or Frenectomy Periodontal Treatment

Localised gingival recession has in the past been attributed Periodontal treatment, both non-surgical and surgical, can
to the presence of a prominent labial frenum (“frenal pull”). be very successful in controlling the destructive nature of
ere is no evidence for this attribution, and the likelihood periodontal diseases in patients who perform high levels of
is that the frenum may compromise adequate plaque con- oral hygiene and modify their risk factors. Patients wishing
trol. Under these circumstances, a simple frenectomy can to undergo orthodontic treatment should have periodontal
be performed to remove the unwanted tissue and aid oral diseases stabilised and maintained prior to embarking on
hygiene. active orthodontic treatment. Orthodontic treatment in the
presence of active periodontal diseases is likely to result in Medico-Legal Issues

further periodontal breakdown.
Once orthodontic treatment commences, oral hygiene It is important to ensure that informed, valid consent is
may become more dicult for the patient because of the obtained when providing any treatment. is is especially
presence of orthodontic appliances, and access issues may important when providing orthodontic treatment for peri-
arise. is may inuence the clinician’s periodontal treat- odontally susceptible patients, for whom there may be
ment decisions towards more invasive surgical pocket reduc- increased risk of further loss of periodontal support.
tion techniques to leave the patient with a periodontium
that is easier to maintain. KEY POINT 12
Periodontally susceptible patients undergoing orthodon- Informed, valid patient consent is especially important when
tic treatment should have their periodontal health carefully providing orthodontic treatment for periodontally susceptible
maintained and monitored for at least 6 months prior to patients.
starting the active phase of orthodontic treatment to ensure
patient compliance and stability of the treatment outcomes. Multiple choice questions on the contents of this chapter
KEY POINT 10
Patients wishing to undergo orthodontic treatment should References
have periodontal diseases stabilised and maintained prior to
embarking on active orthodontic treatment. Bollen AM, Cunha-Cruz J, Bakko DW, Huang GJ, Hujoel PP. e eects
of orthodontic therapy on periodontal health: a systematic review of
controlled evidence. J Am Dent Assoc. 2008;139(4):413–422.
Monitoring and Maintenance Boyd RL, Baumrind S. Periodontal considerations in the use of
bonds or bands on molars in adolescents and adults. Angle Orthod.
Patients who have successfully completed their periodon- 1992;62:117–126.
tal treatment require professional maintenance or sup- Boyd RL, Leggott PJ, Quinn RS, Eakle WS, Chambers D. Periodon-
portive care. While maintenance regimens are tailored to tal implications of orthodontic treatment in adults with reduced
the individual based on a risk assessment, in practice most or normal periodontal tissues versus those of adolescents. Am J
periodontal patients will see their dentist or dental hygien- Orthod Dentofacial Orthop. 1989;96:191–199.
ist every 3 months for non-surgical maintenance and for Corrente G, Abudo R, Re S, Cardaropoli D, Cardaropoli G. Orth-
detailed periodontal charting at least annually. odontic movement into infrabony defects in patients with
Periodontal patients undergoing orthodontic treatment advanced periodontal disease: a clinical and radiological study. J
Periodontol. 2003;74(8):1104–1109.
should be regarded as high-risk patients; they should be
Kessler M. Interrelationships between orthodontics and periodontics.
seen at least every 3 months for professional maintenance Am J Orthod. 1976;70(2):154–172.
care and monitoring (Boyd etal. 1989). Anecdotally, some Machen DE. Legal aspects of orthodontic practice: risk management
periodontists double the frequency of maintenance to six concepts. Periodontal evaluation and updates: don’t abdicate your
weekly during the active phase of orthodontics. duty to diagnose and supervise. Am J Orthod Dentofacial Orthop.
Any sign of lack of compliance in home care by the 1990;98(1):84–85.
patient should result in orthodontic treatment being with- Melsen B. Limitations in adult orthodontics. In: Melsen B, ed.
drawn, even if the treatment is not completed (Machen Current Controversies in Orthodontics. Chicago: Quintessence;
1990). 1991:147–180.
All patients undergoing orthodontic treatment should Melsen B, Agerbaek N, Markenstam G. Intrusion of incisors in adult
continue with their normal dental routines by seeing their patients with marginal bone loss. Am J Orthod Dentofacial Orthop.
1989;(3):232–242.
general dentist or dental hygienist at the prescribed intervals
Tarnow DP, Magner AW, Fletcher P. e eect of the distance from
for screening of healthy dentitions or monitoring and main- the contact point to the crest of bone on the presence or absence of
tenance of compromised dentitions. Referring clinicians the interproximal dental papilla. J Periodontol. 1992;63:995–996.
should not abdicate their responsibility to the orthodontist Wennström JL, Lindhe J, Sinclair F, ilander B. Some periodon-
and, if anything, should be especially vigilant. tal tissue reactions to orthodontic tooth movement in monkeys. J
Clin Periodontol. 1987;14(3):121–129.
KEY POINT 11
Periodontal patients undergoing orthodontic treatment should
be regarded as high-risk patients.
7.3
Dental Implants –
Anatomy, Complications,
Management of Peri-
Implant Diseases
CO L I N P R I E ST L A N D A N D N E I L M E R E D I T H
CHAPTER OUTLINE
The Anatomical Architecture of Natural Teeth and Dental Implant Factors in Peri-Implant Disease
Implants Classiöcation and Diagnosis of Peri-Implant Diseases
Macro- and Micro-Anatomy of Natural Teeth and Dental Diagnosis of Peri-Implant Mucositis
Implants Diagnosis of Peri-Implantitis
Soft Tissue Biotype Management of Peri-Implant Diseases
Implant Complications Patient Prophylaxis
Aetiology and Pathogenesis of Peri-Implant Diseases Professional Support
Management of Peri-Implant Mucositis
Bioölm Formation and Maturation
Management of Peri-Implantitis
Speciöc Microbial Findings with Implants
Individualised Implant Maintenance
Incidence of Peri-Implant Inøammation
Follow-Up and Support
Histopathology of Periodontitis and Peri-Implantitis
Comparing Periodontal Diseases and Peri-Implant Diseases Summary

This chapter outlines the anatomical dierences between teeth and implants, the monitoring and maintenance of implants and the
management of complications including peri-implant mucositis and peri-implantitis.
• Understand the anatomical diòerences, and their • The anatomical architecture of natural teeth and dental
signiöcance, between the supporting tissues of natural teeth implants
and those of dental implants • Dental implant maintenance, complications and
• Understand the key elements of treatment planning and the management
use of diagnostic information including 3D imaging • Peri-implant inøammatory diseases.
• Understand the clinical stages in the routine maintenance of ere is also an online component to this chapter which covers the
implants following:
• Understand the complications arising from dental implant • Development of modern dental implantology
treatment, their possible causes and methods of treatment. • Treatment planning for dental implant therapy
• The insertion and restoration of dental implants
• Grafting and augmentation materials in dental implantology.
271
The Anatomical Architecture of Natural teeth support the soft tissue architecture of the interdental
papilla (Palmer 1999). Such a papilla between two adjacent
Teeth and Dental Implants implants relies on other factors including the underlying
Macro- and Micro-Anatomy of Natural Teeth bone architecture, soft tissue thickness, restorative emer-
and Dental Implants gence prole and the distance from the bone crest to the
contact point between the two restorations (Tarnow etal.
e anatomy of the interface between a natural tooth and 1992). Other factors that play a role in the stability of the
the surrounding soft tissues, periodontal ligament and bone soft tissues around dental implants are as follows:
diers markedly from the anatomy around an implant • ɨe biologic width (now referred to as the “supracrestal
(see Figure 7.3.1). ese macro-anatomical dierences are tissue attachment”) has been investigated in a cadaver
manifest in the dierent orientation and absence of groups study by Gargiulo etal. (2002). e dentogingival junc-
of gingival connective tissue bres, the absence of a peri- tion was reported to have a mean width of 2.04 mm
odontal ligament around an implant, and the direct rela- comprising supra-crestal connective tissue and junctional
tionship between the implant surface and bone seen in epithelial attachment. Encroachment to within 2 mm of
osseointegration. the bone crest appears to result in bone loss in a similar
e collagen bre arrangement in the connective tissues manner at both teeth and implants leading to soft tissue
around implants diers markedly from the arrangement recession.
seen around natural teeth. Gingival bres are inserted into • ɨe attachment of the long junctional epithelium to
the root surface of natural teeth but not generally into an the tooth surface appears to be mediated by hemi-des-
implant surface. e attachment in the implant situation mosomes along the entire length of the junctional epi-
exists at the most coronal point of osseointegration. thelium while such an attachment appears to exist only
e primary orientation of connective tissue bres in the apical region of the peri-implant cu epithelium
around implants is similar to that of circular gingival bres to the implant surface (Stern 1981). is apparently
around teeth, there being a complete absence of oblique reduced attachment at implants may also contrib-
bres, trans-septal or dentogingival bres. is dierence ute to the weaker soft tissue barrier to bacterial ingress
in the arrangement of bres, including the absence of den- (Hermann etal. 2001). e micro-anatomical interface
togingival bres, in particular, and the existence of a pas- between tooth or implant and the surrounding tissues
sive soft tissue “cu” relationship between the soft tissues may play an important role in the dierence in suscepti-
and the implant surface, may play a role in the increased bility to bacterial ingress and the degree of extension of
susceptibility of the peri-implant tissues to plaque-induced the associated inammatory lesion in the local soft tissue.
inammation over the susceptibility of the periodontal tis- • Further histomorphometric analysis conducted on the
sue arrangement around a natural tooth. attachment zones between the soft tissues, bone and
e anatomy of the interdental or inter-implant papil- the tooth or implant have been reported to demon-
lae diers; dentogingival bres associated with natural strate comparable ratios of collagen, blood vessels and
Gingival sulcus Gingival sulcus
Junctional epithelium Epithelial cuff
Dentogingival, crestal Circular and crestal fibres

and circular fibres (parallel, less vascular,
(perpendicular) more scar tissue)
• Figure 7.3.1 The tooth/implant–host interface in health. Note the greater concentration of gingival bres
around teeth compared to implants (Renvert & Giovannoli 2012).
CHAPTER 7.3 Dental Implants – Anatomy, Complications, Management of Peri-Implant Diseases 273
plasma cells. However, analysis at implants demonstrated

reduced proportions of macrophages and polymorpho-
nuclear leucocytes. is was interpreted to reect a
weaker immuno-inammatory barrier at implants than
found around teeth (Ivanovski & Lee 2018).
KEY POINT 1
There are fundamental differences in the soft and hard tissue
attachments between teeth and implants.
Natural teeth are generally surrounded by a band of

keratinised attached gingiva, whereas the positioning of
implants with respect to keratinised tissue remains under
the control of the surgeon. In cases where there has been
a need for signicant bone augmentation and hence, an • Figure 7.3.2 Peri-implantitis around implants with no keratinised gin-
gival margin.
expansion of the ridge volume, the buccal tissues are often
advanced coronally to achieve primary closure of the surgi-
cal wound. Where there was a pre-existing wide band of
keratinised gingiva prior to placing the bone augmentation but it is generally believed that where a thin biotype exists,
material and achieving primary closure, it is likely that after it is more dicult to achieve a stable soft tissue–implant
primary closure, the muco-gingival junction will remain on relationship than would be the case in the presence of a
the labial or buccal alveolar plate, albeit positioned more thick biotype. Denitive measurements within the classi-
coronally. is will result in the implant retaining a reduced cation of thick versus thin biotype have yet to be universally
width of keratinised gingiva. accepted, but generally <1 mm thickness is thin biotype and
In many cases, however, the coronal advancement of the >2 mm is thick biotype. e tissue between 1 mm and 2
labial or buccal ap, with a pre-existing narrow band of kera- mm may provide some confusion when attempting to inter-
tinised gingiva, results in the mucogingival junction being pret the literature and the eects of biotype on tissue suscep-
located on the ridge crest of the alveolar process so that the tibility to peri-implant mucositis, implantitis, recession and
buccal aspect of the implant has a non-keratinised alveolar crestal bone loss.
mucosal cu around the buccal aspect of the implant, abut-
ment or restoration. Implant Complications
It has been suggested that, at sites where the band of
keratinised peri-implant tissue is less than 2 mm in width, ere is a misconception that once successfully integrated,
greater plaque accumulation is found in conjunction dental implants will last a lifetime. is is both inaccu-
with inammation, but further research is required to rate and misleading. Failures and complications may arise
clarify if this tissue arrangement is a signicant aetiologi- because of either biomechanical or biological factors, or a
cal factor in the development of peri-implant inamma- combination of the two.
tion resulting in peri-implant mucositis, peri-implantitis • Biomechanical factors include:
or recession.  • Occlusal overload – can result in peri-implant bone loss
e need for keratinised tissue has been investigated and typically with the radiographic appearance of a verti-
reported by Wennström & Derks (2012), but following review cal or funnel-shaped defect. is may be due to poor
of 19 studies, they concluded that there was insucient com- occlusal design. Such situations may include the use
parable data to draw any scientic and statistical conclusions of distal cantilever pontics and occlusal schemes with
regarding the relationship between the width of keratinised tis- increased load application in the intercuspal position/
sue around implants and the degree of plaque accumulation, centric occlusion (ICP/CO) or interferences during
peri-implant inammation and recession around implants various mandibular excursions from ICP/CO. High
(see Figure 7.3.2). However, it should remain the aim in all levels of occlusal loading can be applied to implants
implant surgery to achieve keratinised tissue around implants by bruxing and other parafunction, including clench-
whenever possible (see Figures 7.3.3 and 7.3.4). ing, or by poor biomechanical prosthesis design. e
consequence of excessive loads can result in bone loss
KEY POINT 2 and also implant, abutment screw and prosthesis frac-
An adequate zone of keratinised tissue around implants may ture. Provision of an occlusal splint should be consid-
help to ensure future peri-implant health. ered in patients exhibiting parafunction.
 • Poor implant angulation – generally occlusal forces
should be applied along the long axis of an implant.
Soft Tissue Biotype is is not always achievable but should generally
e soft tissue biotype refers to the thickness and contour of be the aim. Overloading or angulated loading can
the gingival tissues. ere is no clear denition of biotype, typically result in implant or component fracture.
Exceptions exist to this general rule, for example, disease and suer signicant destructive changes
when implants are joined by a bar or laser-welded with loss of periodontal attachment levels are gen-
sub-structure to support a xed or removable bridge, erally found to be more susceptible to peri-implant
hybrid bridge or over-denture. inammatory diseases, with those who have more
 • Inappropriate components – poor-quality components severe periodontal diseases being the most suscep-
can contribute to implant failure and components tible to peri-implant complications (Sousa et al.
must conform to nationally accepted standards. 2016). However, past periodontal patients who have
• Biological factors: received treatment and who have continued to main-
 • Plaque-induced inammation – this may be due to a lack tain excellent plaque control may continue to enjoy
of patient motivation to perform detailed plaque con- good peri-implant health after implant therapy. ese
trol procedures, poor manual dexterity that may arise patients will continue to be genetically susceptible to
as a patient ages or as their health deteriorates, or dif- peri-implant inammatory disease in the presence of
culty in achieving adequate access for plaque removal reduced oral hygiene and plaque accumulation.
due to poor laboratory design, with inadequate atten-  • in tissue biotype – a thin biotype has been identied
tion being paid to the accessibility of cleaning aids to as a risk factor for the development of peri-implant
enable the patient to maintain plaque control beneath inammation and recession in the presence of sub-
the prosthetic device and around the implant cu to optimal hygiene. It may be prudent to alter the nature
maintain soft and hard tissue health. Resulting peri- of the surrounding soft tissue by the provision of a
implant inammation may arise, leading to the devel- sub-epithelial connective tissue or free gingival graft.
opment of peri-implant mucositis or peri-implantitis. Alternative xenogenic and allograft materials are also
 • Smoking – there is an association between those available to extend the keratinised zone or thicken the
patients who smoke and peri-implant diseases. A adjacent soft tissue.
contributing factor to oral disease in smokers is the  • Uncontrolled or inadequately controlled diabetes –
vasoconstriction in the oral and circum-oral region, patients suering diabetes that remains inadequately
resulting from numerous chemicals present in the controlled by diet, medication or both are more prone
smoke to which the oral tissues are exposed. is to infection. However, well-controlled diabetics who
reduces vascularity and blood ow to the oral and maintain good oral hygiene are not considered to
circum-oral tissues that may cause oxidative stress have any greater susceptibility to infection than non-
of the tissues, increasing their susceptibility to infec- diabetic patients. Patients who fail to demonstrate a
tion and adversely aecting the tissues’ ability to heal. commitment to maintaining both good oral hygiene
Smoking must therefore be considered an important and eective diabetic control are therefore not ideal
risk factor in the aetiology of peri-implant mucositis for implant therapy.
and peri-implantitis, and smokers should be strongly
encouraged to quit before embarking on an implant KEY POINT 3
treatment plan. Implants are susceptible to failures and complications due to
 • Past history of periodontal disease – those patients who either biomechanical or biological factors, or a combination of
are susceptible to chronic inammatory periodontal the two.
A B
• Figure 7.3.3 (A) An implant at UR1 with healthy gingival margins (B) Radiograph of the same implant
showing good bone support
that demonstrated putative pathogens Porphyromonas gingi-

valis, Prevotella intermedia, Prevotella nigrescens, and Aggrega-
tibacter actinomycetemcomitans in 60% of cases. Organisms
not normally associated with periodontitis, including Staph-
ylococcus spp., enteric organisms and Candida spp., were
found in 55% of peri-implantitis sites, whereas healthy sites
around implants demonstrated a microbiota associated with
periodontal health around natural teeth.
In summary, Leonhardt and co-workers suggest healthy
implant sulci harbour a similar ora to healthy gingival
crevices around teeth. However, sites with peri-implantitis
were found to be populated with organisms associated with
periodontitis in almost equal proportions to additional
ora, including Staphylococci, yeasts and enteric organisms
• Figure 7.3.4 Peri-implant health in an edentulous mandible in a
patient with a number of risk factors, including xerostomia, but with (Leonhardt etal. 1999).
excellent oral hygiene. This patient had been provided with a mandibu- It has also been demonstrated by ligature-induced plaque
lar bar and clip-retained over-denture to allow for proper self-care and formation in the dog model that, where the implant sur-
professional maintenance. face is exposed to microbial contamination, the degree of
roughness of an implant surface inuences the nature of the
ora that develops on that surface (Berglundh etal. 2007).
Aetiology and Pathogenesis of It was also found that rougher implant surfaces exhibit
accelerated progression of peri-implantitis. is explains the
Peri-Implant Diseases general preference for implants with a relatively smooth col-
Biofilm Formation and Maturation lar despite the high degree of roughness of that part of the
implant designed for osseointegration within the bone.
ere are over 700 microbial species that exist in the human
mouth from which the biolm can develop (Aas etal. 2005). KEY POINT 4
Periodontitis (and by inference peri-implant diseases) is a Implants can accumulate both a health- and disease-
biolm-associated disease (Darveau et al. 1997, Marsh 2005) associated biolm in the same manner as teeth.
and many microbial interactions take place to protect the
bacterial species and increase their pathogenicity and poten-
tial to induce tissue destruction (Schaudinn etal. 2009). Incidence of Peri-Implant Inflammation
In several large-scale and international research stud-
Specific Microbial Findings with Implants
ies, patients have received implant therapy and have then
Healthy osseo-integrated implants have been found to have returned to the ongoing care of their general dentist. Large
relatively little biolm and minimal inammation associ- numbers of such patients have then been recalled for re-
ated with the peri-implant sulcus (Lekholm et al. 1986; examination to assess the health of the soft tissues and the
Leonhardt et al. 1992). e ora found around healthy bone surrounding the implants. e results show that unless
implant sites are similar to the ora found in gingival health implant patients are given specic implant care (including
around natural teeth (Mombelli & Meriscke-Stern 1990, professional cleaning and oral hygiene advice), a progres-
Rams etal. 1991). It has also been demonstrated that the sive reduction in peri-implant bone can be expected. e
presence of putative periodontopathogens is more common extent of inammation and bone loss around dental osseo-
in dentate implant patients rather than edentulous patients, integrated implants in those patients who fail to get the pro-
suggesting that periodontal pockets present around natural fessional support they need is disturbing.
teeth may serve as a reservoir for organisms from which col- e results vary between studies largely because of a
onisation of titanium implants may occur (Apse etal. 1989, variation in denitions and thresholds. Zitzmann & Ber
Quiryen & Listgarten 1990, Leonhardt etal. 1999). glundh (2008) reported peri-implant mucositis occurred
e microbiological studies carried out in patients who in approximately 80% of the subjects and in 50% of the
have suered bone loss around implants indicate similar implants. It has also been reported that around 50% of
ndings to those reported in periodontitis. In a study involv- implant patients are found to exhibit peri-implant inam-
ing 51 patients with healthy implant-supporting tissues and matory changes (Koldsland etal. 2010) and around 20% of
37 patients with one or more implants with loss of attach- all implant patients and 10–15% of implants were found
ment of three or more threads accompanied by bleeding on to have suered from peri-implantitis (Mombelli et al.
probing and suppuration, subgingival plaque samples were 2012). It is therefore imperative that the periodontal and
collected using paper points. Culture studies were performed implant communities agree to common threshold levels for
peri-implant mucositis and implantitis to allow comparison were analysed separately, a frequency of peri-implantitis was
of research studies on this subject. found to be 36.3%. e authors therefore concluded that
Patients who have a history of periodontitis are suscep- supportive periodontal therapy appeared to reduce the rate
tible to the destructive eects of periodontal inammation of occurrence of peri-implantitis. ey further concluded
around implants as well as natural teeth. ese patients that peri-implant diseases are not uncommon following
must receive meticulous periodontal therapy to reduce the implant therapy. Long-term maintenance care for high-risk
plaque to below the threshold required to initiate inamma- groups is essential to reduce the risk of peri-implantitis. It
tion in that patient. e elimination of this inammation was also proposed that informed consent for patients receiv-
can then stabilise peri-implant disease. Once clinically and ing implant treatment must include patient acceptance of
radiographically classied as stable, implant patients should the need for appropriate maintenance therapy.
be provided with regular ongoing periodontal supportive
treatment in the presence of patient cooperation. KEY POINT 5
In a study of periodontally susceptible patients who were Peri-implant diseases are not uncommon following implant
receiving periodontal supportive therapy, 786 implants were therapy, and long-term maintenance care is essential to reduce
assessed in 239 patients. Data was analysed at both the sub- the risk of peri-implant diseases.
ject and implant level. Peri-implant mucositis was diagnosed
in 24.7% of subjects and 12.8% of implants whereas peri- Histopathology of Periodontitis and
implantitis was diagnosed in 15.1% of subjects and 9.8%
Peri-Implantitis
of implants (Aguirre-Zorzano etal. 2015). ey concluded
that the level of peri-implant inammatory disease was ere are histopathological dierences between lesions
clinically signicant with aetiologically signicant factors of periodontitis around natural teeth and lesions of peri-
being plaque index and implant location. However, these implantitis at implant sites. Results of studies and analysis
gures appear to be no greater than studies of patients with of human biopsy material have shown that peri-implantitis
no history of periodontal disease (Mombelli et al. 2012, lesions are poorly encapsulated and are more closely associ-
Koldsland etal. 2010) thereby demonstrating the benets ated with the adjacent bone (Berglundh et al. 2011) (see
of supportive periodontal care for implant patients who Figure 7.3.5). Inammatory lesions are larger and extend
remain susceptible to peri-implant inammatory disease. nearer the bone crest than equivalent lesions seen in peri-
Atieh etal. (2012) carried out a meta-analysis of 9 stud- odontitis, consistent with the reduced connective tissue
ies with 1497 subjects and 6283 implants included in the bres around implants compared to natural teeth. Lesions
analysis. It was found that the frequency of peri-implant of peri-implantitis have been found to contain larger pro-
mucositis was 63.4% of subjects and 30.7% of implants, portions of neutrophils and osteoclasts than would nor-
and the frequency of peri-implantitis was 18.8% of sub- mally be seen in sites of periodontitis around natural teeth
jects and 9.6% of implants. When the data for smokers (Carcuac etal. 2013).
Lesion contained by Lesion not contained

connective tissue
Complex surface
to manage
Bone resorbs away from
Bone may get infected -
the advancing lesion -
evidence of bacteria in
never gets infected
affected bone
• Figure 7.3.5 The tooth/implant–host interface in disease (Renvert & Giovannoli 2012).
Comparing Periodontal Diseases and there has been a clear association between bone loss, implant
Peri-Implant Diseases failure and various implant surfaces and designs. Sur-
faces including TPS (titanium plasma sprayed) and some
e microbiological, immunological and anatomical nd- hydroxyapatite coatings were clearly linked to clinical fail-
ings of research suggests that there are similarities between ure as were hollow and basket-shaped designs. Several stud-
natural teeth and implants in health, and similarities ies are cited that demonstrate little or no bone loss around
between periodontitis and peri-implantitis, but dierences rough-surfaced implants having a surface roughness Sa value
remain that have still to be completely explained when com- of 1.5 or greater. However, many experienced clinicians are
paring lesions of periodontitis and peri-implantitis. observing a higher level of peri-implantitis in “real-world”
Implant failure has been divided into early, late and non- clinical groups where rougher surfaces have been used.
infectious (overload) (Esposito etal. 1998). ere are a large e question remains: is a conservative, moderately
number of interrelated factors and cofactors that may con- rough implant surface and design sucient to achieve the
tribute to peri-implant disease; these include cardiovascular early integration desired today and yet provide the long-
disease, diabetes, smoking, medication and implant surface term stability and bone level maintenance essential to long-
topography. e complexity of the aetiology makes isolation term clinical success?
of single factors dicult to achieve. Ideal implant anatomy involves an intimate relationship
It has long been established that the regular and eec- between the prosthetic abutment and the peri-implant soft
tive biolm control is required to prevent the development tissue cu. e implant collar should be deeply placed, level
of gingivitis around natural teeth (Löe etal. 1965, ei- with the crest of the bone allowing for close adaptation of
lade et al. 1966, Löe et al. 1967) and that poor biolm the gingival tissue to the implant abutment. Some implant
control will allow the progression from gingivitis to severe manufacturers, in order to increase the connective tissue
loss of periodontal support in a proportion of subjects, volume around the connection between the implant and
but not all. is indicated that periodontal disease may the prosthetic abutment, have adopted a platform-switch
be a disease of a high-risk, susceptible group consisting of design in an attempt to maintain tissue stability. Other
around 15–30% of the population. Chapter 1.3 identies implants exhibit surface design features to encourage the
the epidemiology of periodontal diseases. It is also con- attachment of connective tissue to the collar zone of the
rmed that the cause of this progression is multifactorial implant, whereas other systems employ a collar that exhibits
in nature with genetics, smoking exposure, systemic dis- a far smoother texture than the surface of the implant that
ease, immunological factors, local factors and oral hygiene is designed to encourage bone apposition or soft tissue des-
all playing a role. is complex relationship between the mosomal attachment.
causative factors, periodontal tissues and immunologi- Implants that have a relatively smooth, machined collar
cal defence mechanisms resulting in chronic periodon- attract less plaque deposition and are far easier to maintain
titis around natural teeth has been researched for many plaque free with correct hygiene techniques. Implants with
years. e relationship between implants and peri-implant a uniform rough surface throughout the body and collar
inammatory disease has been researched for only a frac- of the implant encourage plaque accumulation at the collar
tion of that time and therefore it is not surprising that and present a dicult surface from which to remove plaque,
many questions remain unanswered. when exposed to the subgingival environment or when
e current understanding of the relationship between exposed to the oral cavity. When presenting for treatment,
implants, implant restorations and peri-implant soft and the dental hygienist, dentist or periodontist will encounter
hard tissue health is that peri-implant mucositis is largely greater diculty in achieving adequate disinfection and
equivalent to gingivitis whereas peri-implantitis is largely removal of toxins, including lipopolysaccharide endotoxin,
equivalent to periodontitis. from any implant where the rough surface has become
contaminated.
KEY POINT 6 As in periodontally susceptible patients, it remains the
Peri-implant mucositis is the equivalent of gingivitis, and peri- responsibility of the patient to maintain adequate biolm
implantitis is the equivalent of periodontitis. control on a daily basis. ere are many techniques available
to access the more anatomically inaccessible sites to disrupt
It is generally accepted that peri-implant mucositis is the biolm. is is a fundamental requirement to avoid
found where there is plaque accumulation. e quantity plaque biolm accumulation, development of periodontal
of plaque is dicult to assess objectively, as the aetiological or peri-implant inammation and associated periodontal or
ora inhabit the subgingival environment and limitations peri-implant attachment destruction.
exist in objective quantitative and qualitative assessment of
this primarily anaerobic ecological niche of microorganisms. KEY POINT 7
It is the responsibility of the patient to maintain adequate
biolm control around implants on a daily basis.
Implant Factors in Peri-Implant Disease
e association between the aetiology of peri-implant disease Routine, professional follow-up is an essential tool in
and implant surface design is a contentious one. Historically order to maintain a functional and healthy implant/tissue
interface to ensure long-term implant success and to iden- mucositis and peri-implantitis were dened clinically and
tify and manage any potential complications early. Serial histologically. e clinical denitions of these various states
intraoral radiographs are a useful adjunct to clinical exami- of peri-implant health and disease are described in Table
nation in monitoring bone levels, but to be most eective, 7.3.1
the view should be taken in a reproducible technique; with
the lm parallel to the implant long axis, the central beam of Diagnosis of Peri-Implant Mucositis
the X-rays should be directed at right angles to the implant,
and the lm providing a clear and detailed image of the e diagnostic signs of peri-implant mucositis include an
implant thread and the bone. By repeated imaging in such alteration in the soft tissue colour with erythema, changed
a reproducible manner, changes in bone level can be identi- soft tissue contour, bleeding on probing and/or suppura-
ed, ensuring timely periodontal support before signicant tion, commonly associated with increased probing depths
peri-implant support is lost. of up to 4 mm in the absence of radiographic loss of bone
from around the implant.
Classification and Diagnosis of Peri-Implant e incidence reported in the literature varies widely
Diseases depending on diagnostic criteria adopted. Peri-implant
mucositis has been reported to aect between 25% and
e 2018 World Workshop on the Classication of Peri- 80% of subjects and 13% and 50% of implants accord-
odontal and Peri-implant Diseases and Conditions pro- ing to Roos-Jansaker etal. (2006), Zitzmann & Berglundh
posed a new classication system for both periodontal and (2008) and Aguirre-Zorzano etal. (2015). Such wide varia-
peri-implant diseases (Caton et al. 2018) which has now tions in prevalence indicates the need for globally agreed
been globally accepted. Peri-implant health, peri-implant diagnostic criteria.
A B
• Figure 7.3.6 (A) Peri-implantitis around an implant with attached gingivae; (B) radiograph of the same
implant.
A B
• Figure 7.3.7 (A) Peri-implantitis around an implant with no attached gingivae; (B) radiograph of the same
implant.
TABLE Clinical denitions of peri-implant health Diagnosis of Peri-Implantitis

7.3.1 and disease
In addition to peri-implant inammation, with or with-
Condition Clinical features
out suppuration, peri-implantitis presents with bone loss
Peri-implant • absence of signs of inammation that may be detectable either clinically or radiographically
health • absence of bleeding and/or (see Figures 7.3.6 and 7.3.7). Early detection of bone loss
suppuration on gentle probing relies on accurate and reproducible radiography with a
• no increase in probing depth
compared to previous examinations lm parallel to the long axis of the implant. e bone crest
• Note: peri-implant health can exist may then be related to the thread of the implant, provid-
around implants with some pocketing ing accurate interpretation when judging if the crest has
• absence of bone loss beyond crestal remained stable or has reduced. Periodontal probing is also
bone levels a useful examination to determine whether the implant
• Note: peri-implant health can exist
around implants with variable levels thread can be detected. e incidence of peri-implantitis
of bone support varies between studies, but when the criteria for radio-
graphic bone loss is set at 2 mm or greater, then incidence
Peri-implant • presence of bleeding and/or
mucositis suppuration on gentle probing with is generally reported around 20% of subjects and 10% of
or without increased probing depth implants (Atieh etal. 2012, Aguirre-Zorzano etal. 2015).
compared to previous examinations Globally accepted diagnostic criteria need to be adopted
• absence of bone loss beyond crestal to ensure comparability of peri-implantitis studies, thereby
bone levels increasing the number of studies that may be accepted for
•
vary and peri-implant mucositis can systematic reviews.
exist around implants with variable
levels of bone support
Management of Peri-Implant Diseases
Peri-implantitis • presence of bleeding and/or
(established suppuration on gentle probing Patient Prophylaxis
patient) • increased probing depth compared
to previous examinations Daily biolm disruption around all implants and teeth
• presence of bone loss beyond crestal should be achieved using an accepted technique. Brushing
bone levels
with a conventional manual toothbrush is often ineective
Peri-implantitis • presence of bleeding and/or for a number of reasons that include:
(new suppuration on gentle probing • incorrect size of the brush head,
patient) • probing depths ≥6 mm
• bone levels ≥ 3 mm apical to
• use of a scrubbing motion,
the most coronal portion of the • use of hard bristles,
intraosseous part of the implant • use of excessive force,
• • inadequate frequency of brushing,
vary, and recession of the mucosal • inadequate brushing time,
margin should be considered in
probing depth evaluation
• missing areas because of a lack of a standardised sequence
of brushing.
A systematic review of 59 studies revealed an average plaque
Diseases and Conditions 2018)
Reprinted from Journal of Clinical Periodontology 45(S20):8, Maurizio S
removal of 42% (range 30–53%) depending on the particular
Tonetti et al. (2018), with permission from John Wiley & Sons. plaque index chosen. Dierences in bristle tuft design were
found to inuence the outcome with angled designs being
more eêective, achieving a plaque reduction of 62%. Brush
Experimental studies of peri-implant mucositis indicate ing duration was also important in plaque removal.
that inammatory changes are reversible following thorough Systematic reviews of studies investigating the eec-
anti-infective therapy (Pontoriero et al. 1994, Salvi et al. tiveness of powered brushes versus manual brushes have
2012), with elimination of the biolm from the implant, been published. ese have demonstrated more eec-
prosthetic abutment and restoration surfaces. tive plaque removal with powered brushes than manual
Left untreated, peri-implant mucositis appears to be the brushes (Niedermann 2003, Deery et al. 2004). More
precursor to peri-implantitis in many cases, in the same recently the incorporation of accelerometer sensors into
way as gingivitis is a precursor to periodontitis. However, powered brushes altering the brushing mode depending
just as patients suering from gingivitis may experience a on brush position further improves the eectiveness of
stable gingivitis that does not progress to a destructive peri- plaque removal.
odontitis, it appears that peri-implant mucositis does not • A high frequency electric vibration brush can be eêective
necessarily progress to peri-implantitis. However, if peri- in maintaining a high standard of plaque control; how-
implant mucositis is found to be present, treatment should ever, this technique should be supplemented with oss
be directed at its elimination and future prevention to avoid and proximal brushes of various designs between teeth/
the potential for the development of peri-implantitis. implants to obtain the best plaque control possible.
• For manual brushing a single-tufted interproximal brush Management of Peri-Implant Mucositis
may also be eective used at an angle of 45 degrees to the
restoration or tooth surface, the bristles should be splayed e successful management of this early stage of peri-
apart, and then advanced subgingivally before initiat- implant inammatory disease is dependent on clear com-
ing a very small vibratory movement. is requires a fair munication of suitable home plaque control measures and
degree of manual dexterity that not all patients possess. motivation of the patient to achieve improved biolm
• Antimicrobial agents may be used on the brush, though disruption in order to resolve inammation and maintain
the length of time the active ingredient remains in the improved peri-implant health. Once the patient is able and
crevice/cu is likely to be short and will therefore have a willing to perform the necessary hygiene measures, then the
limited antimicrobial eect. peri-implant environment should be professionally cleaned
in a thorough manner using ultrasonic or piezo-electric scal-
ing tips suitable for use against the implant surface. Hand
Professional Support instrumentation is relatively ineective, particularly when
Regular and thorough professional debridement of the the biolm is attached to the microscopically rough surface
implant/abutment/restoration surfaces exposed to contami- of the implant.
nation must take place. is can be achieved using several Adjunctive use of antimicrobials, air polishing or suit-
techniques, all of which have a place in the prevention and able laser therapy may be applied at the clinician’s discre-
treatment of periodontal and peri-implant disease. tion to improve antimicrobial activity. Review of the site
• Ultrasonic or piezo-electric scalers with non-damaging is essential to ensure healing is taking place, and a longer-
tips for implant surfaces including Teon, plastic or tita- term maintenance regime should be agreed upon with the
nium inserts. e inserts must be very narrow to gain patient to ensure the improvement in peri-implant health
access to the relatively inaccessible sites where debride- is maintained. Once a patient has been identied as being
ment or biolm disruption is required, particularly in the susceptible to peri-implant mucositis, their susceptibility
interdental areas and within the peri-implant cu. remains, and they should therefore be considered a higher-
• Hand instrumentation is best limited to removing calculus risk patient and provided with an enhanced professionally
that remains despite piezo-electric or ultrasonic scaling. supported maintenance care plan.
• Following mechanical bioëlm disruption, adjunctive
methods may be employed to achieve as near as possible KEY POINT 8
to complete elimination of the microbial plaque if there Both daily home care and professional support are essential to
is a periodontal or peri-implant inammatory response ensure long-term peri-implant health.
to established plaque. ese adjunctive techniques may
include the following:
 • Lasers may be beneëcial using light energy of a wave Management of Peri-Implantitis
length that is absorbed by particular pigments produced
by many anaerobic, pathogenic bacteria. e applica- Heitz-Mayeld & Mombelli (2014) conducted a system-
tion of laser light energy that is preferentially absorbed atic review and concluded that generally treatment of
by those particular pigments will result in the destruc- peri-implantitis results in an improvement in the clini-
tion of the pigment-containing bacteria. Furthermore, cal condition. However, peri-implantitis in some patients
if there is an associated inammatory response to the appears to present a degree of resistance to therapy. In
presence of those pathogenic bacteria, and the laser these patients there was a recurrence or progression of peri-
light energy is preferentially absorbed by haemoglobin implantitis that required re-treatment or removal of the
in the expanded vasculature, then this inamed tissue implant. e eectiveness of therapy appears to relate to the
will also be destroyed. is will have the eect of reduc- thoroughness of anti-infective treatment with elimination
ing the extent of the inammatory lesion. of the biolm from the surfaces of the implant/abutment/
 • ɨe use of air polishing (a pressurised air jet with restoration being the aim. e most appropriate treatment
abrasive particles) can be eective in removing par- protocol will be individually driven by patient and site-spe-
ticles from the supra- and subgingival environments cic factors.
and from tooth or implant surfaces. Increasing concern has been expressed for sites with peri-
 • Submucosal application of chlorhexidine may also implantitis resulting from the incomplete removal of cement
have a benecial eect on microbial control. e lit- left in the subgingival space around dental implants follow-
erature is equivocal on the benets of antimicrobials ing cementation of the implant restoration (Wilson 2009).
and antiseptics to enhance plaque control and control e cementation of crowns on implants is still a common
periodontal inammation. ere appears to be inad- practice, though screw retention is preferable for retrievabil-
equate scientic evidence and guidance on the use of ity in case of restorative fractures or peri-implant inam-
sub-mucosal application of antibiotic and antiseptic matory disease. Several commonly used luting cements are
preparations to achieve eective control of ora in undetectable on radiographs (Wadhwani et al. 2010) and
peri-implant disease. therefore can only be found by careful periodontal probing
with an appropriate instrument. e cement surface topog- challenge for the patient. In these cases the application of a
raphy is likely to provide a suitable plaque-retentive surface sub-epithelial connective tissue graft may thicken the tissues
for the development of a biolm with resulting inamma- signicantly and provide a more robust barrier to the devel-
tion. Complete removal of all cement deposits is required to opment of peri-implantitis in the future, where formerly
prevent progressive loss of attachment and the development the implant was surrounded by non-keratinised alveolar
of a severe peri-implantitis. mucosa. Modication of the implant surface may also pro-
A detailed assessment of the extent and degree of peri- vide additional benets by removing supra-gingival threads
implantitis should be undertaken combining visual, radio- and rough implant surface and achieving a polished surface
graphic and probing examinations to achieve a clear picture more conducive to plaque removal by the patient. However,
of the underlying bone contour and possible implant sur- such surface modication of the titanium implant surface
face exposure due to bone dehiscence. An assessment should may be challenging because of poor access proximally.
also be made of the degree of biolm accumulation and the Appropriate treatment depends on correct diagnosis,
patient educated on the correct performance of biolm con- identication of relevant contributing factors and assess-
trol. It is very often helpful to remove the prosthesis and ment of the level of bone destruction taking place. While
replace with healing abutments to facilitate easier access management of peri-implant mucositis is within the scope
for home care throughout the period of treatment for the of practice of a general dentist with implant training, the
peri-implantitis. identication of such a lesion from one where peri-implan-
Once the patient is able to carry out home care to the titis is becoming established can be challenging. For that
necessary standard, professional cleaning should be per- reason, the referral of such patients for specialist assess-
formed and the patient reviewed over time to conrm ment and management should be considered at an early
their continued cooperation and healing. It is likely that stage in the disease process, rather than providing incom-
the peri-implant sulcus depth will be deeper where peri- plete therapy that allows further deterioration and loss of
implantitis has been present, and biolm control tech- supporting bone that may endanger the longevity of the
niques may have to be modied to achieve this more implant and restoration. Early referral is far preferable to
challenging biolm disruption and more frequent profes- late referral and will both maintain the patient’s condence
sional support in a less accessible location. More adjunctive in their general dental practitioner and provide the practi-
therapeutic techniques may be applied from the outset in tioner with a measure of medico-legal defence should peri-
order to achieve control of the destructive lesion. e use implantitis endanger the implant and the patient wish to
of a diode laser has been found to be extremely eective enter into litigation.
in conjunction with thorough debridement, and air-pol-
ishing use can also provide an eective means of debride- KEY POINT 9
ment of the rough implant surface, the peri-implant sulcus If peri-implantitis is diagnosed or suspected, early referral to a
and the soft tissue outer wall of the sulcus, such as the periodontal specialist is indicated.
EMS AirFlow, PerioFlow and Piezon approach to guided
biolm therapy. However, lesions of peri-implantitis do
not always respond adequately to an entirely non-surgical Individualised Implant Maintenance
approach to treatment.
Where several threads of the implant are no longer cov- All patients who receive implant therapy should be assessed
ered by bone and there has been an aggressive inammatory for their future risk of plaque-associated periodontal and
response seen clinically in the adjacent soft tissues, accom- peri-implant inammation. Once their degree of risk has
panied by recession, open debridement of the site may have been identied, an individualised supportive protocol
to follow the non-surgical approach adopted initially. or- should be developed with the patient’s involvement to
ough debridement of the implant surface is fundamental to ensure the oral environment presents the lowest risk pos-
achieving a good clinical outcome. sible to the establishment of periodontal or peri-implant
Several authors advocate the use of various chemicals to inammatory diseases.
assist in this implant surface preparation (Salvi etal. 2007, Patients with very few risk factors would include patients
Kotsovilis et al. 2006). e use of citric acid in combina- who have suered no previous periodontitis, have no detect-
tion with mechanical debridement is reported to have been able family history of periodontal disease or premature tooth
successful in achieving a satisfactory outcome when treat- loss, are systemically healthy, do not smoke and maintain
ing peri-implantitis. Some authors have also suggested using excellent plaque control with gingival crevices around natu-
tetracycline, ethylene-diamine-tetra-acetic acid (EDTA) ral teeth of no more than 3 mm at any site. ese patients
and various antimicrobials. should be seen by a dental hygienist to monitor their plaque
Ultimately after healing is established, the site must control, check the health of the oral soft tissues and help to
be assessed for its stability and its anatomical susceptibil- re-motivate the patient to continue their commitment to
ity to further damage including recession, leading to fur- maintaining good plaque control. e frequency of review
ther implant thread exposure, creating a greater hygiene may depend on dental and non-dental factors, including
the oral ndings and the patient’s ability to aord regular to periodontal and peri-implant disease remains because
care and support. Frequency of review may vary between of their genetic prole. erefore they must be prepared
six-monthly and annually. to maintain an absolute commitment to their periodon-
Patients who are considered to have an increased risk of tal and peri-implant plaque control on a life-long basis.
periodontal or peri-implant inammatory diseases include Failure to keep up this high standard of home care will
patients with a history of some of the following risk fac- certainly lead to a reinfection of the subgingival sites with
tors, including previous periodontitis, a family history of a pathogenic ora and resulting destructive inammation
periodontal disease and/or premature tooth loss, systemic with the re-development of periodontitis and peri-implan-
disease including sub-optimally controlled diabetes (Heitz- titis. is can present a problem for elderly patients whose
Mayeld 2008, Kotsovilis etal. 2006) or an indication of a manual dexterity, cognitive function and self-care can
compromised immunological response, a recent history of become compromised.
smoking or continued smoking (Lang & Berglundh 2011,
Ong etal. 2008), the presence of sites exhibiting periodon- Follow-Up and Support
tal inammation with sub-optimal plaque control (Serino
& Ström 2009) and the presence of periodontal pockets of With implant treatment being so widely available, many
more than 3 mm in depth with bleeding on blunt probing implant patients are returning to their own general dentist
and/or suppuration. e deeper pockets provide a suitable for their ongoing dental and implant care and supervision.
ecological niche in which a reservoir of ora can thrive to ini- It is therefore extremely important that all dentists and their
tiate recolonisation of implant and restorative surfaces with oral healthcare teams provide the necessary high standard
putative pathogens (Papaioannou et al. 1996, Gouvoussis of clinical and radiological monitoring and regular profes-
etal. 1997), especially in patients with a history of aggres- sional periodontal debridement of implants and natural
sive periodontitis (DeBoever & DeBoever 2006). High- teeth in conjunction with support of the patients in their
risk patients require a dierent approach, incorporating a home care and plaque removal. is is a task that can be
greater frequency of professional support and a higher level performed most eectively by dental hygienists, and these
of profession intervention (Karoussis etal. 2007, Lindhe & regular maintenance visits are the best support an implant
Meyle 2008, Lang & Berglundh 2011, Ong etal. 2008). patient can receive.
High-risk patients should not normally receive implant
therapy, but should such therapy have been provided, then Summary
they would normally be reviewed and supported by a den-
tal hygienist at a frequency of 2–4 monthly, and additional Dental implants represent a successful and long-term ther-
review with the implant dentist or periodontist would nor- apy for the replacement of missing teeth and, in many cases,
mally take place every 6–12 months. At each review an they are the treatment of choice in providing anchorage
assessment of plaque accumulation should take place with for single-tooth, partial and full prostheses. Several funda-
plaque disclosure preceding observation of the patient’s mental principles remain essential in achieving success in
own eorts to maintain plaque control. Correction of implant therapy, including the early identication of risk
plaque control measures would take place where necessary, factors and any predisposition to periodontal disease, as well
and further observation of the patients corrected techniques as appropriate patient follow-up and management to mini-
should follow. A full-mouth debridement should take place mise the risk of plaque-induced peri-implant inammatory
around the implants and natural teeth to minimise the res- disease.
ervoir of bacteria available to repopulate the oral environ- Multiple choice questions on the contents of this chapter
ment, and in particular, the periodontal and peri-implant are available online at Elsevier eBooks+.
sulci and pockets. Following debridement the use of an air-
polishing system can be useful to remove any residual ora References
or debris.
It is accepted that patients who have active chronic or Aas JA, Paster BJ, Stokes LN, Olsen I, Dewhirst FE. Dening
aggressive periodontitis should not receive implant therapy the normal bacterial ora of the oral cavity. J Clin Microbiol.
due to the higher risk of implant failure and the raised like- 2005;43:5721–5732.
lihood of their implants being aected by peri-implanti- Aguirre-Zorzano LA, Estefania-Fresco R, Telletxea O, Bravo M.
tis. However, patients who have a past history of chronic Prevalence of peri-implant inammatory disease in patients with a
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Appendix 1
World Workshop on Classication of
Periodontal and Peri-implant Diseases
and Conditions 2017 - Staging and
Grading of Periodontitis
Staging
Periodontitis stage Stage I Stage II Stage III Stage IV
Interdental CAL 1 to 2 mm 3 to 4 mm ≥5 mm ≥5 mm
at site of
greatest loss
Severity Radiographic Coronal third (<15%) Coronal third Extending to Extending to mid-third of
bone loss (15%–33%) mid-third of root and root and beyond
beyond
Tooth loss No tooth loss due to periodontitis Tooth loss due to Tooth loss due to
periodontitis of ≤4 periodontitis of ≥5 teeth
teeth
In addition to stage II In addition to stage III
complexity: complexity:
Maximum probing Maximum probing Probing depth ≥6 mm Need for complex
depth ≤4 mm depth ≤5 mm rehabilitation due to:
Complexity Local Mostly horizontal bone Mostly horizontal Vertical bone Masticatory dysfunction
loss bone loss loss ≥3 mm Secondary occlusal
trauma (tooth mobility
degree ≥2)
Furcation involvement Severe ridge defect
class II or III
Moderate ridge defect Bite collapse, drifting,
aring
Less than 20 remaining
teeth
(10 opposing pairs)
Extent and Add to stage as For each stage, describe extent as localized (<30% of teeth involved), generalized, or molar/incisor
distribution descriptor pattern
CAL: Clinical attachment loss.
285
286 APPENDIX 1 World Workshop on Classication of Periodontal and Peri-implant Diseases and Conditions 2017
Grading
Grade A: Grade B: Grade C:
Periodontitis Slow rate of Moderate rate Rapid rate of
grade progression of progression progression
Direct evidence Longitudinal data Evidence of no <2 mm over 5 ≥2 mm over 5 years
of progression (radiographic loss over 5 years
bone loss or years
CAL)
% bone loss/age <0.25 0.25 to 1.0 >1.0
Primary Indirect evidence Case phenotype Heavy biolm Destruction Destruction exceeds
criteria of progression deposits with commensurate expectation given
low levels of with biolm biolm deposits;
destruction deposits specic clinical patterns
suggestive of periods
of rapid progression
and/or early onset
disease (e.g., molar/
incisor pattern; lack
of expected response
to standard bacterial
control therapies)
Smoking Non-smoker Smoker <10 Smoker ≥10 cigarettes/day
cigarettes/day
Grade Risk factors Diabetes Normoglycemic/ HbA1c <7.0% in HbA1c ≥7.0% in patients
modiers no diagnosis patients with with diabetes
of diabetes diabetes
CAL: Clinical attachment loss; HbA1c: glycated haemoglobin.
(Reprinted from Tonetti, M., Greenwell, H., Kornman, K. J. Staging and grading of periodontitis: Framework and proposal of a new classication and case deni-
tion. J Periodontol. 2018 Jun;89 Suppl 1:S159-S172. doi: 10.1002/JPER.18-0006., with permission from Wiley. )
Appendix 2
Implementing the 2017 Classication
of Periodontal Diseases to Reach a
Diagnosis in Clinical Practice
287
288 APPENDIX 2
Implementing the 2017 classification of periodontal diseases
to reach a diagnosis in clinical practice
Implementing the 2017 Classication of Periodontal Diseases to Reach a Diagnosis in Clinical Practice
History, examination and screening for periodontal disease
including BPE and assessment of historic periodontitis (interdental recession)
Code 3 Code 4
Code 0 / 1 / 2
with no obvious evidence of and/or obvious evidence of interdental recession
with no obvious evidence of interdental recession
interdental recession
Appropriate radiographic Appropriate radiographic assessment

assessment
<10% 10%–30% >30%
bleeding on bleeding on bleeding on Full periodontal assessment
probing probing probing Initial periodontal therapy (including detailed 6-point pocket chart)
and review in 3 months with
localised 6-point pocket chart
in involved sextant(s)
Clinical
Localised Generalised
gingival
gingivitis gingivitis Molar-incisor
health <30% of teeth ≥30% of teeth
pattern
Diagnosis should also include a comment on No pockets Pockets ≥4 mm

plaque retentive factors where a BPE code 2 is ≥4 mm and no remain and/or Periodontitis
present radiographic radiographic Localised Generalised
molar-incisor
evidence of evidence of periodontitis periodontitis
pattern
bone loss due to bone loss due
periodontitis to periodontitis
continue with code continue with code Staging and grading, current disease status and risk
0/1/2 pathway 4 pathway factor assessment
(PTO)
© The British Society of Periodontology 2018
www.bsperio.org.uk
APPENDIX 2
Staging Grading
Implementing the 2017 Classication of Periodontal Diseases to Reach a Diagnosis in Clinical Practice
Radiographic assessment
(periapicals or OPG/DPT)
if not clinically justified or if bitewings only available use CAL or bone loss from CEJ
lnterproximal bone loss % bone loss ÷ patient age

(use worst site of bone loss due to periodontitis) (use worst site of bone loss due to periodontitis)
<15%
(or <2 mm Coronal third Mid-third of Apical third of
<0.5 0.5–1.0 >1.0
attachment loss of root root root
from CEJ)
Grade B
Stage I Stage II Stage III Stage IV Grade A Grade C
(moderate
(early/mild) (moderate) (severe) (very severe) (slow rate of (rapid rate of
rate of
progression) progression)
progression)
Assessment of current periodontitis status Risk factor assessment
Currently stable Currently in remission Currently unstable

For example:
BoP <10% BoP ≥10% PPD ≥5 mm or
• Smoking, including cigarettes/day
PPD ≤4 mm PPD ≤4 mm PPD ≥4 mm & BoP
• Sub-optimally controlled diabetes
No BoP at 4 mm sites No BoP at 4 mm sites
Diagnosis statement: Extent - periodontitis - stage - grade - stability - risk factors

e.g.: Generalised periodontitis stage 3 grade B - currently unstable - risk(s): Smoker 15/day
Reproduced with the kind permission of the British Society of Periodontology and Implant Dentistry: www.bsperio.org.uk
289
Appendix 3
European Federation of
Periodontology S3-Level Clinical
Treatment Guidelines - Stepwise
Approach
E
Supportive care/rehabilitation
C
Step 4 EXIT - plan longer-term care (above)
I
Step 3 CHECK - Non-responder sites: Re-RSD/surgery
R
Step 2 INTERVENE - Sub-gingival biofilm & calculus removal ± adjuncts
P
Step 1 RISK - Risk factor control, OHI, adjuncts for GI, PMPR, supra-gingival scaling
Step 0 PREREQUISITE TO THERAPY - Educate, classification, diagnosis, risk assess, care plan
(Reprinted with permission from Springer Nature: Br. Dent. J. Evidence-based, personalised and minimally invasive treatment for periodontitis
patients - the new EFP S3-level clinical treatment guidelines, Kebschull, M., Chapple, I., copyright 2020.)
290
Appendix 4
BSP UK Clinical Practice Guidelines for
the Treatment of Periodontal Diseases
291
292 APPENDIX 4
BSP UK clinical practice guidelines
BSP UK Clinical Practice Guidelines for the Treatment of Periodontal Diseases

for the treatment of periodontal diseases
ORAL HEALTH AND RISK ASSESSMENT, DIAGNOSIS & CARE PLAN
Diagnosis Periodontal health Gingivitis Periodontitis
Extract teeth with hopeless prognosis or unsavable teeth – e.g. grade III mobile
Building foundations for optimal treatment outcomes

STEP 1
I: Explain disease, risk factors & treatment alternatives, risks & benefits including no treatment
II: Explain importance of oral hygiene (OH), encourage and support behaviour change for OH improvement
III: Reduce risk factors including removal of plaque-retentive features, smoking cessation and diabetes-control interventions
IV: Provide individually tailored OH advice including interdental cleaning, + /– adjunctive efficacious toothpaste & mouthwash,
+ /– professional mechanical plaque removal (PMPR) including supra and subgingival scaling of the clinical crown
V: Select recall period following published guidance and considering risk factors such as smoking and diabetes
VI: Oral health educator (I, II), hygienist, therapist (I – IV), dentist, practitioner accredited for level 2 and 3 care (I – V)
Re-evaluate
Non-engaging patient – Engaging patient –

Consider referral
move to
STEP 2
www.bsperio.org.uk
Periodontitis (continued)
Subgingival instrumentation (root surface debridement / PMPR on root)
STEP 2
I: Reinforce OH, risk factor control, behaviour change
II: Subgingival instrumentation, hand or powered (sonic / ultrasonic), either alone or in combination
III: Use of adjunctive systemic antimicrobials determined by practitioner accredited for level 2 and 3 care
APPENDIX 4
STEP 3 Unstable Re-evaluate after 3 months Stable STEP 4
Managing non-responding sites: Maintenance

I: Reinforce OH, risk factor control, behaviour change I: Supportive periodontal care strongly encouraged
BSP UK Clinical Practice Guidelines for the Treatment of Periodontal Diseases

II: Moderate (4–5 mm) residual pockets – re-perform II: Reinforce OH, risk factor control, behaviour change
subgingival instrumentation III: Regular targeted PMPR as required to limit tooth loss
III: Deep residual pocketing (≥6 mm). Consider alternative causes IV: Consider evidence-based adjunctive efficacious toothpaste
IV: Consider referral for pocket management or and / or mouthwash to control gingival inflammation
regenerative surgery
V: If referral not possible, re-perform subgingival instrumentation
12 months
BSP top tips

I: Patients should be made aware that regular effective self-performed plaque removal offers the largest treatment benefit – engage the patient
in a verbal contract to perform daily plaque control
II: Toothbrushing should be supplemented by the use of interdental brushes (where anatomically possible)
III: Individual patient’s abilities, needs, preferences and manual dexterity should be considered when selecting toothbrush & interdental brush
IV: Refer to BSP website for further clarification and glossary of terms
I: Favourable improvement in OH – indicated by ≥50% Defining engaging & I: Insufficient improvement in OH – indicated by <50%
improvement in plaque and marginal bleeding scores OR non-engaging patients improvement in plaque and marginal bleeding scores OR
II: Plaque levels ≤ 20% & bleeding levels ≤ 30% OR (this is a guide) II: Plaque levels >20% & bleeding levels >30% OR
III: Patient has met targets outlined in their personal self-care III: Patient states preference to a palliative approach to
plan as determined by their healthcare practitioner periodontal care
Reproduced with the kind permission of the British Society of Periodontology and Implant Dentistry: www.bsperio.org.uk
293
Index
A Air polishing, implant surface, 280 B

Abscess Alcohol, mouthwash ingredients, 180t Bacteria
periodontal, 126–127, 127f, 127b Alloprevotella tannerae, 50t colonisation of, 12–13
aetiology of, 128b Alveolar bone, 9–10, 10f acquisition, 12
with systemic involvement, 157 American Academy of Periodontology adherence/retention, 12
from periodontium, 73 (AAP), 217 avoidance of elimination, 12
Abutment tooth, 119 classication system, 72 initial survival, 12
Acquired immunity, 34, 38 American Academy of Periodontology/ invasion, 12
Actinomyces spp., 45, 47 Centre for Disease Control maturation of biolm, 12
A. viscosus, 13 (AAP/CDC), 27, 27t multiplication, 12
Acute necrotising ulcerative gingivitis Anaeroglobus germinatus, 50t prosperity, 12
(ANUG), 13 Anaesthesia, 218 virulence factors, 12, 33
Adaptive immunity, 104 Antibiotics components of, 36
Adherence, 193–194. See also Patient as adjuncts to RSD, 225–226 and host response, 32f–33f, 34
adherence classication systems, periodontal vs. host’s inammatory/immune response,
Adhesins, on bacterium, 47 conditions, 223 17–19, 20f
Adhesions molecule expression, 37 local delivery of, 224–227, 224t, 227t interaction with host epithelial cells, 35f
Adolescents, periodontal diseases in minocycline gel, 224–225, 225f pathogenesis, 13, 13f
classication of, 147b as monotherapy, 224 role
diagnosis, 153–154 in periodontal therapy, 226–227 in periodontitis, 205–206
gingival overgrowth, 150–151 rationale for, 222–223 toxins, 205–206
gingival recession, 150, 151f systemic delivery of, 224–225, 224t–225t, Bacteroidales species, 50t
gingivitis, 147–148 227–228, 227f, 228t Basic Periodontal Examination (BPE), 26,
history and examination, 151 Antibodies 75, 76f, 81–83
local and systemic periodontal risk factors, and bacteria aggregation, 17, 19f advantages and disadvantages, 82
148–150, 148b classes of, 17 classication, dentition, 81–82
periodontal health, 147 removal/destruction of antigen by, 17, 19f scores, 82
radiographs, 153 Antigen timing for, 82–83
sBPE codes, 151–153, 152f–153f, 154t removal/destruction of antibodies, 17, 19f B-cell response, 17, 18f
treatment planning and periodontal T cells, 17 Behaviour change, patient adherence and,
therapy, 154–158 Antimicrobials 195–198
EFP S3-level guidelines and BSP on brushes, 280 Beta-defensins, 13
implementation, 154–155 systemic, in children and adolescents, Bidobacterium dentium, 50t
non-surgical therapy, 156–158 156–157, 157f, 157b Biolms, 42–43, 42f, 43b. See also Plaque
plaque control, 155–156 Antioxidants, 38 antigens, immune responses to, 15
Adult Dental Health Survey (ADHS), 28 Anti-resorptive agent-induced osteonecrosis assessment of, 84–85
Adult periodontitis, 72 of the jaw (ARONJ), 111–112 bacterial, prognosis factors, 118
Aesthetic improvement, 245, 246f Antiseptic agents, 178–179 control, self-performed, 172
Aesthetics, gingival recession, 142, 143f chlorhexidine, 178–179, 180t denition of, 42
Age dentifrices (toothpastes), 178, 179t development, 206
DIGE and, 96 mouth rinses, 178 diseased root surface treatment, 208, 209f
periodontal prognosis and, 118 Apically repositioned ap (ARF), 248, 249f formation of, 45–48
and periodontal risk, 61 Apical resorption, intruded tooth, 265, 266f conditioning lm formation, 45–47
Aggregatibacter actinomycetemcomitans, 13, Archaea spp., 50t detachment from surfaces, 48
31, 47–48, 50, 109, 149–150, 150f, Atherosclerosis, 106 irreversible attachment, 47
275 Atopobium rimae, 50t and maturation, 47–48, 275
Aggressive periodontitis, 227, 227f Attachment loss, assessment of, 87–88 reversible attachment, 47
Page numbers followed by ‘f ‘ indicate gures those followed by ‘t’ indicate tables and ‘b’ indicate boxes.
294
Index 295
Biolms (Continued) Calculus (Continued) Chronic periodontitis, 227

secondary colonisation, 47 sBPE codes, 152, 153f self-performed biolm control for, 172
stages, 45, 45b, 46f subgingival, 213 Classication systems
transport of microorganisms, 47 Cameras American Academy of Periodontology
and host response, 34, 206, 207f digital, 189, 190f (AAP), 72
microbial composition of intra-oral, 189, 190f BSP implementation of, 75–77
approximal surfaces, 45 Campylobacter spp., 49 in clinical practice, 75
determination methods, 43–45, 44f C. rectus, 50t staging and grading in, 74–75
ssures, 45 Capnocytophaga, 45, 50 1999 World Workshop, 72–73, 74t
gingival crevice, 45 Cardiovascular diseases Clinical attachment loss (CAL),
in health, 43–45, 44f periodontal treatment and, 107 antimicrobials, 226
in periodontal diseases, 49–51 periodontitis and, 106–107, 107f, 107b Collagen bres, 8
in mouth, 43 Cell–cell signalling, 47–48 arrangement, 272
orthodontic appliance, retention of, 64f Cell-mediated immune responses, 15 Colonisation, bacterial, 12–13
reduced sensitivity to antimicrobial Cell signalling, 36 Commensal, denition of, 33
agents, 48 Cementation Community Periodontal Index of Treatment
removal, bacterial contaminants, 213 crowns on implants, 280–281 Need (CPITN), 25, 26f, 81
subgingival, 104 stage, of crown and bridge, 259 Complementary metal oxide
tolerance of, 48 Cementoblasts, 9 semi-conductors (CMOS), 186, 186f
Black triangle disease, 258, 258f, 267, 267b Cemento-enamel junction (CEJ), 25, 88 Complement system, 36, 37f
Bleeding Cementum, 9 inammatory response to bacterial
gingivae, 83f acellular, 9 biolm, 14, 15f
marginal, 84 cellular, 9 Complex diseases, 57
Bleeding on probing (BoP), 74–75, 76f, 84 contaminated, 210 “Causal pie” hypothesis, 57, 58f
assessment of, 88, 88b removal, 210, 214 Compliance, 245
sBPE codes, 152, 153f root, 210 Computerised tomography (CT), 186–187,
B lymphocytes, 17, 38 surface, 210 187f–188f
Bone loss, prognosis factors, 118 Cetylpyridinium chloride (CPC), 180t Cone beam computerised tomography
Bone support, assessment of, 89–90, 90f Charged coupled devices (CCD), 186 (CBCT), 91, 91f, 186–187, 187f–188f
Borrelia vincentii, 127 Chediak–Higashi syndrome, 39t Contamination
Bridge construction, 258–259, 258f–260f Chemokines, 36b cementum, 210
British Society of Paediatric Dentistry Chemotaxis, 37 sources of, 207, 208f
(BSPD), 147 Children, periodontal diseases in Core Oral Microbiome Database (CORE),
British Society of Periodontology and classication of, 147b 45
Implant Dentistry (BSP), 59, 154–155, diagnosis, 153–154 Corynebacterium, 45
165, 224, 231, 258 gingival overgrowth, 150–151 C. matruchotii, 48
BSPi grades, 59 gingival recession, 150, 151f COVID-19, periodontitis and, 103, 110–111
Brushes gingivitis Critical pathway model, 58, 59f
antimicrobial agents on, 280 necrotising, 148 Crowded teeth, orthodontic treatment, 265,
electric vibration, 279 plaque-induced, 147–148 265f
interdental, 177, 177f history and examination, 151 Crown
powered, 175–176, 176f local and systemic periodontal risk factors, construction, 258–259, 258f–260f
vs. manual, 279 148–150, 148b lengthening, 259–260
single-tufted interproximal brush, 280 non-plaque-induced gingival margin prediction, 261f
techniques, 175–176, 175f. See also lesions, 148 subgingival margins of, 259
Toothbrushing periodontal health, 147 Crown-to-root ratio, 119
Bulleida extructa, 50 radiographs, 153 Curettes, 215, 215f
Bundle bone, 9–10 simplied BPE, 151, 152f Cyclo-oxygenase pathway, 17t
codes, 152–153, 153f, 154t Cyclosporin, gingival enlargement and, 96
C treatment planning and periodontal Cytokines, 14
Cairo classication, of gingival recession, therapy, 154–158 inammatory/immune response, 16t
138, 139t EFP S3-level guidelines and BSP types of, 14
Calcium channel blockers, gingival implementation, 154–155
enlargement and, 96 non-surgical therapy, 156–158 D
Calculus plaque control, 155–156 Debridement
assessment of, 86 Chlorhexidine, 178–179, 180t full-mouth, periodontal pockets, 282
formation, subgingival, 231 submucosal application of, 280 periodontal, 214, 214b
gingival recession and, 141 Chlorhexidine chip, 224–225, 225f professional, 280
interproximal, 126, 126f Chlorhexidine gluconate (CHX), 179, 180t, root surface, 214
local risk factors, 65, 65f 219 Decontamination
removal, in periodontitis, 208–210, 209f Chronic obstructive pulmonary disease methods of instrumentation, 212–213
removal of, 213 (COPD), periodontitis and, 109 treatment objectives, 213–214
296 Index
Dehiscence, 150, 151f. See also Gingiva, E Fissures, microbiota of, 45

recession Ecological plaque hypothesis, 51–52, 52f, Flap approach, 97, 98f
Dementia, periodontitis and, 110 206 Floss
Dental scaling, 214 Eector T cells, 17 anchorage method of, 177, 177f
Dentifrices (toothpastes), 178, 179t EFP. See European Federation of in children and adolescents, 156
Dentine hypersensitivity. See also Gingiva, Periodontology (EFP) dental, 176
recession Eikenella corrodens, 109 holder, use of, 177, 177f
aetiology of, 137, 138f Embryological origins, of periodontal implant, 176
denition of, 136 tissues, 3, 4f loop, 177, 177f
management and treatment of, 143–144, Enamel techniques, 177, 177f
144t acquired enamel pellicle, 45–47 use of, 176
mechanisms for, 137, 137f matrix derivatives, 144 Fluid lubrication, 36
prevalence of, 136–137 space, 6 Fluorides, 180t
sensory transmission of, 137, 137f Enamel matrix proteins (EMPs), 251, 252f. Free radicals, tissue damage, 19, 21f
Dento-gingival junction, microanatomy, 7, 8f See also Regenerative techniques Frenectomy/frenotomy, 269
DentoRisk, 236 Endodontic/periodontal relationships, 263, Frenum
Denture 263f attachment, 65
chrome cobalt, 260 Enzymes gingival recession, high attachment of,
design, 260, 260b inhibitors, 38 140
every style, 260, 261f modication of oral mucosa, 109 Fretibacterium fastidiosum, 50t
partial, 259b, 260–261, 261f tissue damage, 19, 21f Full-mouth disinfection (FMD), 214,
removable, 260 Epidemiology 218–219
Desulfobulbus spp., 50t analytical, 24 Full-mouth ultrasonic debridement
Diabetes mellitus, 104–105 denition of, 23 (FMUD), 215, 218–219
American Diabetes Association (ADA) descriptive, 24 Furcation
diagnostic criteria for, 105b denition of, 24 involvement, 118
classication of, 104, 105t principles of, 24, 24b assessment of, 88–89
diagnosis of, 104 experimental, 24 clinical assessment, 89, 89f
gestational, 105t formulation of hypotheses, 24 probing, 88–89, 89f
gingival enlargement and, 99, 99f periodontal, problems with, 23–30 radiographic assessment, 89, 89f
implant complications, uncontrolled/ probe prognosis factors, 118
inadequately controlled, 274 North Carolina (NC) 15, 27, 28f management of, 132–133, 132b
pathobiology of, 105 WHO, 25, 25f root resection, 133, 134f
periodontal prognosis and, 117 radiographs use in, 27–28 scaling and root-surface
periodontal risk and, 62 surveys, indices used in, 24–26 instrumentation, 132–133
periodontal treatment in, 105–106 radiographs in, 27–28 surgery, 133, 133f
periodontitis vs., 105–106, 106f, 106b Epithelial barriers, 36 tunnel preparation, 133, 133f
prognosis factors, 117 Erythromycin, 96 plasty, 249, 250f
type 1, 104, 105t Essix retainers, 268 Fusobacterium spp., 45, 50, 127
type 2, 104, 105t Ethical issues, 167–168 F. nucleatum, 13, 47–49, 50t, 109
Dialister, 50 Eubacterium spp., 48, 50t
D. invisus, 50t E. nodatum, 49 G
D. pneumosintes, 50t European Federation of Periodontology Gender
DIGE. See Drug-induced gingival (EFP), 27, 27t, 72, 129, 212–213, DIGE and, 96
enlargement (DIGE) 213f, 231 periodontal prognosis and, 118
Digital scanning, 190–191, 191f European Federation of Periodontology S3- Genetics, periodontitis and, 59–61
Disto-buccal (DB) root resection, 250f level clinical practice guideline 2020, Gingiva
Down’s syndrome, gingival enlargement 154–155, 194–195 acute conditions, management of,
and, 100 clinical recommendation, 195, 196f–197f 126–129
Drug-induced gingival enlargement (DIGE), grades of recommendation, 195t before and after non-surgical treatment,
94–96, 162, 164 stepwise approach, 194–195, 196f 244, 244f
associated with amlodipine, 95f strength of consensus, 194, 195t alveolar mucosal problems, 245, 245f
distribution of, 96 Extent and Severity Index (ESI), 26, 26b appearance, 85, 85f
incidence of, 96 assessment of, 85–86
management of, 96–97 F asymmetry, 266–267
non-surgical, 97, 97f Fenestration, 150, 151f. See also Gingiva, bleeding, 83f
surgical, 97–98, 97f–98f recession colour, 85–86
medication Fibreotomy, 266–267 consistency, 85–86
changing, 98 Fibroblasts, 8 contour, 85–86
periodontal status at onset of, 96 Fibromas, gingival enlargement and, diseases, classication systems, 73
risk factors for, 96 99–100, 100f enlargement of, 93. See also Drug-induced
Dysbiosis, 206 Filifactor alocis, 50t gingival enlargement (DIGE)
Index 297
Gingiva (Continued) Gingiva (Continued) Hand instruments (Continued)

aetiology of, 93–94, 94f classication of, 138 hoes, 215, 215f
causes of, 95–100 clinical features of, 136, 136f methods, 215, 216f
and delayed maturation, 96f clinical outcomes of, 142 scalers, 215, 215f
hormonal, 98 correction, non-surgical, 143 vs. ultrasonic instrumentation, 218
management, 98–99 denition of, 136 Health Belief Model (HBM)
mechanisms of, 94–95 free soft tissue grafts, 144 principles of, 172, 172t
brotic, 85, 86f guided tissue regeneration, 144 social and economic factors, 172
healthy, 6f, 85f management, 158 Health/disease balance, 206, 207f
inammation, 86f management and treatment of, Health educational model, 172
assessment of, 86 143–144, 144t Helper T cells, 17
attachment loss, 233f mechanisms for, 137 Hereditary gingivo-bromatosis, 99
levels on, 231–232, 232b Miller’s classication of, 138, 138f, Herpetic gingivostomatitis, acute, 128–129
tooth loss, 233f 139t irregular ulceration and erythema in, 129f
invaginations, 269 non-surgical management of, 143, 144t presentation and management of, 128b
microanatomy of, 4–7, 5f pedicle soft tissue grafts, 144 Histamine, 36–37
attached gingiva, 6 prevalence of, 136–137 Hoes, 215, 215f
dentogingival bres, 4–5 preventive care, 143 Hormonal gingival enlargement, 98
enamel space, 6 smoking, 141 management, 98–99
free gingiva, 5 surgical correction of, 246f Host factors, periodontal diseases, 13–19
gingival connective tissue, 4 surgical management of, 143–144, antibodies/immunoglobulins, 17
gingival groove, 5 144t bacteria vs. host, 17–19
gingival margin, 5 soft tissue biotype, 273 B lymphocytes, 17
junctional epithelium (JE), 7 Gingival crevice, microanatomy of, 34–36, gingivitis and, 19
mucogingival junction (MGJ), 6 35f immune responses to biolm antigens, 15
outer gingival epithelium, 4, 5f–6f Gingival crevicular uid (GCF), 7, 36, 45, inammatory response to bacterial
sulcular epithelium, 5 206 biolm, 13–15
overgrowth Gingival index (GI), 86, 173 complement cascade, 14, 15f
in children and adolescents, 150–151 Gingivectomy, 97, 97f, 247–248 cytokines, 14
management, 158 stages in, 248f epithelial barrier, 13
precipitating factors, recession, 141–143 Gingivitis inammasomes, 15
aesthetics, 142, 143f biolm-induced, 49 mast cells, 15, 17t
calculus, 141 in children and adolescents, 147–148 neutrophils, 15, 16f
dentine hypersensitivity, 142 management, 156 T lymphocytes, 15–17
healing after periodontal treatment, necrotising Host response
141 in children and adolescents, 148 to bacterial biolm, 34, 34f
partial dentures removal, 141 interproximal cratering, 128f contribution of genes to, 38–39
periodontal diseases, 141 management of, 127–128, 128f, 128b normal, 34, 34f
plaque, 141 presentation of, 128b Host susceptibility, 33, 33f
plaque retention and gingival treatment, 157 Human Oral Microbiome Database
inammation, 142 periodontitis and, 19 (HOMD), 45
restorative dentistry, 141, 142f to periodontitis, progression of, 34f Humectants, 180t
root caries and non-carious cervical plaque-induced, management of, 126, Humoral immune responses, 17
lesions, 142–143 126f–127f Hyalinisation, 267
self-inicted trauma/chemical trauma, poor oral hygiene and, 62, 62f Hydrogen peroxide, 179t–180t
142, 142f Gingivoplasty, 249 Hyperplasia
smoking, 141 Grade Adolopment framework, 194 denition of, 94
tooth abrasion, 142 Grading gingivitis, 94, 99. See also Gingiva,
toothbrush trauma, 141 2017 classication system, 74, 74b enlargement of
tooth movement, 141, 141f of periodontitis, 77t Hypersensitivity, dentine. See Dentine
predisposing factors, recession, 139–140 Granule release, 17t hypersensitivity
anatomical factors, 139 Granulocyte-macrophage colony stimulating Hypertrophy
bone morphology, 140 factor (GM-CSF), 15, 16t denition of, 94
frenum, high attachment of, 140 Guided tissue regeneration (GTR), 251, gingival, 85, 94. See also Gingiva,
malocclusion, 140 251f enlargement of
periodontal (gingival) biotype, 139,
140f, 140t H I
quantity of attached gingiva, 139 Haemophilus spp., 45, 47 Imaging systems
recession, 268–269 Hand instruments benets of, 182–183
aetiology of, 137, 138f calculus removal, 280 digital scanning, 190–191, 191f
Cairo RT1 classication, 138 curettes, 215, 215f to enhance adherence, 191–192
in children and adolescents, 150, 151f design of, 215, 215f factors to consider, 184–191
298 Index
Imaging systems (Continued) Inherited conditions, with periodontitis risk, K

oral hygiene on gingival inammation, 39t Keratinocytes, 4
184, 184f Innate immunity, 34, 36–38, 104 Keystone pathogens, 51–52, 52f
photography, 187–190 adhesion molecule expression, 37
place for, 183f cell signalling, 36 L
plaque control, 183f complement cascade, 36 Laser
radiography, 185–187 epithelial barriers, 36 pigment-containing bacteria, 280
types of, 184, 185f uid lubrication, 36 systems, 217
videos, 190 macrophages, 38 Lautropia, 45
Immune responses neutrophils, 37 Legal and ethical issues, 167–168
to biolm antigens, 15 vasoactive peptides, 36 Leptotrichia spp., 50, 50t
cell-mediated, 15 Instrumentation, periodontal Lipoxygenase pathway, 17t
humoral, 17 adjuncts to, 219 Local delivery antibiotics
Immune senescence, 61 dental scaling, 214 evidence for use, 226–227, 227t
Immunity full-mouth disinfection, 214 systemic delivery antibiotics vs., 224–225,
acquired, 38 full-mouth/quadrant approaches, 224t, 225b
adaptive, 104 218–219 Local tissue damage, oxidative stress in, 15,
innate, 36–38, 104 full-mouth ultrasonic debridement, 19, 21f. See also Periodontitis
types, 34 215 Loss of attachment (LOA), 26, 26f
Immunoglobulins, 17, 38, 38f hand instruments, 215, 215f vs. probing pocket depth, 87–88, 88f
Implants, 271–284 calculus removal, 280
anatomical architecture of, 272–273 curettes, 215, 215f M
biological width, 259, 260f design of, 215, 215f Machine-driven instruments, 215–216
biologic width, 272 hoes, 215, 215f magnetostrictive, 216
cementation of crowns on, 280–281 methods, 215, 216f methods, 216
complications, 273–275 scalers, 215, 215f sonic scalers, 215, 216f
biological factors, 274 vs. ultrasonic instrumentation, 218 types of, 215–216, 216f
biomechanical factors, 273–274 machine-driven instruments, 215–216 ultrasonic scalers, 215–216, 216f
diabetes, uncontrolled/inadequately periodontal debridement, 214, 214b Macrophages, 38
controlled, 274 power-driven instruments, 216–217 Magnetostrictive ultrasonic scalers, 216,
inappropriate components, 274 root planing, 214 216f
occlusal overload, 273 strategies Malocclusion, gingival recession and, 140
periodontal disease, past history of, 274 anaesthesia, 218 Marginal bleeding (MB), 84
plaque-induced inammation, 274 choice of instruments, 217–218 Mast cells, 15, 17t
poor implant angulation, 273 hand vs. ultrasonic instrumentation, Medicines and Healthcare Products
smoking and, 274 218 Regulatory Agency (MHRA), 179
thin tissue biotype, 274 subgingival instrumentation, 214 Medico-legal issues, 270
oss, 176 types of, 215–217, 215f Mesio-distal tunnelling, 250f
with healthy gingival margins, 274f Intercuspal position/ centric occlusion (ICP/ Metastatic infection, 103–104
macro- and micro-anatomy of, 272–273, CO) Metronidazole gel, 226, 226f
272f occlusal overload, 273 Microbial composition
peri-implant diseases Interdental cleaning, 176–178, 176f biolms
aetiology and pathogenesis of, brushes, 177, 177f approximal surfaces, 45
275–279, 276f elastomeric toothpicks, 176 determination methods, 43–45, 44f
clinical denitions of, 279t oss, 176, 177f ssures, 45
management of, 279–282 oral irrigators, 178 gingival crevice, 45
periodontitis and, 262, 262f, 262b subgingival cleaning, 178, 178f in health, 43–45, 44f
referral to specialist, in periodontics, 164 Interdental/inter-implant papillae anatomy, in periodontal diseases, 49–51
soft tissue biotype, 273 272 resident oral microbiome, 42f, 48–49,
Incidence, denition of, 24 Interdental papillae, loss of, 267, 267b 48b
Incipient periodontitis, 149, 149f Interleukin 1 (IL-1) transport of microorganisms, 47
Inammasomes, 15 on inammatory/immune response, 15, control on implants, 280
Inammation 16t Miller’s classication, of gingival recession,
gingiva, 86, 86f periodontal prognosis and, 118 138, 138f, 139t
gingival, 231–232, 232b Interleukin 6 (IL-6), 15, 16t Minocycline gel, 224–225, 225f
and inammatory injury, innate Interleukin 8 (IL-8), 15, 16t Mobility
immunity, 104 Interleukin 10 (IL-10), 15, 16t periodontal prognosis and, 119
meal-induced, 61 Intra-osseous defects, 245f tooth, assessment of, 88
peri-implant, incidence of, 275–276 Modied Widman ap (MWF), 247, 247f
plaque-induced, 274 J Mogibacterium timidium, 50t
Inammatory periodontal diseases, 57 Johnsonella spp., 50t Molar/incisor pattern (MIP), 74, 76f
Infra-bony defects, 265–266 Juvenile periodontitis, 72 Motivational interviewing (MI), 196–198
Index 299
Mouth Oral hygiene (Continued) Patient coping skills, 245

assessment, full vs. part, 28 assessment, 200 Patient education
breathing, gingival enlargement and, 100 delivery of, 173–174, 174f, 174b health beliefs, 172
mouthwash, antiseptic, 97 diet advice, 200 interdental cleaning, 176–178, 176f
rinses, 178 instruction sheet, 199f oral hygiene
ingredients, 180t motivation and re-instruction, 235–236 advice, 173
Mucogingival deformities, 73 patient adherence to, 198–200 motivation for, 172–173
Mucositis, peri-implant periodontal-orthodontic interface, 267 techniques for, 173
clinical denition of, 279t poor, 62–63, 62f toothbrushing, 174–175
diagnosis of, 278–279 regime, 199f Pedicle soft tissue grafts, 144
incidence of, 278 techniques for, 173 Peptostreptococcus stomatis, 50t
management of, 280 without professional intervention, 200f Pericision
and plaque accumulation, 277 Oral irrigators, 178 gingival asymmetry, 266–267
Multi-rooted teeth, surgery for, 249–251 Orthodontics soft tissue procedures, 269
Mycobacterium tuberculosis, 51 crowded teeth, anterior splaying/over Peri-implant diseases
eruption, 265, 265f–266f aetiology and pathogenesis of, 275–279
N gingival asymmetry, 266–267 biolm formation and maturation, 275
National Health and Nutrition Examination infra-bony defects, 265–266 classication of, 278
Survey (NHANES), 28 interdental papillae, loss of, 267, 267b diagnosis of, 278
Natural immunity. See Innate immunity patients preparation for, 269–270 implant factors in, 277–278
Natural teeth medico-legal issues, 270 inammation, incidence of, 275–276
anatomical architecture of, 272–273 monitoring and maintenance, 270, management of, 279–282
keratinised attached gingiva, 273 270b follow-up and support, 282
macro- and micro-anatomy of, 272–273, periodontal treatment, 269–270 individualised implant maintenance,
272f periodontics role in, 267–269 281–282
soft tissue biotype, 273 frenotomy/frenectomy, 269 patient prophylaxis, 279–280
Necrotising gingivitis. See Gingivitis gingival biotype and gingival recession, professional support, 280
Necrotizing ulcerative gingivitis (NUG), 50 268–269 microbial ndings with implants, 275
Necrotizing ulcerative periodontitis, 50–51 gingival invaginations, 269 mucositis
Neisseria spp., 45, 47 missing teeth and poor anchorage, 268 clinical denition of, 279t
Neoplasms, gingival enlargement and, 100 oral hygiene, 267 diagnosis of, 278–279
Neutrophils, 37–38, 38f reduced bone support, 267–268 incidence of, 278
chemotaxis, 37 relapse and retention, 268, 268f management of, 280
diapedesis, 37 soft tissue procedures, 269 and plaque accumulation, 277
disorders, periodontal prognosis and, 118 tooth crowding, 267 peri-implantitis
margination, 37 Orthopantomogram (OPT), 185 around implants, 273, 273f
phagocytosing bacterium and subsequent Osseous surgery, 248–249 with attached gingivae, 278f
degranulation, 15, 16f Ostectomy, 248 clinical denition of, 279t
rolling, 37 Osteoplasty, 248, 250f diagnosis of, 278f, 279
sequence of activity, 37 Osteoporosis, periodontal prognosis and, histopathology of, 276, 276f
Non-carious cervical lesions (NCCL), 118 management of, 280–281
142–143 Oxidative stress with no attached gingivae, 278f
Non-specic plaque hypothesis (NSPH), biomarkers, 62 vs. periodontal diseases, 277
205–206 in local tissue damage, 19, 21f periodontitis and peri-implantitis, 276, 276f
Non-surgical periodontal therapy (NST), 253 Periodontal debridement (PD), 214, 214b
Nutrition, periodontal risk, 61 P Periodontal Disease Index (PDI),
Partial dentures removal, gingival recession, Ramord’s, 25
O 141 Periodontal diseases, 11
Obesity, periodontal risk and, 62 Parvimonas micros, 50t assessment, 81
Occlusion, 261 Pathogen-associated molecular patterns radiographs in, 90–91
overload, 273 (PAMPs), 36 bacterial factors, 12–13
Odontoplasty, 249, 250f Pathogen, denition of, 33 classication and diagnosis of, 69–79
Open ap debridement (OFD), 246–247, Pathogenesis diagnosis, 77–79, 78f, 78b
247b denition of, 12 epidemiology, 24
Operator skills, 245 of periodontal diseases, 11–22, 12f problems with, 26–28
Opportunistic pathogen, 33 synergism, 51 host factors, 13–19
Oral dryness, 65 Patient adherence, 193–202 microbial composition of dental biolms
Oral Health Surveys: Basic Methods, 25, 29 and behaviour change, 195–198 in, 49–51
Oral hygiene imaging systems to enhance, 191–192 necrotising, 73
advice importance of, 193–194, 194f pathogenesis of, 11–22, 12f
adherence with, 173 to oral hygiene advice, 198–200 vs. peri-implant diseases, 277
tailoring, 173 prognosis factors, 117 and pregnancy, 107–109, 108f
300 Index
Periodontal health, 257, 257b Periodontitis (Continued) Phenolic compounds, 180t

Periodontal Index (PI), Russell’s, 24 and cardiovascular diseases, 106–107, Phenytoin, 97
Periodontal lesions, pathogenesis of, 34–36, 107f, 107b gingival enlargement and, 95
35f in children and adolescents Photodynamic disinfection therapy (PDT),
Periodontal ligament, 7–8 history and examination, 151 217
and cementum, microanatomy, 7–9 local and systemic periodontal risk Photography, 183, 187–190
bres, 8, 9f factors, 148–150, 148b clinical, 187–190
Periodontal-orthodontic interface, 264–270 management, 156 consent form, 188, 189f
frenotomy/frenectomy, 269 non-surgical periodontal therapy, digital camera systems, 189, 190f
gingival biotype and gingival recession, 156–158 digital “wax-up”, 191f
268–269 sBPE, 151, 152f intra-oral cameras, 189, 190f
gingival invaginations, 269 stage II, III or IV grade C, 149–150, views of, 191f
missing teeth and poor anchorage, 268 150f, 156–157 Photo-stimulated storage phosphor (PSP)
oral hygiene, 267 chronic, 32f, 73 sensors, 186, 187f
reduced bone support, 267–268 clinical presentation of, 205–207 Piezo-electric ultrasonic scaler, 216, 216f,
relapse and retention, 268, 268f and dementia, 110 280
soft tissue procedures, 269 and diabetes mellitus, 104–105, 106f Plaque
tooth crowding, 267 direct and indirect bacterial eects in, 14f assessment of, 84–85
Periodontal patient, monitoring of, 91, 91b diseased root surface treatment biolm control, 236
Periodontal pockets, 282 biolm role, 208, 209f control, 172b
Periodontal risk assessment (PRA), 63–64 calculus, 208–210, 209f in children and adolescents, 147–148,
factors, 236 contaminated cementum, 210 151f, 155–156
low, moderate and high risk, 237, non-surgical vs. surgical treatment, electric vibration brushes, 279
237f–239f, 239 207–208 full-mouth debridement, 279
model, 237t sources of contamination, 207, 208f at home, self-assessment of, 173
multi-level, 63f EFP denitions for, 27t inammation and, 274
technologies, 63–64 features of, 205 periodontal and peri-implant, 282
as third dimension, 63, 64f gingivitis and, 19 development, 206
Periodontal surgery grading of, 77t gingival recession and, 141
apically repositioned ap, 248, 249f histopathology of, 276, 276f hypotheses, 205–206
approaches in, 246–249 host response mechanisms in, 14f ecological, 206
case selection for, 245–246 and implant dentistry, 262, 262f, 262b non-specic, 205–206
medical contraindications, 246 incipient, 149, 149f specic, 205–206
site factors, 246 inherited conditions with additional risk and microbial community, 43
subject factors, 245 for, 39t retention and gingival inammation, 142
tooth factors, 245–246 juvenile, 72 Plaque Control Record, 84–85, 85f
control of disease, 244–245 maintenance/supportive therapy, 155 Plaque indices (PIl), 84, 173
furcation plasty, 249, 250f as manifestation of systemic diseases, 73 advantages and disadvantages, 84
gingivectomy, 247–248, 248f microbial composition of dental biolms simplied, 84
modied Widman ap, 247, 247f in, 49–50, 50t Plaque-induced gingivitis, management,
objective of, 244–245 necrotising, 150 126, 126f–127f
open ap debridement, 246–247, 247b necrotizing ulcerative, 50–51 Plastic surgery, 245, 245f–246f
osseous surgery, 248–249 non-responding sites, 155 Pneumonia, periodontitis and, 109
plastic surgery, 245, 245f–246f pathogenesis, 13f Pocket
pocket elimination procedures, 246 and respiratory diseases, 109–110, 110f elimination, 244
pocket production procedures, 246 staging of, 77t procedures, 246
regenerative procedures, 246 and systemic diseases, 103–112, 103f false/true, 65
root resection/amputation, 249–251, 250f tissue damage in, 12, 12f periodontal, 282
Periodontal tissues treatment planning for, 129–131 assessment of, 86–87
embryological origins of, 3, 4f aims of, 131–132, 131t probing depths, 86–87
interdental, 7f cause-related therapy, 129 probing depth, prognosis factors, 118
Periodontitis, 12, 12b corrective therapy, 129 production procedures, 246
AAP/CDC denitions for, 27t outcomes, 129, 129b sBPE codes, 152, 153f
adult, 72 periodontal reassessment, 132 in smoking patients, 78f, 79
aetiology of, 206–207 stepwise approach, 130–131, 130f Pocket probing depth (PPD), 118
aggressive, 73 structuring, 131, 131f, 131t, 132b Polymorphonuclear leucocytes (Pmnls), 15,
antibiotics for supportive periodontal therapy, 129 16f
aggressive, 227, 227f Periodontium Pontic design, in bridgework, 258, 259b, 260f
chronic, 227 systemic conditions aecting, 111, 111t hygienic, 259, 260f
bacteria systemic medication aecting, 111–112 modied ridge lap, 259, 260f
and host response, 32, 32f PerioFlow tip, 218f ovate pontic, 259, 260f
role in, 205–206 PerioWave system, 217f ridge lap/saddle design, 259, 260f
Index 301
Porphyromonas spp., 109 Prognosis (Continued) Regenerative techniques, 249b

P. endodontalis, 50t questionable, 120 biologic root modiers, 251, 252f–253f
P. gingivalis, 13, 31, 47–49, 50t, 51, revising, 120 grafting and combined therapies, 251,
106–107, 275 weighting, factors of, 120–121 253f
Post-orthodontic retention, 268 Prostaglandin E2 (PGE2), 15, 16t, 36–37 guided tissue regeneration, 251
Power-driven instruments, 216–217 Pyorrhoea, 72 objective, 251
laser systems, 217 Resident oral microbiome, 42f, 48–49, 48b
photodynamic disinfection therapy, 217 Q Respiratory diseases
subgingival air polishing, 217 Quadrant scaling and root planing (QSRP), bacterial aspiration, 109
Vector ultrasonic instrumentation, 210, 214, 218–219 pathogenesis of, 110f
216–217 Quigley Hein Index, 84 periodontal treatment and, 109–110
Pregnancy periodontitis and, 109–110, 110f
adverse outcomes, periodontal treatment R cytokine alteration of respiratory
and, 108–109 Radiographs, 183, 185–187 epithelium, 109
epulis, 98, 98f analogue, 185, 185f enzyme modication of oral mucosa, 109
electrosurgery, 99f in children and adolescents, 153 salivary pellicle destruction, 109
periodontal disease and, 107–109, 108f cone beam computerised tomography, Restorative dentistry
Preterm low birth-weight (PTLBW), risk 91, 91f gingival recession, 141, 142f
factors, 108 conventional, 185–186, 185f referral to specialist, in periodontics, 164
Prevotella spp., 45, 49, 50t, 109 criteria for, referral to specialist, 164 Restorative treatment
P. intermedia, 47–48, 51, 275 digital, 185–186, 186t crown and bridge construction, 258–259,
P. nigrescens, 275 direct sensors, 186 258f–260f
Probes/probing of endo-periodontal lesion, 263, 263f mobility, 261–262, 262f
computerised, 87, 87f furcation involvement, 89, 89f occlusion, 261
constant pressure, 87, 87f of implant, peri-implantitis, 274f, 278f, 279 partial dentures, 259b, 260–261, 261f
errors, 87b indirect sensors, 186 patient engagement, 258
furcation involvement, 88–89, 89f interpretation of, 90 engaging patient, 258
manual, 87, 87f periapical, 90f, 90b non-engaging patient, 258
measurements, 87 viewing and reporting on, 90–91 phases of, 257, 258b
Nabers, 88–89, 89f Ramord’s Periodontal Disease Index (PDI), supracrestal tissue attachment, 259–260,
periodontal epidemiology, 27–28 25 259b, 260f–261f
pocket depth, 86–87 Reactive oxygen species (ROS), in local Risk factors, 57, 57b
loss of attachment vs., 87–88, 88f tissue damage, 19, 21f assessment, 57–58, 63–64
Professional mechanical plaque removal Recession classication of, 58–59
(PMPR), 130, 154 classication system, 139t denition of, 12, 236
Prognosis gingival. See also Gingiva, recession local, 64–65, 64b
assigning, 119–120 in children and adolescents, 150, 151f anatomical factors, 65
classication system, 119–120 management, 158 calculus, 65, 65f
denition of, 117 Referral to specialist, in periodontics false/true pockets, 65
determination of, 120–121, 121b acceptance of, 168 high frenal attachment, 65
factors aecting, 117–119 approaches, 165–166 iatrogenic, 64–65
abutment tooth, 119 audits, 166, 166b–167b oral dryness, 65
age, 118 care, 168 root caries, 65, 65f
anatomical defects, 119 clinical criteria, 163–164 tooth position, 65
bacterial biolm, 118 compliant but non-responding patients, modiable, 59
bone loss, 118 162–163 modifying, 58
crown-to-root ratio, 119 decision to, 162 non-modiable, 59
diabetes, 117 early referral, 164 in periodontitis progression, 59, 60f
furcation involvement, 118 expectation from clinician, 166 predisposing, 58
gender, 118 implants, 164 putative, 58
IL-1 genotype, 118 legal and ethical issues, 167–168 systemic, 59–63, 60f, 60t
mobility, 119 non-compliant but demanding patients, 163 age, 61
non-vital teeth/pulpal lesions, 119 participants in periodontal care and diabetes and obesity, 62
patient adherence, 117 treatment, 162, 162f genetics, 59–61
perio-endo lesions, 119 patient preparation, 166 nutrition, 61
pocket probing depth, 118 patient types, 162–163 poor oral hygiene, 62–63, 62f
smoking, 117 place to visit, 165 smoking, 61, 62f
systemic disorders, 118 protocol for, 163, 163f stress, 62
tooth type, 118 radiographic criteria, 164 true, 58
good, 119 restorative criteria, 164 Root caries, 65, 65f
hopeless, 120 specialist’s report, 167 gingival recession, 142–143
initial, 120 timing of, 164–165 local risk factors, 65, 65f
302 Index
Root planing, 210, 214 Streptococcus (Continued) Toothbrushing (Continued)

Root resection, 133, 134f, 249–251, 250f S. oralis, 13, 47 manual, 174–175
disto-buccal (DB), 250f S. sanguinis (S. sanguis), 13, 48 and motivation, in children and
Root surface debridement (RSD), 210, 214 Stress, periodontitis and, 62 adolescents, 155–156
adjuncts to, 225–226 Subgingiva nylon toothbrushes, 174
antibiotics as monotherapy, 224 air polishing, 217 powered brushes, 175–176, 176f
reasons for failure, 223–224 calculus formation, 231 trauma, gingival recession, 141
Root-surface instrumentation, furcations cleaning, 178, 178f Tooth crowding, periodontal-orthodontic
management, 132–133 instrumentation (SI), 210, 213–214 interface, 267
Rothia, 45 and overhanging restoration margins, Tooth/implant-host interface
RSD. See Root surface debridement (RSD) 141, 142f in disease, 276, 276f
Russell’s Periodontal Index (PI), 24 symbiotic microbiota, 51–52, 53f in health, 272, 272f
Supportive periodontal therapy (SPT), 57, Tooth movement, gingival recession, 141, 141f
S 117, 167 Toothpastes, 178
sBPE. See Simplied Basic Periodontal appointment, 235, 235b ingredients in, 179t
Examination (sBPE) biological basis of, 231, 232b triclosan/copolymer dentifrice, 178
Scalers, 215, 215f clinical examination and diagnosis, 235 Toothpicks
magnetostrictive, 216, 216f frequency of, 235, 235t, 235b elastomeric, 176
piezo-electric, 216, 216f goals, 231 wooden, 176
sonic, 215, 216f objective of, 231, 231b Tooth position, local risk factors, 65
ultrasonic, 215–216, 216f patient’s and professional’s contribution, 232f Tooth type, prognosis factors, 118
Scaling and root planing (SRP), 214 for periodontitis, 129 Transforming growth factor beta (TGF-β),
Scaling and root-surface instrumentation, plan, 234, 234b 15, 16t
132–133 risk assessment, 236–239 Treponema spp., 50, 50t
Selenomonas spp., 50, 50t value of, 232–234 T. denticola, 49
Self-performed biolm control Suppuration, assessment of, 89 T. vincenti, 13
for chronic periodontitis, 172 Supracrestal tissue attachment, 259–260, Triclosan, 179t–180t
interdental cleaning, 176–178, 176f 259b, 260f–261f, 272 Tumour necrosis factor alpha (TNF-α), 15,
oral hygiene connective, 4 16t
advice, 173 Surfactant, 179t–180t Tunnel preparation, furcations management,
motivation for, 172–173 Surgical treatment. See Periodontal surgery 133, 133f
techniques for, 173 Susceptible host, 33, 33f e 2017 classication system
toothbrushing, 174–175 Symbiosis, 206, 207f BSP implementation of, 75–77
Self-performed plaque control, 208, 209f Synergistes spp., 48 in clinical practice, 75
Severity, denition of, 24 Systemic delivery antibiotics, 156–157, staging and grading in, 74–75
Sharpey’s bres, 8 157f, 157b
Sickle scalers, 215, 215f evidence for use, 227–228, 227f, 228t U
Simplied Basic Periodontal Examination vs. local delivery, 224–225, 224t Ultrasonic/piezo-electric scalers, 215–216,
(sBPE) for periodontal diseases, 225t 216f, 280
in children and adolescents, 151, 152f recommendations, 228–229, 228b UniFe, 236
codes, 152–153, 153f, 154t Systemic diseases
Single nucleotide polymorphisms (SNPs), 39 periodontal interactions, 103–112, 103f V
Smoking periodontitis as manifestation of, 73 Vasoactive peptides, 36
cessation advice, 200 susceptibility, 104 Vector ultrasonic instrumentation, 216–217
gingival recession and, 141 Veillonella spp., 45, 48, 50
periodontal prognosis and, 117 T Videos, clinical photographic record, 190
periodontal risk and, 61, 62f Tacrolimus, gingival enlargement and, 96 Vincent’s disease. See Necrotizing ulcerative
pockets in patients with, 78f, 79 Tannerella, 48, 50 gingivitis (NUG)
Sodium valproate, 96 T. forsythia, 49, 50t Virulence factors, 12–13, 33, 38
Sonic scalers, 215, 216f Temporary anchorage devices (TADs), 268
Specic immunity. See Acquired immunity Tetracycline hydrochloride, 224–225, 225f W
Specic plaque hypothesis (SPH), 205–206 T lymphocytes (T cells), 15–17, 38 Wegner’s granulomatosis, 99
Splint antigen-specic, 17 World Workshop Classication of
design, 262, 262b eector, 17 Periodontal and Peri-implant Diseases
indirect, 261–262 helper, 17 and Conditions, 121
types of, 261 response, 17, 18f e 1999 World Workshop classication
Staging Tolerance, denition of, 48 system, 72–73, 74t
2017 classication system, 74b Toll-like receptor (TLR) family, 36 World Workshop in Periodontology, 213
of periodontitis, 77t Tooth abrasion, gingival recession, 142 Wound-healing potential, 245
Strawberry gingivae, 99 Tooth age, calculation of, 232
Streptococcus Toothbrushing, 174–175 Z
S. mitis, 47 brushing techniques, 175–176, 175f Zinc gluconates, 180t

Practical Periodontics

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First edition © Elsevier Limited 2015

Content Strategist: Alex Mortimer

Last digit is the print number: 9 8 7 6 5 4 3 2 1

Foreword, vii 2.4 Periodontitis and Systemic Diseases, 102

3.3 Treatment Planning: Periodontal Problems in

2.2 Periodontal Assessment and Monitoring, 80 4.3 Patient Adherence, 193

2.3 Gingival Enlargement, 93

Section 5: Non-surgical Periodontal 7.2 The Periodontal–Orthodontic Interface, 264

5.2 Periodontal Instrumentation, 212

Section 7: Interaction with Other Dental

7.1 The Periodontal–Restorative Interface, 257

Aetiology of Periodontal Diseases

OVERVIEW OF THE CHAPTER

Introduction of periodontal anatomy at both macroscopic and micro-

• Figure 1.1.1 The embryological origins of the periodontal tissues.

Outer gingival epithelium

8. e attached gingiva: this is a band of between 1 and 9

• Figure 1.1.5 The interdental periodontal tissues in health.

tooth is also known as the “epithelial attachment”.

• Figure 1.1.8 Periodontal ligament bres.

ere are two types of cementum: cellular and acellular.

referred to as “bundle bone”. is cortical bone layer is

OVERVIEW OF THE CHAPTER

Time exposed Modifiable and

• Figure 1.2.1 Interactions that are responsible for disease.

Species-specific virulence factors

Enzymes Toxins Metabolic products

Local gingival • Collagenase Exotoxins Endotoxins • Hydrogen sulphide

Gingivitis Potential periodontal tissue damage

• Figure 1.2.3 Overview of periodontitis pathogenesis.

KEY POINT 2 periodontitis), Aggregatibacter actinomycetemcomitans is

Inflammation Tissue damage Neutrophils Immune response

Damage by plaque bacteria/products

• Figure 1.2.4 Direct and indirect bacterial effects in periodontitis.

Inflammatory response Immune response

• Rapid • Relatively slow

Gingival inflammation Chronic inflammation

Occur together: chronic stimulation because plaque not

• Figure 1.2.5 Host response mechanisms in biolm-induced periodontitis.

• Figure 1.2.6 The complement cascade.

Cytokine Cell of origin Effects upon inflammatory/immune response

Phagosome Killing and Release of

Kill/lyse Lymphokine Regulate

When effector T cell responds to antigen associated

Soluble or cell Activation and

• Figure 1.2.9 The B-cell response.

All antibodies cross-link antigens and

Antigen binding to IgE

IgG antibodies opsonise

• Figure 1.2.10 The removal/destruction of antigen by antibody.

Host Plaque bacteria

Aberrant inflammatory/ Bacterial Bacterial

Risk factor modulation