Inbde notes

Skull cranium
• Cranium is divided into two parts
1. Neurocranium  protection around brain
2. Viscrocranium  face

• Neuro cranium is divided into 2 parts

a) Membranous nuerocranium / calvarium
• Flar bones of root of cranium
• Frontal, parietal & occipital  intramembranous ossification happens
here

b) Cartigenous / chondroneurocranium
• Base of cranium
• Frontal, ethmoidal, sphenoid, temporal, parietal, occipital 
 / frontal suture
Closes  3-9 months after
birth
Closes after post 
 b/w frontal & paretal bone

Bregma  where
coronal & sagital
suture intersect

Closes first
 Lambda  where
saggital and lambdoif
suture intersect

• All sutures closes by the age of 20

• Fontanalles  where 2 bones come together (helps baby pass
2. Viscrocranium
• Develops from 1st & 2nd cranial arch
Facial bones
• Zygomatic, maxilla, pataini, mandible, ethmoid, nasal, vomer,
lacrimal
 Craniosyntosis
• Premature closures of fontanelles & suture

1. Schaphocephaly / dolicocephaly
• Early closure of sagital suture
• A-P growth  elongated skull
• Frontal bossing
• Prominent frontal & occipital bones  boat shaped skull

2. Brachycephaly
• Early closure of coronal & lambdoid suture
• Sup-inf growth  wide skull
• Flat head
• Oblique skull

3. Phagiocephaly
• Early closure of coronal or lambdoid suture of one side
• Skull distored asymtrically
 Brachycephaly

Wide face

Unilater growth
Asymmeteric skull

Scaphiocephaly/dolicoceph

Elongated
face
Fossa of skull
• Fossa are divided into 2

1. Internal fossa
a) Anterior
b) Middle
c) Posterior

2. External fossa
a) Temporal
b) Infratemporal
c) Pterygopalatine
 Floor  frontal, greater

Temporal fossa wing of sphenoid,

pareital, temporal
Superior & posterior border  temporal
line

Contents
• Temporalis muscle
• Sup temporal artery
• Auriculotemproal nerve

Pterion
• Where all bones
meet
• Weakest point
Anterior border 
frontal process of
zygoma
Inferior border
zygomatic arch
Infra temporal fossa
Contents
• MOM, pterygoid plexus, maxillary artery, PSA, IAN,
BUCCAL NERVE, AURICULOTEMPORAL, LINGUAL
• Chorda tympani & otic ganglion
Pterygopalatine fossa
 IO nerve, artery & zygomatic nerve
/
(v2)
superior

 PSA nerve, Max artery

 Nasopalatine nerve, sphenopalatine

artery
/
inferio
r  Foramen rotaundum  V2
 Vidian/ pterygoid canal  Vidian
nerve
 Pharyngeal canal  pharyngeal nerve
 Greater and lesser palatine nerve & artery
& artery
Cranial fossa
Frontal lobe
here Lesser
wing

Greater wing

Pituatary gland
& temporal lobe
here

Brainstem &
cerebellum
Foramens
Supra-orbital foramen (in frontal bone)
• Supra-orbital artery & vein
• Supraorbital nerve (v1)

Infraorbital foramen (in maxilla)

• Infra-orbital nerve (V2), artey & vein

Mental foramen (in mandible)

• Mental artey, vein & nerve

Cribriform plate (in ethmoid)

• Oflfactory tendrils / nerve

Infra orbital fissure

Optic canal (sphenoid )
• Opthalmic nere (cn2) & artery

Superior orbital fissure (b/w lesser & greater wing of sphenoid)

• CN 3
• CN 4
• CN V1, CN 6
• Sympathetic fibers of cavernous plexus

Foramen rotandum (greater wing of sphenoid bone)

• Maxillary nerve ( V2)

Foramen ovale (post greater wing of sphenoid)

• Mndibular nerve (V3)
• Lesser petrosal nerve
• Accessory Meningeal artery
• Emissory vein

Forman spinosum
• middle meningeal artery, middle meningeal vein & nervus spinosus

Foramen lacerum
• Greater petrosal nerve & Deep petrosal nerve
Carotid canal (temporal bone)
• Internal carotid artery
• Internal carotid venous plexus

Internal auditory meatus (temporal bone)

• Facial nerve (CN 7)
• Vetibulocochlear ( cn 8)
• Labryrinth artery
• Vestibulor ganglion

Jugular foramen (temporal bone)

• Glossopharyngeal (CN 9 )
• Vagus ( cn 10)
• Accesory (cn 11)
Hypoglossal canal (occipital bone)
• Hypoglossal nerve (cn 12)

Foramen magnum (occipital bone)

• Medulla
• Spinal cord
• Spinal & vertebral arterys
• Spinal part of cn 11
Principles lines of
skull
• These are the imaginary lines

Principle lines of force

• These are  Vertical lines
• Storngest areas of skull which develop in response to mechanical stress

Principle lines of fractures

• There are horizontal lines (lefort lines)
• Weakest area of skull where fracture is common

Pterion
• Where bones join  frontal, parietal, temporal & sphenoid
• Weakest point
• Just below it is middle meningeal artery
Tongue
 Innervation
Motor innervation
• CN X (vagus nerve pharyngeal branch)  palatoglossus muscle
• CN XII (hypoglossal nerve)  all other muscles

Taste
a) Anterior 2/3
• Chorda tympani (branch of facial nerve CN 7 )

b) Posterior 1/3
• Glossopharyngeal nerve

c) Ant to epigloti
Sensory
a) Ant 2/3
• Lingual nerve (branch of trigeminal V3)

b) Posterior 1/3
• Glossopharyngeal nerve

c) Ant to epigloti
• Internal laryngeal nerve (cn x)
 Muscles of tongue
Extrinsic
1. Genio-glossus
2. Hyoglossus
3. Styloglossus
4. Palataoglossus
 Lymphatics of tongue
• Submental lymph node  mandibualr incisors, tip of tongue, chin
& lower lip

• Submandibular  lateral tongue 2/3 , upper lips, face below eyes

• Inferior deep cervial  Middle of tongue & lie aroun INV

• Superior deep cervical  Posterior of tongue, lie around INV

• Superficial cervical  the superficial neck & lie near the external
jugular vein.
Muscles of
mastication
1. Lateral pterygoid
Insertion
• is located on both the joint capsule of the temporomandibular joint
and the neck of the condylar process of the mandible
• Functions  protrude & depress the mandible, as well as stabilize the
condylar head during closure (opening of mouth )
• It functions  by contracting on one side to move the jaw to the
opposite side, facilitating lateral movements (contralateral movement)
• Since the lateral pterygoid muscle does not insert onto the ramus of
the mandible, it can facilitate opening of the mouth

2. Medial pterygoid
• Inserts  on the medial surface of the ramus and angle of the
mandible
• Function 
•
3. Masseter
• Inserts  on the lateral surface of the ramus and angle of the
mandible.
• The largest and most superficial muscle group within the cheek
region is the masseter muscle, which contributes to most of the
lateral fullness of the cheek
• Pain of the muscles of mastication (masseter and temporalis) is
often associated with TMD

4. Temporalis
• Functions  elevate and retract the mouth to facilitate closing of
the mouth.
• It does not facilitate opening of the mouth.
Nerve supply to mastication muscle
Muscels of facial expression
Muscles of palate
Salivary gland
Sublingual gland
• Opening  Ducts of Rivinus (small ducts)
• Opening  Bartholin’s duct is the major duct associated with the sublingual
• Located  These are under the tongue, within the floor of the mouth
• Secretion  mucous

Submandibular glands
• Opening  Wharton’s duct
• Located beneath the lower jaw
• Secretion  mixed

Parotid gland
• Opening  Stensen's duct
• Symptoms of mumps commonly affect the parotid gland
• Located  in front of the ear and extends to the area beneath the ear and down
the lower jaw
• D. Von Ebner’s glands: pure mucous secretions
• Von Ebner’s glands are minor salivary glands located in
the circumvallate papillae, just anterior to the posterior
third of the tongue. These secrete a purely serous
solution
Blood supply of face
Blood supply of mandible
Blood supply of maxilla
Muscles affected by fractures
• Zygomatic fracture
• Madibular fracture
• Maxiilarty fracture
Facial spaces infection
Dental antomy
 Maxillary central Maxillary lateral
Universal number Universal number
• 89 • 7 10
Facially Facially
• Trapezoidal • Trapezoidal
• Narrowest
• Widest
• i-c greater then m-d
• i-c greater then m-d (longer then max
• Developed by 4 lobes (very convex crown &
lateral)
root)
• Developed by 4 lobes • Rounded disto-incisal
• Rounded disto-incisal & 90 mesio-incisal • Convex cej facially & lingually
• Convex cej facially & lingually • HOC  mesially at junction of middle-incisal
• HOC  mesially at middle third & distally third & distally middle third
incisal third • Lingually
Lingually • Cingulam & deepest lingual fossa &
prominent marginal ridges (also lingual
• Cingulam & marginal ridges pit)
Mesially Mesially
• Triangular • Triangular
• Facial & lingual HOC in cervical third • Facial & lingual HOC in cervical third
Distally Distally
• Flatter cej • Flatter cej
• Contact cervically • Contact cervically
Incisally Incisally
• M-D more than F-L • M-D more than F-L
Cross-section Cross-section
• Triangular • Oval
Pulp Pulp
• 3 pulp horns • 3 pulp horns (one if peg
• One pulp canal lateral)
• One pulp canal
 Anomalies of maxillary latertal incisor
• Peg lateral  smaller lateral incisors (microdontia)
• Lingual pit  most common site of decay
• Palatogingival groove  from lingual fossa to root, very hard to
clean (highway for bacterial  deep pockets)
• Hawk bill  incisal edge more to lingual (looks like mand
incisors)
• Talon cusp  extra cusp on the cingulam
• Dens invaginatus / indente  tooth within a tooth (caved in
enamel, need radiograph to diagnose, caries can spread
quick)
 Mandibular central Mandibualr lateral
Universal Universal
• 24 25 • 23 26
occlusion Occlusion
• 2/3 width of maxillary incisors
• Two opposing tooth  maxillary
• Only tooth with one opposing tooth for
central & max lateral
occlusion (other then max 3rd molar)
Facially • Upper cental on distal marginal
ridge & upper lateral on mesial
• Trapezoidal shape
marginal ridge (ridges are of upper
• Smallest (in mouth) teeth)
• Sharpest M-I & D-I (90degress)
(symmetrical & hard to disguinsh side)
Facially
• Shortest root • Wider and longer than mandibular
• Distal surface  little convex
central (opposite to uppers)
• Apex  distally Lingually
• Four lobes • Less prominent marginal ridges &
Lingually cingual
• Less prominent marginal ridges & cingual • No lingual pits
• No lingual pits
Mesial aspect Mesial
• Incisal edge falls lingual to long • Distal marginal ridge can be seen from
this side (distal twist  crown twist
axis (asked in exam ) around its root base)
• Development depression on root Distally
surface (on mesial & distal surface) • Can see more of facial surface due to distal
Distally twist
• Development depression on root • Deep root depression
surface  deeperon distal aspect Incisally
• Wide  F-L than M-D (opposite of max
• Flatter cej incisors)
Incisally • Incisal edge curves lingually from
• Wide  F-L than M-D (opposite of max mesial to distal  fall lingual to long axis
incisors) Cross section
• Ribbon shape (due to deep developmental
Cross section
depression on root)
• Ribbon shape (due to deep Pulp
developmental depression on root) • Three pulp horns
Pulp • 55% one canal & 45% 2 canals
• Three pulp horns • Most likely incisor to have 2 canals 
which usually split facial & lingual
 Maxillary canine Mandibular canine
Universal Universal
• 6 &11 • 22 27
• Last tooth to erupt in age of 11-12
Facially
Facially
• Mesial surface of crown & mesial surface of
• Pentagon shape
root  straight line
• Cusp tip fall in long axis
• Cusp tip mesial to long axis
• Mesial cusp ridge shorter then distal cusp ridge
• Mesial cusp ridge shorter then distal cusp
• Mesial HOC  junction of middle & incisal & Distal
HOC  middle third (same as maxillary lateral ) ridge
• Concave at CEJ • Longest crown  I-C (in mouth)
• Distal buldge  make large gingival embrassure on this • Mesial HOC  junction of middle & incisal &
side Distal HOC  middle third (same as
• Root apex  distal 58%, straight  24%, mesial 18% maxillary lateral )
• Convex crown • Root apex  striaight 45%, mesial 29%, distal
• Facial ridge / mesial side visible during smile at canian  26%
tilted distally (turning tooth of arch) • Imbrication lines at cervical third
• 4 lobes  3 facial 1 lingual
Lingually
Lingually
• Lingual taper
• Narrow than facial
• Tapers towards lingual
• Visible mesial & distal crown and root
surface
• Large cingulum
• Prominent lingual ridge
• Linear Root flutes on mesial and distal
surface  attachment for pdl
• 2 trianglar fossa
Mesially Mesially
• Cusp tip & root apex fall facial to • Cusp tip lingual to long axis
long axis (opposite mand incisors, • Shark arch  convex facial surface from
canines & max lateral) crown to root
• Root flute
• Long round linear depression in root
called  root flute Distally
• Deep root flute
• HOC  cervical third
• Concave disto-facial line angle
Distally Incisally
• Deeper root flute then mesial • F-L is bigger than M-D
Incisally • Slight distal twist (like mand lat incisor)
• F-L is bigger than M-D • Cusp tip  slight ligual & mesial
• Asymmetric diamond shaped Pulp
• 1 pulp horn
• Widest ant tooth F-L
• 95% 1 canal , 5% 2 canals (lingual &
Pulp facial )(due to deep root flutes)
• 1 pulp horn Cross section
• 100% 1 canal • Oval
• Can have bifurcated roots
Cross section
• Longest root of any mand tooth
Canine facts
• Darker in color than incisors  one full shade
• Has lower value than anterior teeth
• Located underneath orbit  called eye teeth
• Canine eminenc  due to bulky root
• Triangular from side
• Longest tooth & root of all  3cm long
• Last standing tooth
• Contact both anterior & posterior tooth  in ideal
occlusion
 Maxillary 1st premolar Max 2nd premolar
• Largest premolar Universal
• Chance of root break during extraction. (thin &
short roots) • 4 & 13
Universal Facially
• 5 &12
• Blunt facial cusp
Facially
• Pentagon • No mesial concavity
• Cusp tip distal to long axis • Mesial cusp ridge longer then
• Mesial cusp ridge longer then distal (opposite distal (opposite to max canine)
to max canine)
• Mesial HOC  junction of middle & iocclusal &
Lingually
Distal HOC  middle third • Less lingual taper
• Mesial concavity at  CEJ
• Longer lingual cusp (angled
• 3 facial lobes  three cusp
towards mesial)
Lingually
• Lingual taper Distal
• Shorter cusp then facial (1mm short) • Flatter cervcal line
• Lingual cusp points mesially
• Deep root flute
• One lingual lobe  1 cusp
Distally • Shorter distal marginal ridge then
• Flat root flute mesial
Mesially
• Trapezoid ( all max teeth from side view)
Mesially
• Facial HOC cervical • No bifurcation
• Lingual HOC  middle
• Cusp tips line with root tips
• No mesial marginal ridge
• Flat mesial marginal ridge groove
• Landmark  mesial marginal ridge groove (only in 1st
max premolars) • Same cuspal height
• Deep root flute
• Larger palatal embrasure
• No mesial concavity
Occlusally • Flat crown & root
• Hexagonal (asymmetrical)
• F-L greater then M-D
Occlusally
• Lingual taper • Straight & short central
• Prominent D-F line angle
• Facial cusp tip  distal
groove
• Lingual cusp tip  mesial • More wrinkled  due to
• Occlusal table  occupy 55% of occlusal surface (mesial
& distal cups & marginal ridges forms boundaries)
supplemental groove
• Length of distal marginal ridge longer than mesial
marginal ridge
• Cental goove
• Mesial & distal pits
Pulp Pulps
• Two pulp horns • 2 pulp horns
• 85% 2 canals, 10% 1 canal, • 75% 1 canals, 25% 2 canals
5 % 3 canals Cross section
Cross section • Oval shape
• Kidney bean shape
 Mandibular 1st premolar Mandibular 2nd premolar
Universal Universal
• 20 & 29
• 21 & 28
• Called Mini molar
• Smallest of all premolars Facially
• 4 lobes • Blunt cusp tips
Lingually
Facially
• 2 Lingual cusp
• Upside down bell shape / pentagon • Lingual groove  b/w cusp
Lingually Mesially
• Rhomboidal (all mandibular teeth from side view)
• Mesial lingual developmental groove 
• Large lingual cusp
occurs at mesio-lingual line angle
• Buccal/facial cusp not centred to the root
Mesially apex
• Rhomboidal (all mandibular teeth from side • No mesial root depression
view) Distally
• Short marginal ridges
• Short lingual cusp (2/3 height of facial
• Deep root flute ( not flutting on mesial side)
cusp) centred over CEJ
Occlusally
• Buccal cusp centred to the root apex • Pentagon shaped
Distally • Multiple lingual cusps (only premolar)
• Lingual groove (only premolar with it)
• Short marginal ridges
Occlusally 1. Y type
• 1 facial cusp + 2 L-cusps
• Only premolar  prominent • 5 lobes (only premolar )
transverse ridge • Most common
• Prominent mesial & distal pits • Grooves form a off-centred Y
 snake eyes 2. U type
• 1-f cusp & 1- L cusp
• Mesio-lingual developmental
• 4 lobes
groove occlusaly has a cut-out • Cresent shaped goove  like a U
reffered to as  bite out of a • Less common
cookie 3. H type
• Diamond • 1-f cusp & 1- L cusp
• 4lobes
Pulp horn • Flat cental gooves
• 2 pulp horn  sometimes 1 • Supplemental groove  make a H
pulp horn due to short lingual • Less common
cusp Pulp
• 2 or 3 pulp horn
• 1 canal 75%, 25% 2 canals(facial
• 87 % 1 canal , 13% 2 canal
& lingual )
Crosssections
cross-section • Oval
 Maxillary 1st molar Maxillary 2nd molar Maxillary 3rd molar
Universal Universal Universal
• 3 & 14 • 1 & 16
• Widest tooth F-L in entire mouth • 2 & 15
• Made out of 5 lobes (only other is Facially • Heart shaped
mand 2nd premolar) • 3 cusps  2 facial & 1
• Largest disto-lingual cusp • More distal facial lingual
Facially groove  short distal • Shortest crown  occluso-
• Trapezoid cusp cervical dimesion of all
• Mesio-facial cups wider then disto- teeth in mouth
facial cusp
• Closer roots & more
• Disto-facial cusp is taller then
to distal incline
mesi-facial cusp • Root trunk  longer
• Facial groove at centre within line with
palatal root Lingually
• Spread out / bow-legged roots
• Lingual groove more
• Root trunk  4mm
distal
Lingually
• Cusp of carabelli (discovered by • Convex palatal root
george carabeli)  attached to
mesio-lingual cusp • No cusp of carablili
• Lingual groove in b/t  line with
palatal root
Mesially Mesially
• Trapzoidal (tooth with same from
front & side) • Short palatl root
• Palatal root  longest & closer
• M-F/M-B root  thickest • No cusp of
(facilolingually)
• D-F/D-B root  3mm (mesia
carablili
furcation closet to CEJ) Distally
Distally
• Shorter marginal ridges • Short marginal
• Occlusal table visible ridge
• Flat cej • Small root
• Root trunk  5mm
• Flat CEJ
Cusp
• Lingual  holding/ functional Cusp
cusp
• Facial/buccal  non holding/
• M-L  M-B  D-L 
non- functional D-B
• Opposite for mandibular
• M-L  M-B  D-L  D-B  CARABILI
Occlusally Ocllusally
• Rombous  pointing mesial • Primary cusp triangle 
• Lingual half of tooth is wider M-L/PALATAL, M-B,
then facial  due to facial D-B
convergence (only tooth wider
lingually) • Heart shaped  when
• Converge to distal  wide mesial there are 3 cusp (D-L
half cusp absent)
• Oblique ridge (mesiol-ingual to • Long D-L groove
disto-buccal) (gives it strength )
• Central fossa
• Fissured transverse
ridge of oblique
• Distal fossa  mesial to oblique ridge
ridge
• Distal & mesial triangular fossa
• Primary cusp triangle 
Pulp
M-L/PALATAL, M-B, D-B • 4 horns
Pulp • 3 for  heart shaped
• 4 pulp horns  m-b pulp horn tsall &
prominent
• 65 % 4 canals, 35% 3
• 70% 40 canal , 30% 3 Cross section
Cross section • Rhombous
• Rhombus • Triangle for  heart
• Apex close to sinus floor shaped
 MANDIBULAR 1ST MOLAR MANDIBULAR 2ND MOLAR
Universal Universal
• Widest tooth M-D • 18 & 31
• 19 & 30
• Most symmeterical of all molars
• 3 pits  facial, central, mesial
Facially Facial
• Two widespread roots (mesial & distal) • Smaller & shorter
• Mesial root more curved • 2 facial cusp
• Blunt facial cusp • Parrallel roots
• Taller lingual cusp
• Facial groove  only 1
• Mesio-facial cusp largest by size
• Two facial grooves (only tooth to have this)
• Cervical enamel projection  tooth most
• Facial pit  at facial groove
likely to have it (can cause perio pocket)
• Cervical ridge Lingual
• Root trunk  3mm • Short lingual groove
Lingually • Tall lingual cusp
• Short lingual groove • Root trunk  longer then facial (and longer
• Higher lingual height of contour (more prominent then 1st mand molar)
than facial) ( to hold tongue away from teeth
• Root trunkm 4 mm Cusp
Cusp • 2 FACIAL CUSP
• 3 facial cusp • 2 LINGUAL CUSP
• 2 lingual cusp • MB ML DL DF
Mesial Mesial
• Deep root flute • Rhombus  most evident in this tooth
• Biconcave root
• Facial HOC  cervical third
Distal
• Lingual HOC  middle third
• Short marginal ridge
• Visible occlusal table
• Teeth leans to lingual  curve of wilson
• Narrow distal root Distal
Occlusal • Narrow roots
• Pentagon shape • Mesial root visble
• Facial half is large then lingal half due to  • Tapering of root (more then mand 1st
lingual convergence molar)
• Mesial half is wide then distal ( same as
1max molar) Occlusal
• Largest occlusal table • Rectangle shape
1. Y5 tooth • Mesio-facial cervcal bulge  very prominent
• 5 cusp MB, DB, D, DL, ML (key to recongize right or left mand molar)
• 4 grooves • Mesial half wider than distal half
• Grooves form a Y 1. + 4
• Facial groove  b/t buccal cusp • + shaped 3 grooves  facial, lingual &
• Distofacial groove  b/w DB & D (oblique ridge sits central
here)
• 4 cusp
• Lingual groove  b/w DL & ML
• 3 pits  distal, central, mesial
Pulp Pulp
• 5 pulp horns • 4 horns
• 65 % 3 canals  2 mesial 1 • 55%  3 canals
distal • 45 %  4 canls
• 32 % 4 canals  2 mesial , 2 Cross section
distal
• Rectangle  at CEJ
• 3 % 2 canal  1 mesial , 1 distal
• Ribbon shaped  at mesial Root
Cross section
• Rectangle  at CEJ
• Ribbon shaped  at mesial Root Mandibular 3rd molar
• Oval  distal root • Shortest roots of all
posterior teeth in mouth
• Longest roots of all molar
• Most variable morphology of all
teeth
• Greatest distal root inclination
3rd molar fact
• 35%  missing atleat 1 wisdom tooth
• 90%  impacted
Golden proportion
 Prosthodontics

watch vidoes
missed some stuff
 Alginate

• Material of choice for diagnostic cast

• Sodium / potassium salts of alginic acid reacts with calcium sulfate to produce
insoluble calcium alginate
• More bulk of material  less susceptible to dimensional changes
• 2- 3 mins  setting time
• Within 15 mins  pour
• 30-60mins  cast sets
• Irreversible hydrocolloid

Composition

• Potassium alginate 15%  active ingredient

• Calcium sulfate 16%
• Tri-sodium phosphate 2%  control setting rate
• Zinc oxide 4%
• Potassium titanium fluoride 3%
• Type 1  fast setting
• Type 2  normal setting
Phases
• Sol phase  material in liquid or semi-liquid phase
• Gel phase  semi-solid material similar to gelatin dessert
Advantages
• Good taste and smell
• Cheap and easily available
• Easy to mix and manipulate
• Comfortable to patient

Disadvantages
• It can not be corrected if there is inacuracy of impression
• It should be held tightly agaisnt tissue surface until it sets ( elastic
but not so adhesive)
• Poor tear strength
• Poor dimenstional stablity
• Imbibition  absorbs water and expands
• Syneresis  shrinkage & disort  if left in open air causing moisture
Uses
• Impression for Study casts
• Impression for Removable orthodontic appliances
• Impression for Denture construction espicially partial dentures
• Preliminary impression for complete denture

Alginate is sufficiently fluid to record detail, but it is

unsuitable for recording fine detail such as that required
for a fixed indirect cast restoration
Maxillo-mandibular
relationship
Centric relation (inbde exam)
• Postion in which condyle articulates with the thinnest avascular portion
of their respective disc in the most ant-sup postion agains articular
eminence
• Independent of teeth (teeth not imp in CR)

Maximum intercuspation / centric occlusion

• Complete interdigitation of teeth
• Independent of condyler postion

• CR – MI  coincide in only 10% population

• In 90% pt there is slight  incentric
• For single crown  MI
• For complete denture / multiple teeth  CR
How to record cr
1. Bimanual manipulation
• Pt lying back
• Support post mandible with fingers & chin with thumb
• Deprogram their jaw  ask pt to relax their jaw so u can manipulate
it
• Identify first cr tooth contact then repeat until u find a consistant
tooth contact

Occlusal harmony
• Joint, muscle & teeth must work in a harmony like door in its frame
• Hinge as  tmj
• Door  mandible
• Frame  maxilla
Face bow record
• Record the articular relation of maxilla to the cranium and mandible to
the rotational centre of tmj
• Record is attacted to the aritculator  tells where the maxillary cast should go
in relationship to the skull & tmj
• Records  Vertical position, horizontal relationship, midline

Types of face bow

1. Arbitary
• Oriets maxillary cast to skull via external auditory meatus to stablize the bow
• Like ear buds
• Less precise

2. Kinematic
• Complex
• Attached directly to the hinge axis of mandible
• More accurate
Articulator parts
• Upper member  maxilla
• Lower member  mandible
• Hinge  tmj

• Facebow record  to mount maxillary cast

• Bite registration  mount mandibular cast after maxillary is done
• = representation of oral cavity movement
Types
1. Non-adjustable articulator
• Simple  open close movement
• Does not reproduce full movement range of mandibular
• Distance b/w hinge & teeth  shorter than pt
• May result in premature contact

2. semi-adjustable
• Allows u to set bennet angle (15) & horizontal condylar inclination (30)
a) Arocon
• Condyles are part of lower member
• Fossa part of upper member
• Anatomically correct
b) Non-arcon
• Upper & lower member rigidly attached

3. Fully adjustable
• Complex
• Cast poured from alginate  mounted with wax records
• Cast poured from elastic material  mounted with ZOE or
PVS
Dislusion (disocclusion)
1. Condylar guidance  (related with protrusion/ moving jaw
forward)
• Posterior deterement of occlusion
• Represented by horizontal condylar inclination
• Condyle slide downs  articluar eminence (limits movement in
ways)(guides movement)

2. Incisal guidance  (related with protrusion/ moving jaw

forward)
• Ant deteremrnt of occlusion
• Incisal edges of lower incisors are forced to move against
lingual slopes of upper incisors (guides movement)
• Represented by pin & guide table on articulator
3. Canine guidance  lateral movement
• When in lateral movement
• Only canine in working side & all post teeth not in
occlusion

4. Anterior guidance
• Refers to canine guidance + incisal guidance
Anatomic landmarks
of edentulous arch
Labial frenum

Buccal frenum  buccinator

Vibrating line
• From hamular notch to hamular notch
• Fovea palatini  lies 1.3mm anterior to anterior vibrating line (according to lye )
• Fovea palatini  lies either on or behind anterior vibrating line ( according to chan)
• Valsalwa manuvauer to locate

Butterfly line
• due to color change b/w hard and soft palate
• Vibrating line bit post to it

Posterior palatal seal

• b/w vibrating line (posterior boundary) & butterfly line (anterior boundary)
• Used for denture sution  to seal it & retain it

• Cast is carved on the posterior seal area for thicker acrylic to compensate for the arcylic
Coronoid notch
• Disto-buccal area impression / denture

Pterygomandibular raphe
• Band of fibrous tissues
• Connects buccinator (anteriorly) & superior pharyngeal
constrictor (posteriorly)
• Labial frenum  orbicular oris

• Buccal frenum  orbicular oris & buccinator

• Lingual frenum  genioglossus

• Labial vestibule  mentalis (inferior border)

• Buccal vestibule  buccinator

Retromandibular
• Marks distal extension of ridge
• Posterior boundary of buccal vestibule
• Contains attachment from  temporalis, buccinator, pterygomandibular raphe,
sup pharyngeal constrictor
• Covered for retention of denture

Masseteric notch
Alveolo-lingo sulcus
• b/w anveolar ridge & tongue
• Has three regions

1. Ant region
• Lingual frenum – premylohyoid fossa
• Sublingual glands sits above mylohyoid muscle above this area
• Flanges are little short anteriorly & touch mucosa of floor

2. Middle
• Premylohyoid fossa – distal to mylohyoid ridge
• Flange is deflected away from this area  due to constriction of mylohyoid
medially

3. Posterior
• Extends into retromylohyoid fossa
• Flange is longer here & deflected latrally (forming s )
• Denture extension is till  plataoglossus & superior consitrictor (sore throat
Buccal shelf
• Buccinator atttaches here
• Lateral to posterior mandibular alvolar ridge
• Support for denture
• Perpendicular to occlusal forces
Areas to consider in denture
2 things to consider
1. Bone
2. Mucous membrane

Denture bearing areas are

3. Limiting structures
4. Supporting structures
5. Relief areas
• Maxillary denture is supported by 2 bone
1. Maxilla
2. Palatine bone
Mandibular denture supported by
3. Mandible

• Cushion between denture and bone is mucous membrane

• Consists of 2 parts
1. Mucosa
Types
• Masticatory hard palate & crest of alveolar ridge
• Lining cheek, inner lips, soft palate, ventral of tongue
• Specialized  dorsum of tongue

2. Submucosa
• Formed by C.T which may be (dense or loose)
• Bulk of mucous memebrane
Relief area
1. Maxilla
• Incisive papila
• Rugae
• Mid palatine raphe
• Fovea palatinae
2. Mandible
• Mental foramen
• Genial tubercle
• Mylohyoid ridge

Limiting structure
1. Maxilla
• Labial & buccal vestibule
• Labial &buccal frenum
• Posterior palatal seal
2. Mandile
• Labial & buccal vestibule
Stress bearing areas
1. Primary stress bearing area
Maxilla
• Hard palate
• Maxillary tuberosity
Mandible
• Buccal shelf
• Retro molar pad area

2. Secondary stress bearing areas

Maxilla
• Rugae
• Alveolar tubercle
Mandible
Pre-prosthetic
surgery
1. Frenectomy
• When there is high frenum attachment
• Labial  buccal  lingual (common  least)

2. Free gingival graft

• Periodontic plastic procedure
• Necesarry for implant & overdenture cases
• FGG widens the keratinezed tissues
• Keratinzed tissues enable better oral hygiene (as it is not sensitive to
brushing , does not collect bacteria easily)

3. Hypermobile ridge
• Common in ant maxilla
• Excess fibrous tissues  loose & flabby
• Tissue conditioner  if tissue is inflammed
• Electrocautary / laser  to eliminate tissue
4. Epulis fissuratum
• Hyperplastic tissue reaction due to over extended denture
• Commonly in buccal vestibule area
• Treat with tissue conditioner & correcting denture

5. Fibrous / pendulous tuberosity

• Common when large tuberosites touch retro-moalr pads
• Surgical correct it  remove tissue or bone
• Can limit inter-arch space

6. Papillary hyperplasia
• Papillary projections on palate
• Due to  ill fitting denture, POH, leaving denture in all time, local irritation
• Main cause  candidiasis ( treat with statin / azole)
Treat
• OHI
• Use tissue conditioner
• Leave denture out at night
• Clean denture with 1% bleach
7. Retained roots
• Can be left if not infected (no radiolucecny) & intact
lamina dura
• If infected = extract

8. Pagets disease
• Etiology  unknown
• Bone resorption & depostion  causing deformity
• Denture not fitting after time  remake denture
periodically (exam question)
 Combination syndrome
• Pattern of bone resorption in anterior edentulous maxilla
when it is opposing mandibular anteriors only
Signs & symptoms
• Overgrowm tuberosity
• Papilary hyperplasia
• Extrusion of lower ant teeth
• Loss of bone under partial denture
1. Alevoloplasty
• Reshaping of alevolar bone
• Using  bur, ronger, filer
• For spiny or irregular ridges
• Non surgical alveoloplasty  when we compress socket after
extraction

2. Tori removal
• If tori creates a under cut
• Or interfere with palatal seal

3. Vestibuloplasty
• Increase height of alevolar process
• By apically respositioning  mucosa, mentalis, buccinator &
mylohyoid muscle
• Lingual vestibulo plasty is more traumatic & rarely done
4. Bone augmentation / graft
• Place bone graft
• From  ilac cres of hib & rib
• Hydroxyapetite  biocompat bone subsitute
• Horizontal  more good prognosis
• Vertical  more chances of failure
Complete
denture
1. Vertical dimension of rest (VDR)
• Distance b/w nose & chin at rest
• Stable point  tip on nose & chin
• Measured at rest  where elevator & depressor muscles are in state of
equilibrium
• Also called physiological rest position (PRP)
• Iin this position there is usually 3mm gap b/w upper n lower premolars

2. Vertical dimension of occlusion (VDO)

• Distance b/w nose & chin at occlusion
• Indicates superior-inferior relatioship of maxilla & mandibile in
maximum intercuspation (MI)

3. Inter-occlusal space (IOS)

• Difference b/w VDR-VDO
• Distance should be ideally  2-4mm
• VDR = VDO + 3MM
Excessive VDO
• Where IOS is less then 2mm or VDO is more than VDR
This will cause
• Excesiive display of mand teeth
• Fatigue of muscles of mastication
• Clicking of post teeth when speaking
• Strained appearance of lips
• Pt unable to wear denture
• Discomfort
• Difficulty to  speak,chew, swallow
• Gag
• Trauma to supporting tissues

Insufficient VDO
• Where IOS is more then 4mm
Aging appearnce of lower third of face because of
• Thin lips
• Wrinkles
• Chin near to nose
• Overlapping of corners of mouth
• Drooling of saliva
• Angular chelitis
CR record
• Fro edentulous pt, provides ability to increase or decrease the VDO more
accurately in the articulator by stablishing  radius of mandibles arc of closure
• To correct excessive / insufficient VDO problem
• Facbow transfered to articulator

Protrusive record
• Registers the ant-inf condylar path in translation movement
• Forward & downward movement

Christensens phenomenon
• Distal space created b/w maxilla & mandible when mandible is protruded due
to downward & forward movement of condyle down their eminence
• This phenomenon not in dentures

• Comepensating curves created into denture  for all teeth to remain in

contact
Plane of occlusion
• Ala tragus/ campers line  from ala to tragus of nose (ap view)
• Interpupillary line  line b/w pupils (front view)
• The maxillary occlusal rim should be parallel to these lines
(use fox’s plane to establish it)

Balanced occlusion
• In denture it refers to anterior & posterior contact simultaneously
(tripodization) in centric & eccentric movements to maintain denture
sit
• Ant guidance is avoided in CD to prevent dislodgement of base
• On balancing side maxillary lingual cusp contact lingual incline of
mandibular buccal cusp
• On working side  maxillary lingual cusp contact facial incline of
mandibular lingual cusp & mandibular buccal cusp contact lingual
incline of maxillary buccal cusp
Lingualized occlusion
• Articulation of maxillary palatal cusps to mandibular occlusal
surface in centric working & non working mandibular position
• Anatomic teeth in maxilla opposing non-cuspal /flat cusp tooth in
mandible
• Lingual cusp of maxillary teeth sitting in fossa of mandibular
teeth in centric relation
• Forces directed towards lingual side
• Upper palatal & lower central fossa  only contact
Compensating curves
1. Curve of spee
• Anterio-posterior (side view) curve to ensure loading into
long axis of each tooth
• More mesial inclination as to more towards back tooth
(distal)
2. Curve of wilson
• Mediolateral (coronal/front view) curve along posterior
cusp tips to esnure loading into long axis of each tooth
• More lingual inclincation as u move towards back (distal)
 Bennets
Bennet angle
• It is angle obtained after non-working side of condyle is moved anteriorly
& medially relative to sagital plane
• 15 degress
Bennet shift
• Lateral movement of mandible towards working side during lateral
excursion
• Moevemnt of mandible
Bennet movement
• Lateral movement of both condyles towards working side
• Movement of condyles
• Tmj looseness

Lateral side shift

• Collective term for both shift & movement
 Determinants of occlusion
Factors that favour disclusion (separate teeth)  no ecentric contacts of post teeth
Post teeth disocclude & occlude fast

Anterior guidance
1. Horinzontal direction
• protrusive movement forward
• Steep incisal guidance  separate teeth
2. Lateral direction
• Exrusion right & left
• Steep canine guidance

Posterior guidance
1. Horinzontal direction
• protrusive movement forward
• Steep horizontal condylar inclination ( HCI)
2. Lateral direction
• Exrusion right & left
Cuspal anatomy
• Short cusp with shallow inclines  faster seperation
• Steep cusp for ant

Tooth arrangement
• Less curve of spee
• Less curve of wilson

Orientation of occlusion plane

• Less parallel to the orientation of condylar path
• Factors that favor occlusion  ecentric position of post teeth
• Post teeth disocclude slowly when leaving mi

Anterior guidance
1. Horinzontal direction
• protrusive movement forward
• Shallow incisal guidance  separate teeth
2. Lateral direction
• Exrusion right & left
• Shallow canine guidance

Posterior guidance
1. Horinzontal direction
• protrusive movement forward
• Shallow horizontal condylar inclination ( HCI)
2. Lateral direction
• Exrusion right & left
Cuspal anatomy
• Long cusp with steep inclines  slow seperation
• Shallow cusp for ant

Tooth arrangement
• More curve of spee
• More curve of wilson

Orientation of occlusion plane

• More parallel to the orientation of condylar path
 Record bases & occlusal rims
• Primary impression  diagnostic cast  custom tray secondary
impression & border moulding  master cast  record base & rims

• necessary for proper denture making and phoentics

 Premature contact in denture
• Denture deviates to the same side of contact
• Anterior contact  A-p movement
• Posterior contact  lateral movement
 Gag in complete denture
Mandibular Dentures:
• Overextension or excessive thickness of the distolingual flange can trigger a gag reflex. This happens
because the denture may contact sensitive structures at the back of the tongue.

Maxillary Dentures:
a. Posterior Palatal Seal
• This area can cause discomfort and a gag reflex if overextended
• Proper adjustment is necessary to ensure a comfortable fit without extending too far back.

b. Buccal and Labial Flanges

• Overextension here can cause irritation of the cheeks and lips, leading to sores or a feeling of
fullness.

c. Vibrating Line
• If the denture extends beyond the vibrating line (the junction of the hard and soft palates), it
can stimulate the gag reflex.
d. Frenum Areas
• Overextension near the buccal or labial frenums can limit movement and cause irritation
 Sturctures that interfere with flanges
Structures that can interfere with maxillary (upper) denture flanges:
1. Frenum  The frenum can interfere with the proper denture border extension
along the maxillary buccal and anterior vestibules.
2. Coronoid process  This can impinge on the maxillary denture if the posterior
region of the buccal flange is too wide, especially during mouth opening.
3. Buccal exostosis  These bony prominences can prevent dentures from fitting
well, leading to a poor adaptation to the buccal vestibule.

Structures that can interfere with mandibular (lower) denture flanges:

4. Frenum  Similar to the maxillary denture, the mandibular frenum can limit the
denture's proper extension.
5. Mylohyoid ridge this ridge can interfere with the lingual flange of the lower
denture.
6. Tongue  A large or active tongue can affect the stability and fit of the lower
denture.
7. External oblique ridge  This ridge can interfere with the buccal flange of the
lower denture
Proper Extension
• The correct extension of the denture base into the peripheral tissues helps in stability. The
buccal and lingual flanges should extend into their respective sulci as far as the functional
movements of the oral tissues allow.

Residual Ridge
• Stability in lower dentures is heavily dependent on the residual ridge. The more robust and
well-formed the residual ridge, the better the stability and retention

Retro mylohyoid space

• This space, located posterolaterally, helps in providing stability by preventing lateral
displacement of the denture.

Tongue Position
• The position and movement of the tongue can significantly affect the stability of the lower
denture. A properly trained tongue placing slight pressure onto the lingual flanges can help
stabilize the denture.

Occlusion
• Proper occlusion is crucial. Balanced occlusion helps distribute forces evenly, reducing the
 Phonetics
1. Labiodental / fricative sounds
• Contact b/w max incisorrs & wet / dry line of lower lip
• Dry part of lip  where we applu lip balm or lipstick
• Wet part  labial mucosa where minor salivary gland begins
• Sounds  F, V , PH
• These sound requires contact b/w lower lip & icisal edge
of max ant teeth

• Testing these sound with rim or wax trial help determine

where the incisal edges of max ant teeth should be
• Ask pt to say 50 – 59
• If problem saying this  adjust wax rims
2. Sibilant / lingo-alveolar sounds
• Contact b/w tip of tongue to anterior palate / lingual
surfaces of ant teeth
• Sounds  S, Z, SH, CH, J
• 60-69
• These sounds help determine vertical length and overlap
of anterior teeth

• If pt tries these words & whistling sound comes out of pt

mouth  narrow arch form
• If there is lisp ( S becomes SH sound)  too wide arch form

• When pt pronouns S sound there should be interincisal

3. Linguodental sound
• Sound  TH
• Contact b/w tip of tongue & upper & lower teeth

• These sound help determine labio-ligual position of the

ant teeth (how forward or backward teeth are)
• Tongue not visible  teeth too far forward
• Tongu sticks out  teeth are too backward
4. Bilabial sounds
• Sound  M, P, B
• From contact b/w lips
• Insufficient lip support by teeth or labial flange  affect
production of these sound

5. Gutteral sounds
• Sound  G & K
• Contact b/w back of tongue to throat
• Denture extend way war to palate these may b affected
1. Support
• Resitance to vertical seating force
• Force towards apex
Upper arch
• Palate
• Alevolar ridge
Lower arch
• Buccal shelf
• Retromolar pad
• Denture base  provide suport

2. Stability
• Reistance against horizontal dislodging forces
For upper & lower arch
• Height of ridge
• Depth of vestibule
3. Retention
• Resistance agains vertical dislodging forces
• How to keep denture in place
• Peripheral seal  retention in denture
Adhesion
• Atteaction b/w unlike molecules
• Saliva to tissue
• Saliva to denture base
• Initmidate contact b/w saliva and bas = best seal
• Occlusal prematurities may break seal

Cohesion
• Attraction b/w like molecules
• Saliva to saliva
• Thick and ropy saliva = unfaavorable
• Thin & watery saliva = good retention

Surface tension
• Combination of adhesion & cohesive formes that maintain film integrity
• Water molecules are attracted to eachother then air
• Eg :- little layer of water b/w two glasess = good seal
• We need to disrupt layer at the menuscus (weakest point of film layer)
Overextenison
1. Due to extended flange
• Sore spot or ulcer
• Relieve the denture
• Follow up
2. Extension too far back
• Denture teeth set too far up till ramus past retromolar pads
• Denture which dislodges from occlusal forces
• This is why third molar not needed in denture

Underextension
1. Short flanges
• Unretentive denture  no proper seal  no enough surface area
• Best inidcator for succes of denture is  ridge
• Ridge can provide  support, stability, retenion
• Wide broad ridge is best for this
 Materials used
Heat cured Acrylic
Powder
• Polymer  PMMA (polymethyl methacrylic)
• Initiator  benzoyl peroxide
• Pigment  salts of iron, cadmium or organic dyes

Liquid
• Monomer  MMA (methyl methacrylic)
• Inhibitor (prevents polymerization in powder form) 
hydroquinone
• Cross linking agent  Glycol d methacrylate
• Activator  Dimethy-p-toluidine
 Denture processing
• Shrinkage occurs its normal (polyemerization)
• Polymerization  moonmers cross links to make polymers
• Excessive shrinkage  more monomer
• Ideal ratio of monomer : polymer  1:3

• Polyermization  mma bonded closer together and occupy

less space

Porosity in denture
• Underpacking of resin durin time of packing
• Being heated too quickly = immediate vaporization of
 Teeth
Acrylic Porcelain
Pros Pros
• Bond to the acrylin resin of • More esthetic
denture base • More stain & wear reistance
Cons
• Not as good aesthetic as Cons
porcelain • Brittle
• Wear oppositing teeth

Retention
• Mechanical
• Anterior teeth  pins
• Posterior teeth  daitorics
Lab processing
• Trial dentures sealed in master cast  flasking
• Seperating medium placed b/w layers 
• After this place the flask in boiling water to melt the
wax  leaving the teeth which are going to be invested
top layer of stone
• Acrylic is packed  to take place of melted wax & the denture
base
• Acrylic first  compressed then it is heated
All material
Partial dentures
 Kenedys classification
Class 1
• Bilateral edentulous free end saddles area posteriorly to remaining natural
teeth
• Bilateral distal extesion
Class 2
• Unilateral edentulous free end saddles area posteriorly to remaining natural
teeth
• Unilateral distal extension
Class 3
• Unilateral edentulous area with natural teeth both anterior and posterior to it
• Unilateral bounded edutulous sapce (BES)
Class 4
• Single but bilateral edentulous area present anterior to remaining natural
teeth (crossing midline)
 Applegates 8 rules
• Rule 1 Classification should follow rather than precede any extractions of
teeth that might alter the original classification (do extraction before
classification)
• Rule 2 If a third molar is missing and is not to be replaced, it is not considered
in the classification
• Rule 3 If a third molar is present and is to be used as an abutment, it is
considered in the classification (abutment 3rd molars considered)
• Rule 4 If a second molar is missing and is not to be replaced, it is not
considered in the classification (2nd molar not considered if not needed)
• Rule 5 The most posterior edentulous area (or areas) always determines the
classification
• Rule 6 Edentulous areas other than those that determine the classification are
referred to as modifications and are designated by their number
• Rule 7 The extent of the modification is not considered, only the number of
additional edentulous areas (doesn’t matter how big edentulous area is )
• Rule 8 No modification areas can be included in Class IV arches (no mods in
class-4)
Parts of rpd
Parts of partial denture
• Connectors
• Saddle
• Direct retainers (clasp)
• Indirect retainers
• Rests (occlusal & incisal)
• Denture base
Saddle
• Part of partial denture which carries artificial teeth
• Two types
1. Tooth-borne
2. Mucosa-borne

Connectors
3. Major connectors
• Joins one side to dental arch to another  Provides unification
• Rigidity to denture  primary fuction
• Not placed on movable tissue
• All major connectors should cross midline at right angle
• Beading  scribing 0.5mm rounded line in cast at borders of maxillary major
connectors only  provide strength & tissue contact
• Maxilla  6mm away from gingival margin
• Mandible  3mm away from gingival margin

2. Minor connectors
Direct retainer
• Provides retention against dislodging forces (clasp)

Indirect retainer
• Prevents movement/rotation of bases away from the residual
ridge

Denture base
• Unit of partial denture that covers the residual ridges and support
denture teeth
 Mandibular
major connectors
 Lingual bar
Indications
• 7mm or greater lingual vestibule depth
• Lingual measured from  lingual gingival margin of teeth to
frenum start
• Simple & most common
Contraindications
• Inoperable lingual tori
• High lingual frenum attachment
• Interferences during functional movements of the floor of the mouth
Advantage
• Minimul tissue coverage and contact with oral tissue
Disadvantage
• Mayb flexible if poorly construted
 Lingual plate
Indications
• Lingual vestibule depth less then 7mm
• Presence of lingual tori
• Additional tooth loss anticipated
• Class 1  all post teeth missing only ant left
Contraindications
• In lingually inclined mandibular anterior teeth
• Wide embrassures and diastema
Advantage
• More rigid, provide more support & stabilization
Disadvantage
 Sublingual bar
Indications
• The height of the floor of the mouth in relation to the free
gingival margin is less than 6mm
• If it is desired to keep the free gingival margins of anterior teeth
exposed and there is inadequate depth of the floor of the mouth
Contraindications
• Lingually tilted remaining natural teeth
• Inoperable lingual tori
• High attached lingual frenum
Lingual bar with continuous bar (cingulum bar)
• Also called kennedy bar
Indication
• Used in periodontally treated anterior teeth with wide inter-proximal
embrassures
• When liguo-plate is contraindicated due to poor axial alignment of
anterior teeth
Contraindication
• Severly crowded anterior teeth
Advantage
• Horizontal stablization
• Minor amount of support to the prosthesis
Disadvantage
 Cingulum bar
Indication
• Improper axial alignment of the
anterior teeth requiring excessive
block out of interproximal undercuts
Contraindications
• In lingually tilted anterior teeth. –
Wide diastema between mandibular
anterior teeth.
 Labial bar / swing lock
• Has hinge on one end & locking system on other  swing lock
Indication
• Missing canine
• Unfavourable soft tissue contour
• Questionable periodontal prognosis
• Large inoperable lingual tori
• Severe & abrupt lingual undercuts
• Lingually inclined lower anterior & premolars
Maxillary major
connectors
 Single palatal strap
INDICATIONS
• Used only when 1 or 2 teeth are being replaced on either side
• In CLASS III situations
• Need for palatal support is minimal
CONTRAINDICATION
• Anterior replacements with distal extension bases
ADVANTAGES
• Because the palatal strap is located in three planes it offers great resistance to
bending and twisting forces
• Distribution of stress over a broad area
• Retention of the partial denture is enhanced by the intimate contact between the
metal and soft tissue
• The strap also contributes some indirect retention.
DISADVANTAGES
• The patient may complain of excessive palatal coverage
• Another possible disadvantage is an adverse soft tissue reaction in the form of
 Anterior-posterior palatal strap
INDICATIONS
• Kennedy’s Class I and CLASS II arches
• CLASS II modifications I arches
• Class IV arches
• In case of inoperable tori
DISADVANTAGES
• Even though the metal over thin rugae area may be thinner than
in some other major connectors, interference with phonetics may
occur in some patients
• In addition, the extensive length of borders may cause discomfort
to the tongue
 Palatal plate
• Most rigid of all
INDICATIONS
• Class 1
• Periodontally compromised tooth
• When flat or flabby ridges or a shallow vault is present
• When the last remaining abutment tooth on either side of a Class I arch is the canine or first
premolar tooth
• In individuals with a full complement of mandibular teeth
• Cleft palate patients

CONTRAINDICATION
• Presence of tori which cannot be surgically removed a full palatal coverage cannot be given
ADVANTAGES
• It reproduces the anatomic contours properly
• uniform thickness and thermal conductivity of the metal are readily acceptable to the tongue
and underlying tissues
DISADVANTAGES
• Adverse soft tissue reaction in the form of inflammation or hyperplasia may occur
 Horse shaped platal connector
• Least rigid of all
INDICATIONS
• Can be in case of a large inoperable palatal tori
• When several anterior teeth are to be replaced
• In case of patients with exaggerated gag reflex
• When periodontically weakened anterior teeth need some
stabilizing support
DISADVANTAGES
• Its lack of rigidity allows lateral flexure under occlusal forces…
induce torque or direct lateral force to abutment teeth
• Bulk to enhance rigidity results in increased thickness in areas
that are a hindrance to the tongue
 Single palatal bar
INDICATION
• Limited to replacing one or two teeth on each side of arch and placed
no further anteriorly than the second premolar position
• Perhaps the only indication for its use is as an interim partial denture
until a more definitive treatment can be considered.
CONTRAINDICATION
• In distal extension situation
• when anterior teeth are to be replaced
DISADVANTAGES
• Most difficult for the patient to adjust as to maintain the degree of
rigidity it has to be made bulky
• Due its narrow anterior-posterior width it derives little vertical support
from the bony palate and must be therefore supported positively by
Single palatal bar
 Anterior-posterior palatal bar
INDICATIONS
• when support is not a major consideration and when the anterior and posterior
abutments are widely separated
• Presence of torus palatinus
• The patient's mental attitude: the a-p bar may be used as a compromise for the
patient who strongly objects to the greater bulk or area coverage of the full palatal
connector
CONTRAINDICATIONS
• In reduced periodontal support of the remaining teeth that necessitates additional
support from the palate.
ADVANTAGES
• The main advantage is its rigidity. In comparison to the amount of soft tissue
coverage, it is by far the most rigid maxillary major connector
DISADVANTAGES
• it is frequently uncomfortable
• Derive very little support from the palate
Anterior posterior palatal bar
 Minor connectors
• Connects major connectors to rest, indirect retainers & clasps

1. Proximal minor connector

2. gridwork minor connector
3. Embrasure minor connector
Rest
• Rigid extension of rpd framework that contact occlusal, incisal or
lingual surface of abutment teeth
• Direct forces through long axis of abutment teeth
• Provide support
• Resistance to vertical seating forces

• Rest seat  prepared on the abutment tooth to receive rest

Types
• Occlusal rest
• Lingual / cingular rest
• Incisal rest
1. Occlusal rest
• Shape  Semi-circular or spoon shaped
• On occlusal surfaces of molars & premolars
• Should be  1/3 of mesio-distal width
• Should be  half of inter-cuspal width
• Depth  1.5mm for base metal
• Floor inclines apically towards center
• Angle formed with vertical minor connector less than 90degress

2. Cingulam rest
• Shape  Inverted V or U shaped design
• Cingulum of anteriors (moslty canine)
• Should be  2.5 - 3mm mesio-distal length
• Should be  2mm labio-lingual width (ledge)
• Depth  1.5mm
• CI  mandibular incisors
• Good  good distribution of occlusal load, easthetics, strength from closeness to
3. Incisal rest
• Shape  rounded notch at incisal angle
• Should be  2.5 mm mesio-distal length
• Depth  1.5mm
• Used as indirect retainer
• Less favoruable levargae than lingual
• Esthetic compromise
 Rest seat placement
Class I  bilateral Distal Extension
• Mesial rest seat on the abutment teeth adjacent to the edentulous space
• Rationale  Helps direct the forces towards the axis of the tooth and disperses the load more
evenly across the occlusion

Class II  Unilateral Distal Extension

• Mesial rest seat on the abutment teeth adjacent to the edentulous space
• Rationale Similar to Class I, this placement helps balance and stabilize the denture,
preventing undue stress on the abutment tooth

Class III (Tooth Bounded on Both Ends)

• Either mesial or distal rest seat on the abutment teeth adjacent to the edentulous space
• Rationale  Typically, the choice depends on the specific occlusal and structural considerations
of the patient's teeth; both placements can offer good support and stability

Class IV (Single, Bilateral or Cross-Arch Replacement of Anterior Teeth

• Mesial rest seats are generally preferred for better distribution of forces towards the teeth and
supporting structures
 Mesial rest Distal rest
• Help direct forces towards other • Generally, not preferred for
teeth, providing better distal extensions as they direct
distribution and reducing stress forces away from other teeth
on the abutment teeth and can create excessive
stress on the abutment tooth.

General Consideration
• Rest seats should be designed and placed to distribute occlusal loads
towards the long axis of teeth, optimizing the denture's stability and
minimizing the risk of damaging abutment teeth.
Metal plate
• Contacts proximal surface of abutment tooth
• Type of minor connector
 Guide planes
• Flat parallel surfaces of abutment tooth that provide the path of
insertion & removal
• Not always present naturally, need to prepare tooth for creating
guide planes
• 1/3 bucco-lingual width
• Extends 2-3mm vertically down from marginal ridge
 Indirect retainer
• Provides retetnion against rotational movement
• It is directly perpendicular & anterior to the fulcrum line (axis of
rotation)
• It is mostly the  rest

• There is a rotational movement centered around an

imaginary line drawn through the most distal rests

• teeth used for indirect retention, farthest acceptable teeth from

the fulcrum line
Direct retainer
Clasp assembly
1. Rest  support
2. Minor connector  stability
3. Clasp
a) Retentive arm  retention
b) Reciprocal arm  stability
Types of direct retainer
1. Extracoronal
• Clasp desgin  should encirle tooth atleast 180degress
• Most common
2. Intracoronal (with in crown)
• Key & keyway pattern
• More esthetic  because no clasp
• Female part  part of survey crown (abutment)
• Male part  part of framework
• Precision attachments provide esthetics, stability, and retention.
Retentive clasp / arm
• Located generally on buccal side
• Originate from minor connector & rest
• Contacts tooth below height of contour / survey line
Parts
• Occlasl  support
• Middle  stablization
• Gingival  retetnion

Only the tip of clasp shoud be below HOC in undercut for retentio, every other
part above HOC
Only active when dislodging forces are applied otherwise it is passive

Reciprocal clasp/ stablising clasp

• Originate from minor connector & rest
• Above HOC
• Mostly located on lingual surface
• Provides stability
 Clasp design
1. Supra-buldge
• Originate above survey line
a) Circumferncial (akers)
b) Ring
c) Combination
d) Embrassure

2. infra-buldge
• Originate below survey line
a) I bar
b) T bar
c) Bar type
Akers clasp

Ring clasp
• Used when undercut is adjacent to bounded edentulous space

Embrasurre clasp
• Kind of when we join two akers clasp
• Placed in embrassure b/w two teeth
• Rest on both the teeth

T bar
 Clasp assemblies
1. RPI system
• Rest  on the mesial than distal side
• Proximal plate  distal
• I – bar  buccal
• Provides ideal class 2 lever system

2. RPA
• Rest
• Proximal plate
• Akers clasp

3. RPC
• Rest
• Proximal plate
 Clasp selection
Wrought wires
• More flexible
• Seperatly postioned & soldered onto the meta frame work
• Puts less torque on teeth
Used / recommended
• Perdiontically compromised teeth
• Endo treated teeth

Akers claps
• Bounded edenulous spaces
• Rest  adjacent to edentulous spaces

Distal extension
Cobalt chromiun
• 2.3 % shrinkage  pores & irregularties

Cold working
• Manipulating metal at ambient temp
• Clasp is cold-worked everytime it is seated or dislodges
• One of reason for it to break
 Altered cast technique
• The altered cast technique involves making a secondary impression of the edentulous areas (where
teeth are missing) of a partially edentulous arch after an initial impression and framework try-in.
• The new impression is then integrated into the master cast to better capture the tissue's functional
form.
• In summary  the altered cast technique is essential in creating a more functional, comfortable,
and stable prosthesis for patients with partial edentulism
• The original cast is cut to enable integration of the new final impression. This technique offers
various benefits, including a reduction in food impaction, maximum stability, minimal stress on
abutment teeth, and preservation of residual ridges

When It Is Used
• This technique is particularly useful in cases where the residual ridges are soft or irregularly
shaped, and a conventional impression might not capture the true tissue dynamics
Purpose and Benefits
• Improved Fit  It helps achieve a more accurate and intimate fit of the denture to the supporting
tissues, thus enhancing comfort for the patient.
• Reduced Movement  By accurately capturing the edentulous ridge, the altered cast technique
minimizes movement of the denture, leading to improved function and stability.
• Better Tissue Adaptation  The technique ensures that the final denture base adapts well to the
soft tissues in a functional state, reducing sore spots and improving overall retention.
 Atwoods classification
• Atwoods gave classification for ridge resorption

• Class 1 pre-extraction
• Class 2 post-extraction
• Class 3 high well round
• Class 4 knife edge
• Class 5 low well rounded
• Class 6 depressed
 Post extraction effects on the ridge
• The alveolar ridge decreases in width

The alveolar ridge perimeter increases

• Following tooth extraction, the alveolar ridge begins to resorb as it
no longer receives stimulatory forces from the teeth
• As a result, height and width both decrease
• The mandible resorbs in an outward direction, resulting in an
increased perimeter as the alveolar ridge height decreases.

The mental foramen opens superiorly on the bone

• Due to aging, tooth loss, and subsequent bone resorption, the
mental foramen moves closer to the alveolar border more
• Extraction has no effect on the coronoid process
• In edentulous pt  coronoid process elongates superiorly &
retracct posteriorly
• Maxilla resorbs & ridge narrows
• Mandible reorbs fasters & its width remain constant
 Cusp angles in different ridges
1. Resorbed narrow ridges
• making 0° non-anatomic denture teeth the ideal choice. Resorbed ridges
provide less retention for dentures, and utilizing a sharper cuspal inclination
increases lateral forces during mastication, which can lead to dislodgement.

2. Semi-resorbed ridges
• 20° Semi-anatomic denture teeth with shallow 20° cusps are utilized in
complete dentures on

3. Healthy ridges with moderate resorption

• 22° Semi-anatomic denture teeth with 22° cusps are utilized in partial
dentures, implant overdentures, or complete dentures on

4. Healthy ridges with minimal resorption

• 30° Denture teeth with fully anatomic anatomy have 30° cusps and are
utilized in partial dentures, implant overdentures, or complete dentures on
• A crown preparation that has insufficient occlusal clearance may
result in a crown that is thin, poorly contoured, and prone to
fracture or perforation. Provisional crowns should be
fabricated before the final impression and can be used to assess
if the occlusal clearance is sufficient. Insufficient occlusal
clearance is not a typical reason for a crown not fully seating
Fixed prostho
Components of bridge
Abutment
• Tooth from which bridge attaches
Retainer
• Part which attaches to the abutment
Pontic
• Fake tooth
Connector
• Attach retainer to pontic
 Tooth preparation
Occlusal reduction
• Provides with structural durability
• Reduce occlusion
• Maintain anatomy
• Funtional cusp reduction / bevel (secondary plan of reduction)
(upper lingual lower buccal)
• Rounde angles  structural durability

Axial reduction
• Retention & resistance

Margin / finish line

•
 Principles of tooth prep
1. Biologic
• Health of oral tissue
Be aware of
• Mechanical injury  common where thin gingival tissue is (lingual of molars & facial
of premolars )
• Thermal injury  use water, sharp instruments (no dull), intermittent light pressure
• Chemical injury  soaked retraction cord, cements
• Bacterial injury  leakage under crown

2. Mechanic
• Integrity & durability of restoration
Retention form
• Features that prevent removal of crown along long axis of tooth (kheechna)
• Long surface of prep should be parallel to long axis of tooth
• Eg :- sticky foods

Resistance form
Taper or parallelism
• Angles of convergence formed b/w two opposing axial walls
• Most operator controlled
• Smaller the degress of taper = more retention (6-10
degress ideal taper , provides retention)
• More taper = less retention
• U can give more taper if prep is taller
Height or length
• From occlusal / incisal surface to margin
• Taller prep = more surface area – retention
• More imp than then width
• 3mm minimum for  incisors , premolars \
Width
• Mesdio-distal or facio-lingual dimention of base
• Wide base & short height = less retention

Height to base ratio

• Minimum  0.4

If u have short crown

• Buccal grooves for  retention
• Proximal grooves for  reistance
Thickness of crown
 Reduction Clearance
• Amount of tooth structure • Space available b/w tooth prep
removed during tooth prep & opposing tooth
• 1.5 – 2mm • 1.5 – 2mm
3. Esthetic
• Metal
• Gold  best material
• Ceramic
• Margin of tooth  edge or shelf on the preparation
• Margin of restoration  part of restoration which forms its
outer limit that adjoins to the cavosurface margin of prep
tooth

Location
• Supra-gingival  above crest
• Equigingival  at crest
• Sub-gingival  below crest
 Types of margin
1. Feather edge
• Very acute thin margin
• Best marginal seal
• Less invasive
• Insufficient clearance for material
• Difficult to visualize
• Not generally used
• Too thin margin = not enough space for material = overcontouring of restoration

2. Light chamfer
• 0.3 – 0.5mm thick
• For gold crowns & metal only
• Wide gold collars of pfm crowns

3. Heavy chamfer
• 1 – 1.5 mm thick
• PFM & some all ceramic crowns
• Too thin margin = not enough space for material = overcontouring of restoration = bacteria
accumulation
4. Shoulder
• 1-1.5mm thick
• Porcelin or pfm
• All – ceramic crown
• Maximum esthetic  due to elimination of metal display
• Aggressive prep  pulpal damage / embaressment
 Indirect restoration
Inlay
• Within cusp
• Does not cover the cusp

Onlay
• On the cusp
• Covers cusp

¾ & 7/8 crowns

• Hybrid b/w onlay & full crown
• Conserve tooth structure
• 3 out of 4 walls covered (usally buccal left)
• Less restoration margin proximity to the gingiva
• More easily seated
 Occlusal schemes
• Occusal point contacts  broad & flat ( to avoid wearing of
opposing tooth

Scheme used
• Cusp – marginal rdige  class 1
• Cusp – fossa  class 2
Components of bridge
Abutment
• Tooth from which bridge attaches
Retainer
• Part which attaches to the abutment
Pontic
• Fake tooth
Connector
• Attach retainer to pontic
 Types of pontic
1. Hygenic / sanitary pontic
• Used in post mandible
• Good hygiene  space b/w pontic & ridge (2mm)
• Poor esthetics
• Reguire enough VDO / restorative space

2. Saddle / ridge lap

• Should never use
• Like a saddle on horse
• Wraps around the ridge
• Very bad for hygiene  extremly hard to clean = peridontal problem

3. Conical
• Conical  on point of contact to ridge
• Similar to hygenic but good marginal esthetic (not as hygenic as that )
• Used in molars
4. Modified ridge lap
• Anteriors
• Good esthetics

5. ovate
• Superior esthetics
• Only for anteriors
• Pontic embed into divet in the soft tissue and ridge
(require surgery)
• Requires good ridge
• Emergence profile  more natural like
Saddle /

2mm

Hygienic / sanitary pontic

 Types of connectors
1. Rigid
• Either cast in 1 piece
• Or soldered together
2. non-rigid
• Inidcated when it is impossible to obtain common path of
insertion b/w abutments (one tooth tipped)
• Eg :- male & female part in bridge

• Connectors for PFM should have atleast 3mm of height

indications for a non-rigid connector include:

1. Pier abutment causing a fulcrum-like situation and potential

failure of weakest abutments
2. Misaligned abutment requiring a non-rigid connector to prevent
devitalization
3. Long-span FPD vulnerable to distortion from porcelain shrinkage
4. Mandibular arch FPD consisting of anterior and posterior
segments needing a non-rigid connector due to mediolateral
mandibular flexion
5. Disparity in abutment retentive capacity requiring non-rigid
connector use
Impression
material
 Tissue management for impression
1. Fluid control
• Cotton rolls
• Suction
• Anti-sialogauge (atropine)

2. Tissue displacement
• Retraction cords  strect circumferential PD fibers
Impregnate cords with
• Alluminium chloride (AICL)  hemodent
• Iron sulphate FeSo4  viscostat
• Epinephrine
• Electro surgery  CI in pacemaker, insulin pumps, &
Reversible hydrocollide / AGAR
• Reversible
• High acccuracy
Change b/w two phases
• Sol phase  solution
• Gel phase
Soft  heat
Hard  cool

Imbibtion  water absoprtion (swell)

Synersis  loss of water (shrink)
 Irreversible hydrocollide / Alginate
• Most inaccurate
• Not for final impression
• Not for crown & bridge

• Primary ingredient  diatomaceous earth (60%) (strength)

• Active ingredient  potassium alginate 15% (active ingredient )
• Setting time  3-4 mins in pt mouth
• Pouring time  10min in gypsum
• Tri-sodium phosphate 2%  control setting rate

• Mix powder into water  to reduce bubbles

• Increase Setting time  cold water & more water

• Decrease setting time  hot water & less water
• Imbibtion  water absoprtion (swell)
Polysulfide rubber
• Water by product

Mositure tolerant
• Hydrophobic
• Synersis  shrink

• Pouring time  30-45mins

Condensation silicone
• Alcohol byproduct  can cause shrinkage
• Pouring time  30mins
Addition silicone (PVS) (polyvinyl
siloxane)
• Best material
• No byproduct
• Best fine detail
• Best elastic recovery
• Best dimensional stability
• Inhibited by sulphar in latex gloves
 Polyether
• Very stable
• Easily influenced by water & humidity
• Hydrophillic
• Imbibition  swell
• Very stiff  break cast teeth
• Pouring time  60mins
 Gypsum
• Mined as  calcium sulphate dihydrate (CaSO4 2H2O)
• Converted to calcium sulphate hemi-hydrate (CaSO4 ½ H2O)

• All gypsum products are chemically same but differ in size and shape of particles
• Mixing  20 sec if vaccume mix , 30 sec if hand spatula
• Setting time  45-60mins
• Disnfect with  1:10 bleach, glutaaldehyde or idophor spray

Gauging water
• Extra water needed to attain workable mixture , does not chemically react with
gypsum

• Type 1  impression plaster

• Type 2  model plaster
• Type 3  dental stone
• Type 4  dental stone with high strength & low expansion
Water/powder ratio

1. Increase water
• Less strength
• More pores
• More setting time
• Less expansion

2. Decrease water
• More strength
• Less pores
• Less setting time
• More expansion
Setting time

1. Increase
• Cold water
• Less spatula
• More water

2. Decrease
• Hot watwr
• Less water
• Slury water
• Increase spatulation
Impression plaster type 1
• Low expansion
• Sets quickly  less expansion
• For mounting cast on articulator
• Sets faster  5-10mins
Model plaster Type 2
• To make cast
• To fabricate  Mouth guards & essix
Dental stone type 3
• To make diagnostic cast
Type 4
• Best abrasion resisance
• Least expansion
• Less requirement of guaging water
• Used for fabrication of dyes

Dye  positive reproduction of prep teeth

Type 5
• Also used for die fabrication
Metal alloys
Nobel metals
1. Gold  tarnish resistance
2. Platinum  increase strength & melting temp
3. Palladium  strength

• Silver is not considered nobel in dentistry  greening of

porcelain
Metal aollys
1. High noble alloy
• Grater than 60% noble
• Atleas 40% of which is gold

2. Noble alloys
• More than 25 % noble

3. Base metal alloy

• Less than 25% noble
• Nickle chromium (Ni-Cr)
• Nickle chromium berrylium ( Ni-Cr-Be)
• Cobalt chromium (Co-Cr)
 Types of gold
Type 1
• pure gold
• 98-99% gold
• Soft
• Class 5 restoration

Type 2
• 77% gold
• Inlays , onlays
• Medium hard
Type 3
• 72% gold
• Crowns
• Hard

Type 4
• 69% gold
• Extra hard – strongest
• Casting of rpds
• Bridges , post , clasp
Mechanical
properties
Compressive strength
• Ability to resit fracture during compression
• Eg:- crown in occlusion

Tensile strength
• Resist fracture during pulling

Flexural strength
• Resisit fracture during bending
• Connector of bridge during occlusion

Fracture toughness
• Ability to resisit propogation of crack
Modulus of elasticity
• Measure of stiffness or rigidity
• Stress / strain (fromula)
• Sustain defromation without permanent change in size or shape

Brittle
• Fracures easily without any substantial dimesional change
• Porcelain

Ductility
• Easily deforms under tensile strength
• Wire

Malleability
• Deforms easily under compressive stress
• Gold

Percetage elongation
• Ability to be burnished (plastic deformity)
• When stress exceeds yield strength of material
Coefficient of thermal expansion
• Measures the fractional changes in size per degree change in
temperature
• Higher CTC means more tendecy to change
• Tooth CTC  11.4

• A possible break in marginal seal of any restoration becomes

imminent when there is marked difference b/w tooth & restoration

• If oral cavity is to become hot this is the how the expansion happens & shrink
when cold
• Composite MetalToothCeramic
• Composite  30
• Amalgam 25
• Gold  14 (best) (closest to tooth)
• Tooth  11.4
• Porcelain  6
 Desirable properties
• High yield strength  does not deform permanently
• High elastic modulus  does not flex
• Casting accuracy  gold is more accurate then base metal
• CTC close to that of tooth
• Biocompatible  ni & be allergies
• Corrosion resistance  more noble more resistant
• Minimal teeth wear  porcelain wear teeth much faster
 Provisonal
restoration
• Temporary crown / provisonal
• For esthetic & funtion
• Not as esthetic as definitive crown

Principles
1. Biologic
2. Mechanical
3. Esthetic
Method
1. Direct
• Inside mouth
• Easy
• More time consuming
2. indirect
• Outside mouth
• Improvied pt comfort
• Avoid thermal & chemical exposure
• Good marginal seal

Mould
1. Prefabricated crown
• Polycarbonate
• Aluminum
• Stain less steel  common in paedatrics

2. Cellulose acetate crown form

• Thin transparent
• Plastic material
• Filled with temp crown material

3. Putty or shim
• Impression taken before prep
Material
1. Polymethyl methacrylate (PMMA)
• Used in indirect method
• Gives off heat  exothermic
• Indirect

2. Polyethyl methacrylate (PEMA)

• Not common

3. Bis-acryl composite (luxatemp)

• Direct method
• Good for single unit
• Short span bridge
• Brittle  worse mechanical properties
• Less shrinkage
• Less odour & shrinkage  good property
Before final crown placement
1. Anesthetize or not
• Anaesthesia  harder to confirm occlusion
• Numb lip = effect aesthetic

2. Clean prep
• Remove provisonal cemet
• Proviosnal cement has eugenol  inhibts with resin
cement polymerization
• Properly clean prep
Crowns
 Metal ceramic / PFM
Bonding of porcelain to metal
Monomolecular oxidative layer
• Should be present b/w metal & porcelain to bond
• ethetic challenge due to its dark color

Material present
1. Metal layer
• Lingually  metal
• Facially  0.3-0.4mm metal

2. Porcelain layer
• Opaque porcelain  masks the dark color of oxide layer (minimum 0.1mm)
• Body or dentine porcelain  most of shade, builds most of crown
• Shoulder margin  buccally / facailly . chamfer margin 
lingually

• All internal line angles  rounded

 metal-ceramic failures
1. Adhesive failure (b/w different material)
• Metal & porcelain  if oxide layer not formed b/w them
• Oxide - metal  if metal is contaiminated
• Oxide – porcelain  if porcelain contaminated

2. Cohesive failure ( b/t same material)

• Porcelain –porcelain  voids or inculsions
• Oxide – oxide  too thick layer (it should be monolayer 1 cell thick)
• Metal – metal  never happens

3. Long span bridges

• Fractue easily unde flexture stress  due to low ductability of
porcelain
 All ceramic crowns
• Esthetic

Types
1. Ceramics with glass or silica
• They are etched with  hydrofloric acid
• Treated with  silane coupling agent & bonded to tooth

2. Non glass ceramic

• No bonding but luted to teeth using cement (no glass = no bonding =
no etching)
• Stronger
• Not as esthetic
•
Prep
• Shoulder margin  facial & lingual
Base porcelain layer
Dentine porcelain layer
Enamel porcelain layer
 Veneers
• Cover only facial surface
• For esthetics

Intra enamel preperation

• Preparation should be in enamel as acid etched enamel
have more pridictable bonding then dentine bond
• Conservative prep design  does not extend to dentine
• Round line angles

Gingival third reduction  0.3mm

Facial reduction  0.5mm
 Discoloration in veneer
Microleakage
• Leakage of gingival fluids or bleeding during cementation is a common cause. This leads
to discoloration at the margin. The problem can be minimized by using a rubber dam
during cementation.

Inappropriate Cement Color

• Dual-cure cement can change from colorless to yellow/orange over time. Light cure
cement is recommended for thin aesthetic veneers to avoid this issue, although this
happens over a longer period than what was described in your practice question.

Marginal Caries
• Though possible, caries formation at the veneer margin is less likely within a short
period (e.g., eight weeks) since cementation.

Veneer Fracture
• Inappropriate preparation design, inadequate occlusal thickness, and rough margins
could lead to veneer fractures, but this would not cause discoloration specifically at the
 Fractures in veneer
Incisal Edge
• Fractures at the incisal edge of the veneer are common, especially if this area is
subjected to excessive biting forces or if the preparation design is inadequate,
leaving the edge too thin.

Margin Areas
• Fractures can occur at the margins if there are sharp line angles, rough margins, or
if the veneer was not bonded properly during cementation.

Surface of the Veneer

• In some cases, surface fractures can occur due to trauma or improper handling
during the veneer placement process.

Middle Third
• Although less common, fractures can also develop in the middle third of the
veneer, often associated with excessive loading or poor distribution of biting forces
 Maryland bridge / resin bonded bridge
• Two wings
• Replace one missing tooth  2 wings lingually bonded to adjacent
teeth
• Conservative then conventional bridge (less removal of tooth
structure than that )
• Debonding is main problem with this
Shade selection
 Munsell color system
1. Hue
• Color family
• Wht color it is
• Red blue etc

2. chroma
• Saturation or intensity of color
• dull greyish blue or more vibrant / pure blue
• How close or far it is from centre of color value

3. Value
• Lightness or darkness of color
• More important for crown shade selection
• 0  black
 Effect of light
Metamerism
• Colors appears different under different lights
• During crown matching this can happen
• 5500k (ideal value)  refers to color temp (low temp redish hue) (high temp
bluiish hue)
• Color rending index  100% means get best color extraction from object

Fluoresence
• Object emits visible light when exposed to UV light
• Composite filling  can be identified by this
• Material with better fluroscence ability  match more to tooth color

Opalescence
• Light effect of a translucent material
• Appear blue  in reflected light
• Appear red-orange  in trnasmitted light
 Order of shade selection
1. Value
• Middle third of crown

2. Chroma
• Gingival third

3. Hue
• Incisal third
• Least important of all
 Characterization
• Reproducing natural defects on crown

1. Staining
• Adding colour stains to crown
• Loss of fluroscence
• Increase metamerism
• Decrease value  more darker

2. Glazing
• Surface layers of procelain melt slightly coalescing particle & filling in defects
• Treating the surface texture rather than color

• You can always make color darker  by decreasing value

• But u can not make it light  not reversible
 Crown delivery
1. Esthetics  shade matching

2. Proximal contacts
• Both on cast & mouth
• Open space / no contact send back to lab
• Heavy / no space  adjust is before moving onn (it will not seat)

3. Margin

4. Fit

5. Retention & resitance form

6. Occlusion

7. Contour
Cements / luting
in crown
 Zinc oxide eugenol
• Soothes pulp
• Temporary cement
• Eugenol  inhibits polymerization in resin
• Eg :- temp bond
 Zinc phosphate
• Considered gold standerd
• Phosphoric acid  irritates pulp (post cementation pulpal
sensitivity)
• Powder  zinc-oxide (base)
• Liquid  phosphoric acid
• Does not chemically bond to tooth

• Mixed on chilled glass slab  due to exothermic reaction

 Zinc poly-carbooxylate
• Powder
• Liquid

• Weak chelation bond to tooth  calcium mineral of tooth

• Minimal pulpal irritation
 Glass ionomer cement
• ACID-BASE REACTION

• Adheres to dentine & enamel

• Weak chelation bond  to tooth
• Release fluoride
• Soak fluoride from water, toothpaste  reservoir
Crown
• PFM , GOLD, ZIRCONIA
 Resin modified glass ionomer
• High strength
• Low solubility than  gic
• Not to be used with all ceramic crown  expansion from
water absorption
• Exception  zirconia
Crown
• PFM , GOLD, ZIRCONIA
 Resin cement
• Compressive strength
• Bonds to dentine
Cure
• Light  more color stable then both (good for anterior
veneers)
• Chemical
• Dual  emax

Crowns
• Lithium dissilicate  emax
• Feldspastic procelain  veneers
 Crowns & cement
• Zirconia  ceramic but no silicate (rmgi , gi)
• Metal  gold & pfm (rmgi , gi)
• Lithium dissilicate  emax (DUAL CURE)
• Feldspastic procelain  veneers (LIGHT CURE RESIN
CEMENT)
 Steps for veneers
Tooth side Crown side
Etch  phosphoric acid Etch  hydrofloric acid
• Not etch dentine only enamel • For crown

Primer / bond Coupling agent  silane

• Inside of crown
• Improve bond strength to the
crown

Resin cement
• Light cured to avoid any
discoloration
Lab process
 Reproduction / replica
Negative Positive
• Negative reproduction of oral • Exact replica of the oral cvity or
cvity or teeth from which we teeth
make a positive reproduction • Eg :- cast, die
• Eg:- mould, impression
• After impression & master cast we make die

Die Positive reproduction of preparation

a) Ditching  exposes the margin of prep (scraping stone
below margin)
b) Die spacer  painted over cast prep tooth (allows room
for cement space)

1. Waxing
• Positive of the object u want to make
• Wax build up internal stress as it is manipulated which relaxes
with time  causing distortion of shape & contour
• Eg:- wax crown
2. Spruing
• Making a path with wax fro metal to go into the prosthesis as it is
casted
• Wax sprues  attached to crown at area od thickest bulk (cusp or
edge)

3. Investing
• Making negative
• Cover wax & spru with inveting material
• Gypsum bonded investment  gold crown
• Phosphate bonded  PFM crown
• Silica bonded  base metal

4. Burnout
5. Casting
• Melt metal into investment

6. Recovery
• Breaking open investment  retrieve cast framework

7. Quenching
• Put very hot cast metal into cold water
• Makes it more malleable to work on it
• Finishing, polishing, delivery
 Porosity issues during lab process
• Porcelain  inadequate condensation of procelain

• Acrylic  too fast heating

• Shrinkage porosity of metal  too thin sprue  prevent

adequte flow of metal into investment

• Back-pressure porosity of metal  too short sprue 

prevents venting of gas = gas still in that area – no
mterial flow there
Post & core
Post
• Portion which goes into the root

Core
• On the coronal portion
• Form the core of the crown
• Function  retain / support crown

Retention of post
• More length = more retention
• More width = no aeefect on retention
Post Width
• Not more then 1/3 of root width (proportionist)
• Surrounded by Atleast 1mm of sound dentine (preservationist)
• Restriction of post width to conserve the tooth structure
(conservationist)

Ferrule
• Ferrule should be circumfential  band of dentine around the tooth
• 1.5 mm – 2mm  height atleast
• 1 mm  width atleast

Advantages
• Anti rotation effect
• Hugging effect
• Gp left  3-5mm at apical portion
Implant
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Occlusion

Articulator Records

● Representation of the maxilla, mandible, and TMJ ● Facebow record: captures the relationship of the maxilla to the skull and mandible to
● Can be non-adjustable, semi-adjustable, or fully-adjustable the rotational center of TMJ
● Interocclusal record: captures the relationship between maxillary and mandibular teeth
Centric relation Maximum intercuspation

● Position in which the condyles are the most anterior and superior against the ● Position in which the teeth are fully interdigitated, also known as centric occlusion
articular eminence ● Not dependent on the condyles
● Not dependent on the teeth

Condylar guidance Incisal guidance

● Type of mandibular guidance ● Type of natural occlusion

● During protrusion, the mandible is guided by the condyle sliding against the ● During protrusion, the incisal edges of mandibular anterior teeth are guided by the
articular eminence lingual surfaces of maxillary anterior teeth
● Component of anterior guidance
Canine guidance Group function

● Type of natural occlusion ● Type of natural occlusion

● During lateral movements, the upper and lower canines contact on the working side, ● During lateral movements, multiple upper and lower posterior teeth contact on
and all posterior teeth disclude on the non-working side the working side, and all posterior teeth disclude on the non-working side
● Component of anterior guidance

Balanced occlusion Lingualized occlusion

● Type of denture occlusion ● Type of denture occlusion

● In centric and eccentric movements, there are anterior and bilateral posterior ● Lingual cusps of maxillary posteriors are in contact with mandibular posterior
contacts (tripodization) central fossa or marginal ridges
● Avoid anterior (canine and incisal) guidance for denture occlusion

Vertical dimension

VDO = vertical dimension of occlusion Excessive VDO Insufficient VDO

● Distance between two selected points (usually a dot on the patient’s nose and a dot on the
● Mouth appears too full ●
Lower face appears collapsed
patient’s chin) in which the teeth are in MIP
● Lip incompetence

● Angular cheilitis
VDR = vertical dimension of rest
● Difficulty with speech, swallowing, ● Fatigue
when chewing
● Position of the mandible in which the muscles are in a relaxed, equilibrium state
chewing
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Occlusion

Determinants of occlusion

1. Anterior guidance (combines incisal and canine guidance)

2. Posterior guidance
3. Cuspal anatomy
4. Tooth arrangements (compensating curves)
5. Orientation of occlusal plane

Curve of Spee: anteroposterior curve, teeth are inclined mesially as

you move distally Curve of Wilson: mesiolingual curve, teeth are

inclined lingually as you move distally Mutual protection:

● Anterior teeth protect the posterior teeth
○ During protrusion and lateral movements, the anterior teeth
disclude the posterior teeth
● Posterior teeth protect the anterior teeth
○ Protect from bite forces, due to sturdier roots and large occlusal
surfaces
Complete Dentures

Maxillary edentulous anatomy Mandibular edentulous anatomy

CC BY 4.0
Stress-bearing areas:
Stress-bearing areas:
● Primary = palate, residual ridge
● Primary = buccal shelf
● Secondary = maxillary tuberosity, rugae
● Secondary = residual ridge
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Complete Dentures

Pre-prosthetic surgery & treatment

● Frenectomy: incision of frenum that is attached too high

● Hypermobile ridge: tissue conditioner, electrosurgery, laser surgery
● Epulis fissuratum: hyperplastic tissue from ill-fitting denture → adjust denture, tissue conditioner, removal of tissue
● Fibrous tuberosity: interferes with interarch space → removal
● Inflammatory papillary hyperplasia: irritation and poor hygiene with dentures, candidiasis → hygiene measures, tissue conditioner, antifungals
● Alveoloplasty: surgically reshape and smooth the alveolar bone
● Tori removal: necessary to remove undercuts
● Vestibuloplasty: repositioning the vestibule lower to increase height of alveolar process

Favorable characteristics Unfavorable characteristics

● Support: resistance to vertical displacement toward the denture-bearing area ● Occlusal interferences
○ Upper arch: palate, alveolar ridge, denture base ● Thick, ropy saliva
○ Lower arch: buccal shelf, retromolar pad, denture base ● Overextension
● Stability: resistance to lateral displacement ○ Denture flanges too long → sore spots, ulcers
○ Ridge height, vestibule depth, denture flange ○ Denture too far back → dislodged by occlusion
● Retention: resistance to vertical displacement away from denture-bearing area ● Underextension
○ Peripheral seal of dentures ○ Denture flanges too short → no retention
○ Thin, watery saliva ● Triangular-shaped alveolar ridges
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Complete Dentures

Combination syndrome

Specific pattern of bone

resorption in the anterior
edentulous maxilla when it
opposes the mandibular anterior
teeth:

1. Overgrowth of
maxillary tuberosities

2. Papillary hyperplasia
of hard palate

3. Extrusion of lower
anterior teeth

4. Loss of bone under

partial denture bases

Removable Partial Dentures

Kennedy classification Applegate’s rules

Class I: bilateral distal extension 1. Extract first, then Kennedy classification

2. Do not consider missing 3rd molars in classification if replacement is not planned

3. Consider 3rd molars in classification only if using as abutment

Class II: unilateral distal extension
4. Do not consider missing 2nd molars in classification if replacement is not planned

5. Classification is determined by the most posterior edentulous area

Class III: unilateral 6. All other edentulous areas are considered “modifications”
bounded
edentulous space 7. Number of modifications matters, not the extent

8. Class IV cannot have modifications

Class IV: bilateral

bounded
edentulous space
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Removable Partial Dentures

Major connectors Rests & component diagram

Function to provide rigidity and unite components of the partial denture Rest seats are
prepared into
Maxillary: the surfaces of
● Complete palatal plate abutment teeth
● Horseshoe to support a rest
● Palatal strap
● Occlusal:
Mandibular: for posterior
● Lingual bar (lingual vestibule >/= 7 mm) abutment
● Lingual plate (lingual vestibule < 7 mm) teeth
● Labial bar ● Cingulum:
for anterior
abutment
teeth
● Incisal:
indirect
retainer
Proximal plates & guide planes Precision attachments

Proximal plate: plate that Intracoro

contacts the proximal surface nal
of abutment teeth attachme
nts that
Guide plane: the vertical replace
surfaces of abutment teeth are the
made parallel, to contact denture
proximal plates, and to provide a rests and
path of insertion/removal for RPD clasps

● Male
portion
fits into
female
portion
● Used
for
estheti
c
cases,
show
less
metal
Retainers
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Clasps

Retentive clasps
● Provides retention
● Contacts tooth below height of contour
● Tip
engages in
undercut to
resist

Dislodgem
ent of RPD

RPI = Rest,
Proximal
plate, I bar
● Rest typically placed
on mesial of abutment
tooth

Reciprocal clasps
● Provides stability
(bracing)
● Contacts tooth above
height of contour
● Braces abutment
tooth to prevent
torque
from retentive clasp
Crowns

Types of reduction Margin types

● Occlusal reduction ● Featheredge: uncommon

● Functional cusp bevel ○ not enough clearance for materials, cannot visualize
○ Upper teeth: lingual cusp ● Light chamfer: 0.3-0.5 mm
○ Lower teeth: buccal cusp ● Heavy chamfer: 1-1.5 mm
● Axial reduction ● Shoulder: 1-1.5 mm
○ Mesial, distal, facial, lingual
● Margin/finish line
Rule of ferrule Posts

● Refers to the circumferential band ● Retain a core

of tooth structure in crown ● Strengthens bond between coronal buildup material and tooth
preparations ● Used in situations where there is insufficient tooth structure
● The minimum amount of ● Ideally the post diameter is ⅓ the root diameter, with 1 mm of dentin circumferentially
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Crowns

Principles of preparation

1. Biologic principles 2. Mechanical

principles 3. Esthetic
principles
● Conserve as much tooth structure as ● Retention form: preventing removal of ● Subgingival
margins
possible crown along
long axis of tooth ● Ideal
porcelain thickness 1.0 mm
● Supragingival margins ● Resistance form: preventing removal ● Porcelain
occlusion
● Good occlusion of crown along oblique axes ● Minimize
metal display
● Good preparation → water spray, sharp ● 6-10 degree taper
burs, light pressure ● Length/height
provides retention
● Avoid overcontouring ● Minimum 0.4 height-to-base ratio
● Avoid tooth fracture

● Reduction: tooth structure removed

during preparation
● Clearance: space
between
preparation and
opposing tooth
Shade components Provisionals Delivery steps

● Hue: color family Methods: 1. Shade

● Chroma: saturation ● Direct: made in patient’s mouth
2. Internal fit
● Value: lightness or darkness ● Indirect: made outside of the
● Metamerism: color looks different depending on lighting mouth, usually in lab 3. Proximal contacts
● Fluorescence: emits visible light when exposed to UV light 4. Margins
● Opalescence: appears blue in reflected light, red in transmitted light Materials:
5. Resistance and retention form
● Polymethyl methacrylate
● Polyethyl methacrylate 6. Occlusion
● Bis-acryl composite 7. Contour
8. Cement
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Fixed Partial Dentures

Components Pontics

● Abutment: bridge attaches to these teeth Hygienic pontic Conical pontic

● Retainer: crown that goes on ● Posterior location ● Anterior or posterior location
abutment tooth ● Cleansable, unesthetic ● Cleansable, unesthetic
● Pontic: “floating” tooth between ● Good for thin ridge
abutments
● Connector: connects retainers to
pontic
○ Rigid: cast or soldered into one
piece Saddle pontic Ovate pontic
○ Non-rigid: multiple pieces, used ● Anterior or posterior location ● Anterior location
with multiple paths of insertion ● Uncleansable, esthetic ● Cleansable, esthetic
● Cantilever: one retainer with 1+ pontics
● Pontic placed in
healing socket to

Ante’s law: PDL surface area of

form depression
abutment teeth should be >/= PDL
surface area of missing teeth
Cements

Cement Type Crown type Indications

Glass ionomer Metal, PFM Medium strength, adhesive, fluoride release, good for high caries risk patients

Resin modified glass ionomer Metal, PFM, zirconia Medium strength but stronger than glass ionomer, adhesive, fluoride release, low
solubility, good esthetics, versatile cement
Conventional resin All-ceramic, some zirconia High strength, adhesive, low solubility, used when a strong bond is desired, best
esthetics, technique sensitive
Self adhesive resin Metal, PFM, zirconia, all-ceramic High strength, adhesive, low solubility, good esthetics, no etching or priming required

Zinc phosphate Metal, PFM, zirconia High strength, higher solubility, non-adhesive, known for pulpal irritation

Impressions

Aqueous hydrocolloids Non-aqueous elastomers

Agar Alginate Polysulfide rubber Condensation silicone

● Reversible ● Irreversible set ● Produces water as byproduct ● Produces alcohol as byproduct
● Changes between “sol” and “gel” form ● Relatively inaccurate ● (syneresis) ● Undergoes shrinkage
● Highly accurate ● Should be poured within 10 ● Hydrophobic Addition silicone (polyvinyl siloxane)
minutes Polyether ● No byproducts
● Decrease setting time with ● Stiff material ● Best in terms of fine detail,
hotter or less water elastic
● Increase setting time with colder ● Hydrophilic recovery, dimensional stability
or more water ● Takes in water (imbibition) ● Inhibited by sulfur (latex gloves
Orthodontics
 Growth & development
Growth
• Antaomical phenomenon
• Refers to increase in size (hypertrophy), number (hyperplsia) or weight
• Quantatative

Development
• Physiological & behavioral phenomenon
• Refered to as increase to complexity
• Qualitative

Pattern
• Proportion
Cephalocaudal growth gradient
• Head and body proportion
• Body parts closer to cranium grows faster
• Body parts away from cranium grows more later
• Axis of increased growth from head towards feet

1. 2 months in utro
• 50-50% head to body porportion
• Cranium is large in relative to face

2. 3-months in utro
• Trunks and limbs grows more than head
• Head size decreases to 30%

3. At birth
• Head 25% of body

4. Adult life
Scammons curve

• Based on principle of differential growth  tissue growing at

different rate at different time
• Shows growth pattern of 4 major tissue systmes of body
• Development of maxilla & mandible lies between neural &
general
1. Lymphoid
• Proliferate rapidly in late childhood and reach at 200% of adult size (by age 10)
• By the age of 18 yrs it goes to 100% of adult size (regresses)

2. Neural
• Completely grows by age of 6-7yrs

3. General
• Muscle, bone & viscera
• Follow S-shaped curve
• Rapid growth which occurs up to 2-3 yrs
• Slow phase/steady growth  middle childhood 3-10yrs
• Rapid phase  puberty/adolescent 10th year
• Steady growth/terminate  18-20 yrs

4. Genital
• Show negligible growth until puberty
5. Maxilla
• Follows closer to neural curve

6. Mandible
• Closer to general curve

• Maxilla develops earlier then mandibile

 Distance & velocity curves
Distance curve
• Tracks actual Height each year
• Grows with time does not decrease

Velocity curve
• Tracks change in height
• Speed of height increasing per year
• Puberty  speeds up

For girls
• Mature early
• 12 yrs  peak growth
For boys
• Later
 Growth timing
1. Chronological age
• Not good indicator of maturity

2. Dental age
• Dental development
• Poor inidcator of maturity

3. Skeletal age
• Measured by  CVM staging, hand-wrist xray
• Better indicator of maturity

4. Biological age
• Best indicator
 Area of growth
Growth sites
• Where growth happens
• Only grows on specific site
• Cannot be a growth center
• Eg:- mandibular condyle, maxillary sutures

Growth center
• Ability to control its growth
• Can independently happen  without any help
• Genetic controlled & not not influnced by environmental factors (functional
appliances)
• Eg :- synchondrosis

• Growth centre can become growth site but growth site can not become
Concepts of growth
1. Endochondreal ossification
• Cartilage growth
• For bone to be made the cartilage is needed
• More under direct genetic control
• Eg :- mandibular condyle & cranial base

Zones
• Zone 1  zone of resting cartilage (chondrocytes cells here)
• Zone 2  zone of proliferaltion (hyperplasia here)
• Zone 3  zone of maturation (hypertrophy here)
• Zone 4  calcified cartilage (mineral deposition here)
• Zone 5  ossification  empty spaces penetrated by vessels
(osteblast here)
2. Intramembranous ossification
• Ecm directly secreted into C.T and then ossify
• No cartilage needed
• Increase in diameter
• Influenced more by environmental factors
• Eg :- cranial vault, maxilla & majority portion of mandible
Theories of growth
• Tell us where the growth control lies
6 theories
1. Genetic
2. Bone remodeling
3. Sichers  sutural theory
4. Scotts  cartilagnous theory
5. Moss functional matrix theory
6. Petrovics servosystem theory

Growth site
• Only grows on specific site
• Cannot be a growth center
• Eg:- mandibular condyle, maxillary sutures
Growth centre
• Can grow anywhere
• Genetic controlled & not not influnced by environmental factors (functional appliances)
• Can be growth site
• Eg:-
1. Bone/suture theory
• Genetic control lies in the bone (sutures  maxilla & cranial vault)
Why not accepeted
• When sutures were transplanted from one place to another there there was no growth
• And the growth should not be influenced by environmental factor  but was influenced by the
functional appliances
• Sutures – growth sites
• Eg:- in proganthic maxilla of 10yr old patient we give head gear (FA) to control/stop the growth

2. cartilagenous theory
• Genetic control lies in cartilage while bone grows passively
• Cartilage  condylar, nasal septum, synchondrosis
• 50% accepted 50% not accepted
• Synchondrosis  growth centers
• Nasal septum transplanted to abdomen pouch = sometimes growth happen sometime not, then to
prove it the nasal septum was damaged at the nose = maxillary growth affected, hence this theroy
as some potential
• Condylar cartilage transplanted = no growth hence it is growth site
Why not accepeted
• Only synchondrosis  growth centre
• Condylar  site
3. functional matrix theory / soft tissue theory
• Not genetic control in bone or cartilage the control is in soft tissue while
bone& cartilage grows passively
• Mostly accepted

• Eg :- in cranial vault the growth is dictated by the brain  it sends signals

for apposition & remodeling to happen

• Eg :- disruption in reabsorption of CSF  if accumulation = small brain &

big vault

• Eg :- big eyeball = big orbit

• Eg:- bigger the nasal & oral cavity = more they are gonna push maxilla &
mandible downward & forward
• Increased Functional growth = increased soft tissue growth = increased
 Development of
craniofacial complex
1. Formation of bone
• Begins in embryo
By two ways
• Intramembranous ossification  in membranes of C.T
• Endochondreal ossification  with in cartilage

2. Growth of bone
• Appositional growth  adding layers over previously formed

3. Growth of cartilage
• Appositional growth  adding new matrix to surface
• Interstitial growth  mitotic division & deposition of matrix (does not happen in
bone)

4. Growth of alveolar process

• Exists only to support teeth
• Teeth not erupted  no alveolar process formed
Craniofacial complex is divided into 4 parts
1. Cranial vault
2. Cranial base
3. Naso-maxillary complex
4. Mandible
1. Cranial vault
• Skull flat bones are seperated by loss C.T = fontanelles
• Fontanelles  allow the large head to pass through birth canal by squeezing
• Fontanelles  are lined by periosteum on bony side

• Periosteum (membrane which lines bone surface) contains osteoblasts = growth of cranial
vault post-natally

Type of ossification
• Intramembranous ossification

Growth post-natally
1. Surface apposition
• Ecm secreted into the periosteum & is mineralized = bone
• Primary mechanism
2. Remodeling
• Occurs due to growth of brain  sends signals to start remodeling
• Bone resorption from internal surface & deposition on outer surface
• Deficient growth  microcephaly
2. cranial base
• Ethimoid + sphenoid + occipital bone
• Synchondrosis  bands of cartilage (histologically looks like 2-
sided epiphyseal plate)
• Synchondrosis is  growth centre

Types of synchondrosis
1. Inter-sphenoidal
• Fuses & closes first  inactive by age 3
• Ossifies before birth

2. Spheno-ethmoidal
• Ossifies by  7 yrs
• Contributes to  anterior cranial base growth
3. Spheno-occipital
• Inactive later  18-23yr
• Responsible for growth of  posterior cranial base

4. Intra occipital
• Not imp
• Closes by age  4

Type of ossicfication
• Endochondreal ossifcation
3. Maxilla

Pre-natally
• Develops from 1st pharygeal arch (mandibular arch)
• Form fronto-nasal process (by intramembranous ossification) ( 1st structure to
develop)
Fronto-nasal develops into 3 processes
1. Median nasal process  nose & philtrum
2. Lateral nasal process  lateral part of nose
3. Maxillary process  lateral parts of upper lip & bulk of cheek

Post-natal growth
4. Displacement
• Forward & downward push of maxilla by anterior cranial base & soft tissues
(nose & lips)
• From time of birth to 6 yrs
2. Apposition
• At sutures (two sutures which connect maxilla to cranium &
cranial base) bone deposition
• Palate, tuberosity, alveolar ridges

1. Remodelling
• Anterior surface  resorptive
• Posterior surface  depositary
Growth type
• Intramembranous ossification
Entire anterior area of maxilla is resorptive surface except small part
around anterior nasal spine (there deposition takes place)

The succedaneous teeth

• Are the permanent teeth that replace the deciduous teeth
Non-succedaneous teeth
• Permanent molars are not succedaneous teeth because they do not
replace any primary teeth

1. How do permanent molars accommodate in the jaw

• Continuous deposition of bone on the posterior surface = bone
formation = space for permanent molars develops

Growth of palate  from maxillary process

1. Primary palate
• Deposition of bone in tuberosity region increase in height &
elongation of maxillary arch in post direction
4. Mandible
• Develops from 1st baranchial arch  2 mandibular processes
(which fuses together to from lower lips & jaw) & meckels
cartilage

• On 8th week of intrauterine life there is condylar cartilage which is

separated from mandible
• On 4th month this gets incorporated
• At the time of birth the quantity of cartilage is decreased
Meckel's cartilage
• Guides the development of mandible ( but no direct role in
development )
• Provides framework for growth
• Fate  incus & malleus & spheno-mandibular ligament
Site of intramembranous ossification  point where inferior
nerve divides into mental & incisive nerve (lateral to Meckel's
cartilage), first anteriorly then posteriorly
• Upward & posterior ossification
• No apposition in post-natal growth of mandible as there is no
suture
• Apposition at  post ramus, coronoid, chin, alveolar ridge
Lengthening of ramus by remodelling & endochondral
ossification (growth over condylar cartilage)
• Anterior surface of ramus  resorption
• Posterior surface of ramus  deposition
Types of growth
• Endochonreal & intramembranous ossification
Mandible
• Major site of growth  condylar cartilage
• Resorption  along ant surface of ramus
• Apposition  along post surface of ramus

Timeline of growth
• infancy  ramus is located where primary first molar will erupt
• Progressive posterior remodelling  space for primary 2nd molar
• If remodelling ceases  no enough space for 3rd molar =
impaction
• At age 6  greatest increase in size of mandible  distal to first
molar
• In maxilla for 2 & 3rd molar space  deposition
• In mandible  resorption

• Condylar growth = molar eruption

Counter closwise growth
• Decreased Lower anterior facial height
• Deep bite
• Codylar growth more than molar eruption
Clockwise growth
• Increased Lower anterior facial height
• Open bite
• Codylar growth less than molar eruption
Planes of growth
1. Transverse plane
• Width
• Age  10 -12
• 1st to stop

2. Antero-posterior / sagital plane

• Length
• Age  14 -16
• 2nd to stop

3. Vertical
• Height
• Age  18 – 20
Cranio-facial
anomalies
 Five stages of embryonic cranio-facial
development
1. Neural crest problems
a) Germ layer formation  day 17 in utro  Fetal alcohol syndrome (FAS)

b) Neural crest formation  day 18 – 23  anencephaly

c) Neural cells migration  19 – 28  hemifacial micro somia, treacher collin

syndrome , mandibulo-facial dystosis

2. Lack of fusion
a) Organ system froamtion  day day 28-38 week 4-5  cleft lip

b) Primary palate  week 6  cleft palate

3. Suture problems

a) Final differentiation of tissue  day 50 – birth  crouzans

syndrome, craniosyntosis, achondroplasia
Syndrome
• Pattern of anomalies which occur in a predictable pattern due to
single etiology
• Genetic
• Eg :- Downs syndrome

Sequence
• Group of anomalies that stem from a single major anomalies that
alters the development of surroning structure
• One thing leads to other
• Eg :- pierre robin sequence (under developed mandible)
Fetal alcohol
syndrome
• Occurs in child whose mother consumed alcohol during 1st trimester of
pregnancy (day 17-20 days)
• Irreversible defects
• No safe level of alcohol during pregnancy
• Ethanol  deficiency of midline tissue of neural plate (germ layer
formation & initial organization of structure)

• It is a severe form of condition referred to as fetal alcohol spectrum disorders

(fasd)

Triad of
• Growth retardation
• Facial abnormalities
• CNS disfunction

Treatment
Features
• Flat nasal bridge
• Railroad track ears
• Thin upper lip
• Smooth & flat philtrum
• Epicanthal folds
• Short pelperable fissure
• Short nose
• Micrognathia
• Small teeth
• Flat midface
• Short stature
• Mental retardation
• Behavioural disturbances
• Congenital heart defect  VENTRICULAR SEPTAL DEFEACT
• Microcephaly
 Treacher collin
syndrome/mandibul
ofacial dysostosis
• Genetic mutation
• Generalized loss of mesenchymal tissue due to TCOF1
gene
• Happens due to defect in neural crest cell migration
• Thalidomide & isotretinoin (also known as accutane) 
(anti-acne drug)
• Affects development of facial bones & tissue

• Under-developed mandible
Treatment
• Surgical treatment to advance midface
Features
• Autosomal dominant  affects both gender
• External ear malformed (sometimes middle & inner ear also )
• Hypoplasia of facial bone  malar & mandible  Agenesis of
mandible
• Bird like / fish like appearance
• Macrostomia
• High palate
• Malocclusion
• Coloboma of eyelid (some structure of eyelid not developed)
• Auditory ossicles absent
• Cochlea & vestibular appartus deficient
• Cleft palate  35%
• Microtia  small ears
• Downward slanting eyes
Craniofacial
microsomia/
hemifacial
microsomia
• Characterized by deficient development of lateral face,
typically external ear deformed
• Both the ramus & associated soft tissue deficient or
missing
• Affecting nural crest cells taking longest migration path 
affecting lateral & lower areas of faces due (no midline
defects)
• One side normal development & on side deficient
development
Causes
• Problem in neural crest cells (loss of neural crest cells
during migration)
• Neural crest cells which develop 1st pharygngeal arch

Features
• Facial assymetry
• Deformed ear  microtia
• Defects in great vessels  teralogy of fallot  aorta,
pulmonary arter & arotic arch
Downs syndrome
/ trisomy 21
• Extra chromosome  21
• Midface deficiency
• Upslanted pelpebral fissue  upwards eye
• No increased caries risk
• Increased periodontal risk
• Relative macroglossia  in relation to maxilla
• Developmental delays & physical disabilities synd
Celft lip & palate
Developemnt of face
• Formation of face starts at week 4 after formation of facial
processes/prominances at the head part of embryo
• Frontal process  at week 4
• Below frontal process is  stomodeum (future mouth), cardiac buldge & 5
pairs of pharygeal arches (lateral to stomodeum & above cardia buldge)
• At end of week 4 two localized epithelial thickness appear on lateral sides of
frontal prominences
• Lateral epithelial thickness are called  nasal placodes
• Mandibular arch gives  maxillary process & part left behind becomes
mandibular process
• On 5th week tissue aroun placodes rapidly proliferates & increases in
thickness  converting placodes to  nasal pits (these eventually becomes
nostrils)
• Mesial bulge at mesial side of nasal pit  mesial nasal process
• On lateral side  lateral nasal process
• Around 7-8th week mesial nasal process of both sides fuse to make  middle
• Medial nasal process also fuses with maxillary process to make
lateral side of lips
• Development of palate
1. Primary palate
2. Seocndary palate
• Primary + secondary = definitive palate

Primary palate
• Also called premaxilla
• Formed from fusion of two medial nasal process
• Maxillary incisors
Secondary palate
• Formed from maxillary processes
• Two maxillary process form  palatine shelves
• Palatine shelves fuse together to form  palate
Cleft lip
• 1:800 incidence
• Common in males
• Formation of lip  week 4th - 6th

Etiology
• Defect in fusion between medial nasal process & maxillary process

Types
• Complete  lip with nostril
• Incomplete  limited to lip only

• If cleft lip on middle  defect in fusion between 2 medial nasal process

• If cleft lip on lateral  defective fusion of medial nasal process with
maxillary process
Cleft palate
• Defect in hard or soft or both
• Communication between oral & nasal cavity
• Formation  6 – 8 week

Etiology
• Failure of fusion between palatal shelves & primary palate
Types
• Complete  entire pale  hard + soft (palatine shelves + primary
palate)
• Incomplete  posterior palate (palatine shelves not fused)

•
Diagnosis
• Ultrasonography
• 3d ultrasonography
Causes
a) Heridetary
b) Pregnency
• Smoking
• Folic acid deficinecy
• Aspirin
• Dilantin
• 6-mercaptopurine  cleft palate only
 Management
Stage 1
• From birth to 18 months
Stage 2
• 18 months to fift year of life
Stage three
• During mixed dentition time
• 6-11
Stage 4
• During permanent dention
• 12-18 yrs
 Classification
• Davison & ritchi
1. Group 1
• Pre-alveolar
• Cleft only involving lip
• Unilateral
• Bilateral
• Madium
2. Group 2
• Post alveolar clefts
• Hard & soft palate
Pierre-robin
sequence
• Micrognathia  small mandible (primary problem )
• Glossoptosis  backward displacement of tongue
• Cleft palate  due to tongue backward = no fusion b/w
shelves
• Breathing & feeding problem

Like a sequence
• Micrognathia  glossoptosis  cleft palate  breathing &
eating probs
Craniosynostosis
syndromes
• Group of craniofacial malformation
• Early closure of suture
• Syndromic craniosynostoses are often sporadic and are the result of de
novo autosomal dominant mutations involving  fibroblast growth
factor receptors (FGFRs) & TWIST genes

Syndromes most frequently associated with craniosynostosis include

• Apert  fusion of fingers & toes (Syndactyly)+ crouzans features
• Crouzon
• Pfeiffer
• Carpenter
• Saethre-Chotzen

Treatment
• Surgical relasing the prematuraturly fused sutures 6-9 months of age
Crouzans syndorme
• Linked with mutation of fibroblast growth factor receptor
2 on chromosome 10
• Autosomal dominant
• Arises because of prenatal fusion of posterior & superior suture of
maxilla along the wall of orbit

Causes
• Environemental  vit-D excess
• Genetic
Features
• Craniosyntosis
• Brachycephalic  short skull
• Mid face deficiency  Midface / maxilla underdeveloped
• Frontal bossing
• Hypertelorism  widely separated eyes
• Proptosis  bulging eyes out of socket
• Mandible fully developed  class 3
• Distorted cranial vault  heavy accumulation of csf
• Mental retardation
• Delayed eruption
• Crowding
• Cleft palate

Treatment
• Surgery to release sutures coupled with distraction osteogenesis to advance
Apert syndorme
• Autosomal dominant
• Similar to crouzans
• Also called  acrocephalosyndactyly

Features
• Craniosyntosis
• Acrocephalic  tall skull
• Byzantine arch  narrow palate & high vault
• Syndactyly  fusion of fingers & toes
• Mid face deficiency  Midface / maxilla underdeveloped
• Frontal bossing
• Hypertelorism  widely separated eyes
• Proptosis  bulging eyes out of socket
Hurler & Hunter
syndrome
• Also called  mucopolysaccharidosis
• Build up of glycosaminoglycans (GAG) due to enzyme
deficiency

Hurler
• Deficiency of  alpha-L-iduronidase
• Autosomal resessive
• Death in first decade of life

Hunter
• Mutation in  iduronate-2-sulfatase
• X - linked
• Death in second decade
 Signs & symptoms
Hunter syndrome Hurler syndorme
• Broad nose • Frontal bossing
• Enlarged tongue • Depressed nasal bridge
• Enlarged head • Hyper-telorism
• Large & rounded cheeks • Thick tongue
• Thick lips • Gingival hyperplasia
• Hearing loss • Gaps b/w teeth
• Compressed & damaged spinal • Short neck
cord • Corneal clouding
• Stiff joints • Excessive hear growth
• Heart valve issues • Reily body inculsions
• Restricted growth
Development of
occlusion
1. Gum pad stage
2. Primary dentition
3. Mixed dentition
4. Permanent dentition
Gum pad stage
• From brith to 6 months
• End with eruption of 1st primary tooth
Primary dentition
• From 6 months – 6 yrs.
• Till the 1st permanent tooth erupts

Young children have

• minimal overbite
• Minimal overjet
• Sometime  edge to edge
• Spacing is a normal characteristic of primary dentition but its most
noticeable

1. Primate space
• It’s a feature of primary dentition
• Physiological space present between teeth
• Most noticeable space
• Present between b & c in upper arch
• Between c & d in lower arch
• Best utilized in lower
• Lost up till the age of 6

2. Developmental spacing / interdental spaces

• Present between incisors
3. Leeway space
• Difference between the sum of the mesiodistal crown widths of
the primary canines and molars & the permanent canines and
premolars
• Upper arch  1.5 for inbde
• Lower arch  2.5 for inbde (sabse zyada 2nd primary molar
se ati hai)
• By 11-12yrs this space is lost
In primary dentition
• We determine class by 2nd primary molar
• Most distal surface determine relationship
• In primary we have 3 occlusal relationships

1. Mesial step
• Distal plane of primary 2nd mandibular molar is mesial to distal
surface of maxillary molar
• Convert to Class 1 in permanent  if minimal growth
differential
• Convert to Class 3  by shifting of teeth & forward growth
of mandible (majority of time class 3)
• Mesial step  49%
2. Distal step
• Distal plane of primary 2nd mandibular molar is distal to the distal surface of
maxillary molar
• Can convert to class 2 in permanent  if minimal growth differential
• Can convert to end to end  by shifting of teeth & forward growth of mandible
• Distal step  cusp is ahead
• Never in class 1
• Distal step  14%

3. Flush terminal
• Upper & lower E are in one line
• When the distal surfaces of the upper and lower second primary molars were
in the same vertical plane in centric occlusion
• Can convert to end-to-end relation in permanent  if minimal growth
differential
• Convert to class 1  by early mesial shift
• Flus terminal  37%
Late childhood -
mixed dentition
years
• 6-12 yrs
• Where we see both decidious & permenant TEETH
• Ends with exfoliation of last primary tooth

Divided in two stages

1. 1st transitional stage

• Emergence of 1st permanent molar
• Transition of incisors
• Initiation of ugly duckling stage

a) Anterior transition
• Changes seen in inciosrs Permanent tooth buds  lingual & apical to
there primary teeth
• Incisors  erupt lingual except (upper centrals)
• Upper centrals  labial eruption (pushed by tongue)
b) Posterior transition
• Changes seen in 1st permanent molars
• Molar relationship established by guiding of terminal plane
• Mesial step
• Distal step
• Flush terminal

Teeth shift
• Early mesial shift  1st molar closes primate space by
(age 6)
• Late mesial shift  1st molar utilizes leeway space (age
12)

Differential jaw growth

2. 2nd transitional stage
• Exfoliation of primary molars & canines
• Eruptions of permanent canines & premolars
• Eruption of 2nd permanent molars
• Changes seen in canines to 2nd molar
Ugly duckling
stage
• Also know as broadbents phenomenon
• Midline diastema in maxilla  which really looks ugly (2mm or
less)
• 8-9 yrs age (11-12 yrs inbde)
• When canines are erupting  they puts pressure on roots of
lateral inscisors to tilt mesially & crown tilts distally  then lateral
puts pressure on roots of centrals causing the crown to tilt
distally = midline diastema
• This is self-correcting mal-occlusion because when canine fully
erupts puts pressure on crown of lateral & lateral puts pressure
on crown of central = correction (reverse action)
Diastema
• 98%  6 yrs old have it
• 49%  11 yrs old

Causes
• Tooth size-discrepency
• Mesiodens
• Abnormal frneum attachment
• Normal stage of development

Treatment
• Space closes  eruption of permanent canines
• Closes spontanously if  gap 2mm or less & lateral incisors in good position
If diastema due to frenum
• Align teeth first
• Frenectomy after permanent canines have erupted

Methods
• Lingual arch with finger spring
• Hawlay + finger
 Eruption of
permanent teeth
• From 12 years – death or edentulism
• When all primary teeth exfoliates
• Eruptive movements begins soon after roots start to develop

• Ideal overjet  10-20 %

• Ideal overjet  1-3mm
• Ideal occlsuion  class 1

Types
1. Pre-emergent eruption
• Tooth not out of gingiva
• Erupting tooth not yet erupted

Two process are important for this phase

• There must be resorption of bone and roots of primary teeth overlying erupting
permanent tooth
• Propulsive mechanism that must move the tooth in direction to the path that has
Primary failure of eruption
• Posterior teeth fail to erupt due to defect in propulsive
mechanism
• There is no hinderance in path of eruption, the path is clear but
propulsive mechanism is mutated/defected
• Happens due to mutation in parathyroid hormone receptor 1
gene (PTHR 1)
• They do not respond to orthodontic movement

Cleido cranial dysplasia

• Failure of teeth to erupt because of failure of bone resorption
• Heavy fibrous gingiva & multiple supernumreary teeth which also
impede noraml eruption
• Path of eruption is not clear
Dilaceration
• If eruption is mechanically blocked
2. Post-emergent phase
• Once the tooth has emerged into the mouth, it erupts rapidly unit it
reaches the occlusion level & is subjected to forces of mastication
• At that point the eruption is slowed down & it reaches occlusion level of
other teeth & is in complete function

Post emergent spurt

• Stage of relatively rapid eruption from the time of tooth first penetrates
the ginigva until it reaches the occlusal level

Juvenile occlusal equilibrium

• Teeth that are in function erupt at a rate that parallels the rate of vertical
growth of the ramus
• Eruption of teeth that are in function are in parallel to the vertical growth
of ramus
• Slow phase
Ankylosis
• Due to any trauma
• Ankylosed teeth apear to be submerged over a period as other
continue to erupt while it remains at same vertical level
• Pdl fibers distruction  tooth directly attached to bone by
cementum
• Dull sound on percussion
• More common in primary dentition
• Anterior teeth affected
• Loss of lamina dura  radio-opaque surronding
Adult occlusal equilibrium
• Pubertal growth spurt ends  tooth continue to erupt in extremely
slow rate through-out life
• Final phase in tooth eruption
• Occlusal wear of teeth compensated by the eruption
Eruption pattern
& failures
 Eruption pattern
1. Incisors
• Both maxillary & mandibular permanent buds lie lingual & apical
to primary incisors

2. Canines
• Permanent mandibular canine  erupt facially to primary mand
canine
 Failure or delayed tooth eruption
Systemic causes
• Heridetary gingival fibromatosis
• Downs syndrome
• Rickets
• Hyperthyroidism  premature exfoliation of primary teeth

Local
• Congeintal abscen
• Abnormal position of crest
• Lack of spee  crowding
• Supernumarary teeth
• Dilaceration
Ectopic eruption
 Late lower
incisor crowding
• Gets worse by  20-40s
• Due to  late mandibular gowth & lower lip pressure against it

Theory
Arch dimesion
changes
1. Inter-canine width
• From cusp tip of canine to canine
• Increase as premanent teeth erupt
• Stabilizes after eruption of canines
• Age  10 -12

2. Inter-molar width
• Central fossa – fossa for upper
• Mesial cusp tip-mesial cusp tip lower
• Increase as molars erupt & then stablizes
• upper molars erupt  divergly
• Lower  convergently
3. Arch length / depth
• Facial of incisors to the line that runs from mesial surface of 1st
molars
• Decreases during transition from mixed to permanent
• Due to closure of leeway space

4. Arch perimeter / circumferance

• Measure by tangent line from mesial of molar around the curve to
other molar
• Maxillary  increases from mixed to permanent
• Mandibular  decreases from mixed to permanent
Early stages of
development
Development of occlusion
1. Pre dentiton preiod
2. Decidious dentiton
3. Mixed dentition period
4. Permanent dention period

Late fetal development & birth

• At time of birth the mandible of child is retrogathic (in most
cases) with no prominent bony chin  to easily pass through birth
canal
• And the head is elongated (eliptical shape)
• Alveolar arches of the infant at the time of birth are called  gum
pads
 Infancy & early
childhood – the
primary dentition
year
• Growth after birth continued by increasing height & weight in steady rate

3 circumstances need special attention

1. Premature birth
• Infants weighting less then 2500gm are at greater risk of problems in post natal
period
• Infants less than 1500gm does not survive
• If they survive  then they grow normally over period of time
2. chronic illness
• Skeletal growth is a process need energy
• 90% of available energy must used for survival & activity other 10% used for growth
• Any chronic illness alter this balance, and leave less energy for growth, chronic
illness reduce the growth rate while acute illness lead to period of growth cessation
3. Nutritional status
• For growth to occur, there must be a nutritional supply
• Chronically in adequate nutrition has effect similar to chronic illness
• On other hand once a level of nutritional adequacy has been achieved, additional
nutritional intake is not stimulus to more rapid growth
Maturation of oral
function
Physiological function of oral cavity  Maturation of oral function  anterior to posterior
1. Respiration
• New born are nasal breather  mandible positioned downward & tobgue downward and
forward, this allow air to flow through pharynx to nose
• Later breathing through nose becomes physiologically possbile

2. Mastication
Juvenile chewing pattern
• Mandible moves laterally as it open the mouth in young child then comes to midline and
then closes
• This pattern develops by the time primary molars erupt
• Well established by  16 months
Adults
• Opens mouth straight and then moves laterally

3. Speech (anterior to posterior)

• First sound  bilabial sounds = M/P/B
• Later  ta/da
• Then sibilant sound  s/z (requires tongue to be not on palate but near palate)
4. Swallowing
• Occurs at last month of fetal life
• Amniotic fluid is swallowed  to activate imune system
Suckling
• Small nibbling movement of lips
• Dissappera during 1st year of life
Infantile swallow
• Active contraction of musculature of lips, tip of tongue broeught
in contact with lower lip with minimal/no posterior movement of
tongue or pharyngeal musculatre
• Disappear during 1st year of life

• Non-nutritive sucking  thumb/finger till 6 months – 2yrs

• Difference bt sucking & suckling
• Difference bt adult & juvenile chewing
• Difference bt infantile and mature swallow
• Difference between adult and infant swallow
Cervical vertebral
maturation cvm
• CVM method is used to determine the craniofacial skeletal maturational
stage of an individual at a specific time point during the growth process
• Seen on lateral cephalometric radiograph
• First vetebrae is not visible
• We can see c2, c3 & c4
• Mostly used to asscess mandibular growth

Two sets of variable are analyzed

1. Presence or absence of concavity at the lower border of the body of
C2, C3, C4
2. Shape of the body of C3 & C4 (most reliable)
• Trapezoidal  least mature
• Rectangular horizontal
• Squared
• Rectangular vertical  typically of adult
Stages  total 6
1. C-S 1 (Pre-pubertal)
• Lower borders of all vertebrae are flat
• C3-C4  trapezoidal
• Peak Mandibular growth occurs 2yrs after this stage
• Target maxilla in this stage

2. C-S 2 (Pre-pubertal)
• Concavity at lower border of  C2
• Absent concavity  C3 & C4
• C3 & C4 trapezoidal
• Peak mandibular growth  1 yrs after this stage

3. C-S 3 (Pubertal)
• Concavity  C2, C3 & C4
• C3 & C4  one can be horizontal rectangular
• Peak stage of mandibular growth
4. C-S 4 (pubertal)
• Concavities  C2, C3 & C4 present
• C3 & C4  horizontal rectangular
• Peak mandibular growth happen 1-2 yrs before this stage or ended here

5. C-S 5 (post-pubertal)
• Concavity  C2, C3 & C4
• C3 & C4  atleast one of them is squared
• Peak mandibular growth ended 1yr before this stage

6. C-S 6 (post-pubertal)
• Concavity  C2, C3 & C4
• C3 & C4  atleast 1 one of them is vertical rectangular
• Peak mandibular growth as ended atleast 2yrs before this stage
• Shows patient should go to orthoganthic surgery
Dental analysis
Primary dentition
• 6 months – 6 yrs
Mixed
• 6-12
• Most of times  canines & premolars not erupted
• We do mixed dentiton anaylysis  to predict width of canine &
premolars
Permanent
• After 12

• We use different methods to predict width of unerpted teeth to

avoid any malocclusion
How to prevent malocclusion
1. Periodic observation of the patient
• We observe and see how the eruptions are happening
2. Space maintainer
• Premature tooth loss  maintain space to prevent mesial shift
• Preventive ortho
3. Serial extraction
• Interceptive ortho
• C then D then 4
Space analysis
• Space availabe – space required = tooth size arch length
discrepency

1. For permanent
Space available
• Divide arch into 4
• From mesial of 1st permanent molar to mesial of canine  A
• From mesial of canine to mesial of right central incisors  B
• From mesial of left central incisors to mesial of canine  C
• From mesial of canine to mesial of 1st permanent molar  D
Space required
• Mesi-distal width of all teeth
•
Boltons
• According to bolton there exisits a ratio between mesio-distal width of
maxillary & mandibular teeth
• Helps in determining tooth size discrepency
• Too large  IPR (commonly done in lower incisors)
• Too small  buildup (peg laterals )

• We take mesio-distal width of all maxillary and mandibular teeth

separtly (1st molar to 1st molar)
• Sum of mandibular 12
• Sum of maxillary 12

Ideal overall ratio

• Sum of mand12/sum of max 12 x 100
• If value is more then 91.3% = excess in mandibular tooth material
• If value less then 91.3 = excess in maxillary tooth material
Ideal overall ratio
• Sum of mand12/sum of max 12 x 100
• If value is more then 91.3% = excess in mandibular tooth material
• If value less then 91.3 = excess in maxillary tooth material

Amount of overall excessive maxillary tooth material

• If x is less than 91.3
• Desired sum of maxillary 12 = actual sum of man / 91.3 x 100
• Actual sum of max 12 – desired sum of max 12

Amount of overall excessive mandibular tooth material

• If x is more than 91.3
• Desired sum of man 12 =. Actual sum of max 12 x 91.3 / 100
• Actual sum of man 12 – desired sum of man 12
Ideal anterior ratio
• Sum of mand 6 / sum of max 6 x 100 = 77.2 %

Amount of anterior excessive maxillary tooth material

(mm)
• If y is less than 77.2
• Desired sum of max6 = actual sum of man / 77.2 x 100
• Actual sum of max 6 – desired sum of max 6

Amount of anterior excessive mandibular tooth material

(mm)
• If y is more than 77.2
• Desired sum of mand 6 = actual sum of max 6 x 77.2 / 100
• Actual sum of mand 6 – desired sum of mand 6
2. Mixed dention
Radiographic method
• Based on cephalometric & peri-apical radiographs
• Cohen
• Limma & monnerat
• Hukaba
Non-radiographic
• Based on correlation & prediction equation  prediction table
• Moyers
• Tanaka & johnson
• Bernab ce, flores mc
Combination
• Combination of both
• Hixon & oldfather
Moyers
• We use lower 4 incisors as predictors to predict value of unerupted canines
& premolars (mesio-distal widths of incisors)
• Sum of incisors is used to predict size of unerupted 345 of one side by
using the prediction table
• Why not we use upper  due to variation (peg lateral etc)
• Developed for northern white children

Space required
• Use the value of 345 we predicted and measure incisors value mesi-distally
• Add values
Space available
• From mesial of 1st permanent molar to mesial of canine  A
• From mesial of canine to mesial of right central incisors  B
• From mesial of left central incisors to mesial of canine  C
• From mesial of canine to mesial of 1st permanent molar  D
Advantage
• No need of radiograph
Disadvantage
• Has tendency to over-estimate size of unerupted teeth
Tanaka & johnson
• Predicts the size of uneerupted canine & premolars
• Measure lower incisors mesioditally and add them
• Divide the sum of incsiors by 2
• Add 10.5 for mandible = value of 345 of one side
• Add 11 for maxilla = value of 345 of one side

Space required
• We have value of 345 of one side
• Then measure incisors mesio-distally
Space available
• From mesial of 1st permanent molar to mesial of canine  A
• From mesial of canine to mesial of right central incisors  B
• From mesial of left central incisors to mesial of canine  C
• From mesial of canine to mesial of 1st permanent molar  D
Formula
Advantage
• Good accuracy for eruopean population
• No radiograph or prediction table
Disadvantage
• Overestimation the required space for caucasion females (both
arches)
• Under-estimates the space availble for  african american males
(lower jaw)
Huckaba
• Use of radiograph & study cas to determine the width of
unerupted teeth

X = actual width of unerupted teeth

X’ = radiographic width of unerupted teeth
Y = actual width of erupted teeth
Y’ = radiographic width of erupted teeth

X = X’ x Y/Y’  use this formula for estimating size of unerupted

tooth
Step 1  total space required
• Mesiodistally measure each tooth from 2nd premolar – 2nd
premolar
• Add all values seperately for maxilla & mandible

Step 2  total space available

• Divide arch into 4
• From mesial of 1st permanent molar to mesial of canine  A
• From mesial of canine to mesial of right central incisors  B
• From mesial of left central incisors to mesial of canine  C
• From mesial of canine to mesial of 1st permanent molar  D

Step 3  calculate space

• Space avaiable – space required
Diagnosis &
treatment
planning
Aims & objectives of orthodontics (jackson’s triad)
1. Functional efficiency
2. Strucctural balance
3. Esthetic harmony

Line of occlusion
• Somooth catenary curve passing through central fossa of upper
molars & cingulam of canine & incisors
• Same line runs along buccal cusp of lower molars & incisal edge
of incisors in lower teeth
Andrews keys
Key 1  molar realtion
• Mesio-buccal groove of maxillary teeth should occlude with buccal groove of lower 1st molars
(class 1 )
• Mesiolingual cusp of upper should occlude with central fossa of lower

Key 2  crown angulation or mesiodital tip

• Gingival portion of the long axis of each tooth crown is disal to the occlusal portion of that axis
• Gingival zenith  distal
• Dant bilkul straight nhi halka distal hoti hai

Key 3  crown inclination or labio-lingual/ bucco-lingual torque

• Upper incisors  +ve torque (root palatal & crown labial)
• Lower  -ve torque (root labial & crown lingual)

Key 4  absence of rotation

• No rotation of any tooth in arch

Key 5  absence of spacing in arch

Key 6  occlusal plane should be flat (flat curve of spee)

Angles class of
malocclusion
Class 1
Class 1
• Normal molar relationship but line of occlusion not
normal/following/ not specified
• Neutro-occlsuion
• 50 – 55 % (70% accroding to first aid)

Super class 1
• When the mesiobuccal cusp tip of the upper first molar occludes
distally to the buccal groove of the lower first molar in a position
between Class I and full Class III
Incisor classification
Class 1
• Lower incisal edge to occlude with cingulam plateau of upper
inciosrs

Canine classification
• We see mesial slope of upper & distal slope of lower canine

Class 1
• Mesial slope of upper canine occluse with distal slope of lower
canine
• Max canine lies b/w 1st premolar & mand canine
Class 2
Class 2
• Also refered as  disocclusion, retrognathism, overbite
• Mesio-buccal cusp of maxillary first molar ahead of buccal groove
of mandibular molar (b/w first molar & 2nd premolar)
• Not specified  line of occlusion
• Convex profile
• Disto-occlusion
• 15% (25% first aid)

• Half unit  when the upper mesiobuccal cusp is ahead of buccal

groove but is in end-end contact with lower mesio-buccal cusp

• Full unit  when the upper mesiobuccal cusp is ahead of buccal

groove but is in the embrassure ahead of mesio-buccal cusp of
Sub division
• If there is class 2 one one side and class 1 on other, we denote
the abnormal side by sub-division

Class 4 molar relationship

• If one side class 3 & other class 2
Incisors classification
Class 2
• Lower incisal edge is behind the cingulam of upper incisors
• Div 1  upper incisors proclined (labioversion)
• Div 2  upper incisors retroclined (linguoversion)

Canine classification
Class 2
• Mesial slope of upper canine is ahead of distal slope of lower
canine
• Max canine mesial to mand canine
 Difference between class II
Div 1 Div 2
• Proclined upper incisors • Retroclined upper incisors
• Increases overjet • Decreased overjet
• Increased deep bite • Decreased deep bite
• Majority cases short upper lip • Normal upper lip & deep mento-
• V-shaped arch labial groove
• Mandible deficient (not in • Broad upper arch
every case • Normal mandible
Class 3
Class 3
• Mesio-buccal cusp of maxillary fisrt molar behind the buccal
groove of mandibular 1st molar (b/w 1st & 2nd molar)
• Refered as  mesiooclusion, prognathism, underbite
• Chin may be in protrusive position
• Concave profile
• Mesio-occlusion
• Half unit
• Full unit
• 1-5%

Subdivision
• If there is class 3 one one side and class 1 on other, then we
denote abnormal side by sub-divison
Incisors classification
Class 3
• Lower incisal edge is ahead of upper incisors
• Edge to edge is also class 3
• Overjet  0 or in negative

Canine classification
Class 3
• Mesial slope of upper canine is behind the distal slope of lower
canine
Pseudo class 3
 Drawbacks of angles classification
• Considered mal-occlusion in A-P plane
• Used 1st maxillary permanent molar as fixed point
• Cannot be applied inf decidious dentiton
• Does not differentiate between skeletal & dental mal-occlusion
• Does not highlight etiology of mal-occlusion
• Individual mal-occlsuion have not be considered (lv, dv etc)
Malocclusion
Malocclusion
• Not a disease but variation from what is considered ideal
Etiology
• 60 %  unknown
• 5%  known
• 35%  normal
Malocclusion happens in all three planes
1. AP
2. Transverse
3. Vertical
Speech problems
related to
malocclusion
1. S, Z
• Ant open bite
• Gaps in incisors

2. T, D
• Irregular incisors  specially lingual position of max incisors

3. F, V
• Skeletal class 3

4. TH, SH, CH
• Ant open bite
Molar uprighting
• Long term loss of mandibular 1st molar = causes 2nd molar to tip
mesially , migrate, rotation

Why molar uprighting is needed

• Improve direction & distribution of occlusal forces
• Decreases amount of tooth reduction needed for parallelism of
abutment
• Decrease possibilitys of procedure - endo, perio, prostho
• Improves periodontal health
• Improves alveolar contour
• Improves crown – root ratio
Treatment methods
• Uprght with fixed edgewise orthodontic appliance
• Tipped molar  should be banded
• Time  6-12 months

Condition which complicate molar uprighting

• High mandibular plane  cause open bite
• Open bite
• Periodontal comproimise
• Root resorption
• Severe skeletal discrepancies
Impacted tooth
• Most common  maxillary canine (after 3rd molars)

May cause
• Adjacent tooth  root resorption
• Orthodontic problems
• Easthetic issue
• Future prostho issue  related to restoration of missing tooth

Diagnosis
• Opg
• Cbct
• Bite wings  slob technique
Soft tissue vs angles
paradigm
Angle
• He believed that diagnosis & treatment planning should focus of
skeletal & dental components & soft tissue realtionships are
byproduct

Soft tissue paradigm

• According to that proportion of soft tissue integument of the face
& relationship of dentiton to lips & face are the major
determinants of facial appearance

1. Macroesthetics  beautiful face

2. Miniesthetics  beautiful smile
3. Microesthetics  beautiful teeth
 Comparsion
Angles Soft tissue
• Primary goal  ideal dental occlusion • Normal soft tissue porprotion &
adaptations
• Functional occlusion
• secndary goal  ideal jaw realtionship

• Ideal soft tissue porportion define ideal

• Hard & soft tissue relationship  ideal hard tissue
hard tissue porportion produce ideal
soft tissues
• Clinical examination of intra-oral & facial
• Diagnotic  ceph, casts
soft tissue
• Plan ideal soft tissue relationship and then
• Treatment  ideal dental & skeletal plan dental & skeletal to achieve this
reationship & assume soft tissue will be
ok
• soft tissue movement in relatioship to
• Function  tmj in realtion to occlusion display of teeth
• Stability  related primarly to dental • Related primarly to soft tissue
Ackermen –
proffit
1. Facial proportion & esthetics
• Lip posture
• Smile arc

2. Alignment & symmetry

• Symmetry
• Spacing
• Crowding
• Rotations

3. Transvers
• Post cross bite
• Midline

4. Sagital (A-P)
• Overjet
• Angle class

5. Vertical
• Over bite
Irregularity index

Midline diastema
• Gap between central incisors
Cause
• Low frenum attachment
• Supranumerary teeth
Overjet
• Horizontal overlap of upper incisors over the lower incisors
• Normally  2-3mm
• Mild  3-4
• Moderate  5-6
• Severe  7-10
• Extreme  more than 10

Reversed overjet / anterior crossbite

• Lower incisors ahead of upper incisors
• Denoted by minus sign
• Mild  0
• Moderate  -1 - -2
• Severe  -3 - -4
Overbite
• Vertical overlap of upper inciosrs over lower incisors
• Normal  1-2 mm / 33%

Open bite
• No overlap of upper over lower incisors & there is vertical separation/gap
• Moderate  -2 – 0
• Severe  -3 - -4
• Extreme  more than -4

Deep bite
• More than normal vertical overlap
• Moderate  2-3
• Severe  5-7
• Extreme  More than 7
Cross bite
• Abnormal realtion of teeth bucco-lingually or labio-palatally

1. Posterior cross bite

• When maxillary posterior teeth are lingually positioned in realtion
to mandibular teeth
a) Lingual  upper teeth lingual to lower teeth
b) Buccal  upper teeth completely buccal to lower (scissor bite)

2. Anterior
• When upper anterior teeth are palatally positioned in realtion to
lower anterior teeth
• Reverse overjet
Face proportion
1. Vertical thirds

a) Upper third  hairline to glabella

b) Middle third  glabella – subnasale

c) Lower third  subnasale – menton

• In lower third  1/3 upper lip & 2/3 lower lip & chin

2. Horizontal fifths
• Middle fifth  inner canthous – inner cantous
• Medial 2/5th  inner canthous – outer canthous
• Lateral 2/5ths  outer canthous – lateral helix of ear

• Vertical line from inner canthous  coincide with alar base of nose
• Vertical line from outer canthous  coincide with gonial angle of
mandible
 Skeletal
classification
Class 1
• Jaws well related to N-vertical line

Class 2
• Prognathic maxilla (10%)
• Retrognathic mandible (85%)
• Both (5%)

Class 3
• Prognathic mandible (20%)
• Retrognathic maxilla (60%)
• Both (20%)
Facial convexity
• Plane formed by glabella + subnasle + soft tissue pogonion
(chin point)

• Class 1  straight (below 10degree)

• Class 2  convex (more than 10)
• Class 3  concave (
 Facial
divergence
• Inclination of lower face relative to forehead
Profile angles
1. Nasolabial angle
• B/w nose & upper lip
• Should be 90degree
Determined by
• AP position  maxiall & upper incisors
• Vertical postion  nasal tip

2. Mentolabial angle
• B/w lower lip & chin
• Should be  120 degress
Determined by
• Lower incisors postions
• Vertical position Lower facial third

3. Cervicomental angle
• B/w chin & neck
• Should be  90-120 degrees
Consideration
• gender
• Soft tissue sag
Lips
Position
• Protrusive
• Retrusive
• Draw rickets E line  tip of nose to chin
• Upper lip  behind
• Lower lip  on line

Posture
• Competent  seal without strain at rest
• Incompetent
• 3-4mm sepration at rest & mentalis strain on closure  incompetence

Porportion
• Thick
Incisor display
At rest
• 2-4 mm ideal

At smile
• 100 % incisor & 1-2 mm gingiva  ideal (more than 2mm gummy
smile)
• 75 % incisors  not ideal
Buccal corridor
• Dark space b/w maxillary post teeth & corner of mouth on smile
• Wide  lots of space (in narrow arch)
• Medium
• Narrow  no space / little (in wide arch)
Cephalometric
• It is the diagnostic tool taken by the radiograph
Two types
1. Lateral (lateral view)
• Visulize hard & soft tissue structures
• To see skeletal relation of jaws
• To see the position & inclination of incisors & molars
• Evaluate treatment results
• Orthodontic diagnosis & treatment planning
• Establishing facial types
• For research

2. Pa view (frontal view)

• To evaluate the facial asymmetry
• Provides information related to skull width
• Vertical proportions of skull, craniofacial complex & oral structures
Cephalostat
• Machine used to take cephalogram
Distance
• Between xray source & mid sagital plane should be  5ft / 60inch
• Betwwen film cassette & mid sagital plane  15cm
Landmarks
1. Sella (S)
• Mid point of sella turcica
2. Nasion (N)
• Anterior most point at fronto-nasal suture
• Point between frontal & nasal bone
3. Orbitale (Or)
• Lowest point on the Inferior margin of orbit
4. Ans (anterior nasal spine)
• Anterior most tip of maxilla / nasal spine
5. Pns (posterior nasal spine )
• Posterior most tip of palatine bone
6. Point A (subspinale)
• Deepest most point between ANS & alveolar process of maxillary incisors
• Inner most point on the contour of maxilla
7. Point b (supramentale)
• Deepest most point between the chin & alevolar processes of mandibular incisors
• Inner most point on the contour of mandible
8. Pogonion (POG)
• Anterior most point of chin
9. Menton (Me)
• Inferior most part of chin
• Button of the chin
10.Gnathion (GN)
• Point between pogonion & menton
• Anterio-inferior point at chin
11.Gonion (GO)
• Point which is present at the angle of mandible
• Intersection point between ramus & lower border of mandible
12.poroin
• Highest most point at external auditory meatus
13. Bolton point (BO)
• Not commonly used
• Highest point in the upperward curvature of occipital bone at
around centre of foramen magnum
• Highest point in the concavity behind the occipital condyle
14. Basion (BA)
• Lowest point of ant margin of foramen magnum & points towards
odontoid process at c2
15. Articulare (AR)
• Intersection b/w zydomatic arch & posterior border of ramus
16. Candilion (CO)
• Most posterior & superior point at the outline of condylar head
17. Pterygomaxillary fissure
• Point at base of fissue where where anterior & post walls meet
Planes
Horizontal planes (5 planes)
1. Anterior cranial base/S-N plane
• From sella to nasion

2. Frankfort horizontal plane

• From porion to orbitale

3. Palatal plane
• Ans to Pns

4. Functional occlusal plane

• Maximum intercuspation of 6, 5, 4
5. Mandibular plane
• Gonion to gnathion
• Gonion to menton
• Steep mand plane  long anterior vertical dimension, ant open
bite
• Flat mand plane  short anterior facial vertical dimension, deep
bite
Analysis
Steiners analysis
• 3- way analysis
• We do dental, skeletal & soft tissue analysis
1. Skeletal analysis
• Reference line  ACB/S-N PLANE

SNA
• sella-nasion-point a
• Tells position of maxilla with respect to anterior cranial base
• Range  78-86 degress
• More than 86 (84 first aid) skeletal class 2 / prognathic maxilla
• Less than 78  retrognathic / class 3

SNB
• Sella-nasion-point b
• Tells position of mandible with respect to anterior cranial base
• Range  76-80 degress
• More than 80  prognathic mandible / class 3
ANB
• Relationship of maxilla to mandible
• Difference between SNA & SNB
• SNA – SNB
• Range  0– 4  normal class 1
• More than 4  class 2
• Less than 0  class 3
• Anb 2  ideal class 1
SN-OP angle
• angle between sn & functional ocllusal plane
• Range  9-19
• Tells diversion pattern between individual (high, low, normal
angle case)
• Range  9-19
• Less than 9  hypodivergent /low angle  deep bite
• More than 19  hyperdivergent /high angle  skeletal open bite

SN-MP angle
• Angle between sn & mp
• Range  28-36
• More than 36 hyperdivergent
• Less than 28 hypodivergent
2. Dental
• We see position and inclination of incisors

UI-NA angle
• Angle formed by intersecting the long axis of upper incisors & N-A
line
• Range  18-26 degrees
• More than 26  proclined
• Less than 18  retroclined
UI-NA distance
• Tells position of the upper incisors in respect to NA line
• Distance from NA-line to the most labial surface of upper incisors
• Range  2-6
• More than 6  forward
LI-NA angle
• Angle between NA line and long axis of lower incisors
• Range  21-29
• More than 29  proclined
• Less than 21  retroclined

LI-NB distance
• Distance between NB line and most labial part of lower incisors
• Range  2-6
• More than 6  forward
• Less than 2  backward

Inter-incisal angle (II)

• Angle between upper and lower incisors formed by intersection of long axis of
upper and lower incisors
• Range  125-145 (reversed)
• More than 145  retroclined
Holdaway ratio
• Ratio between LINB & NB-pog
• Distance of labial side of lower incisors to NB-line should be qual to distance
from NB-line to POG
• Significance  how much do u have chin support for your lower incisors
• 1:1

3. Soft tissue
• Upper lip & lower lips
• We see if lips are normal or not

S-plane
• Most prominent part of the soft tissue chin to the base of the mid of the nose
• Range  -2 - + 2
• More than +2  protrusive
• Less than -2  retrosive
Cephalometric superimposition
• To evaluate skeletal & dental channges over time
 Index for orthodontic
treatment need (IOTN)
1. Aesthic componenet
• 1-10
• We compare patients frontal picture with the given grading pictures
• Grade 8- 10 definite treatment
• Grade 1-7 no treatment

2. Dental health component

• Scale from 1-5
• Grade 4 & 5  needs treatment
We see MOCDO
• M  missing tooth (most points given )
• O  overjets
• C  cross bite
• D  displacement
Biology of tooth
movement
Steps for tooth movement
1. Force to tooth
2. Pdl stressed
Compression side  osteoclast
Tension side  osteoblast
3. Bone remodels
4. Tooth moves

Types of movement
5. Physiological
6. Pathological
7. Orthodontic

Tooth movement to happen we need 3 things

8. Force magnitude
9. Time/force duration
• Pdls are like rubber bands  on side where we apply force =
stretched(tension) and on opposite side compressed (pressure)
• Bone subjected to tension = deposited
• Bone subjected to pressure = resorped
1. Mild force

Pressure side
• Pdl compressed to 1/3 to its original thickness,vascularity
increased, fibroblasts & osteoclasts will come here = bone
resorption adjacent to ligament (frontal resorption) (resorption of
lamina dura)

Tension side
• Pdl stretched, distance b/w alveolar process and tooth widens,
increased vascularity, fibroblast & osteoblast will come = osteoid
deposition which then will calcify and form woven bone
• Secondary remodelling changes
• 3-5 days  movement happens
Extreme/heavy forces

Pressure side
• Crushed pdls, compressed blood vessels, loss of nutritional
supply = hylanization(area of sterile necrosis) , necrosis of
cellular elements, undermining resorption (removal of bone under
the alveolar bone = loss or cementum & root resorption)

Tension side
• over-stretched pdls, teared blood vessels = ishcemia, osteoclastic
activity = loose tooth, pain & hyperemia of gingiva
• 7-14 days  movement happens
 Force
distribution
• Amount of force delivered to a tooth & the area of pdl over which
that force is distributed
• Force / area = pressure
1. Uncontrolled tipping
• Crown goes in direction of force and root goes opposite to it
• Heaviest force is felt at the root apex & crest of alveolar bone on the opposite
side
• Ideal uncontrolled tipping force = 50grams (35-60g dr farhan)
• Finger spings, brackets with round wire
• Mc/Mf = 0 (Mc is zero, because there is not couple here)
• Centre of rotation is slightly apical to centre of resistance
• Crown goes in direction of force & root in opposite

2. Controlled tipping
• Partially tipped & partially translated
• Ideal force = 75grams
• 75 % pdls on compressed side
• 25 % on tension side
• Eg :- retroclination & proclination
• Mc/Mf = 0 – 1 ( movement of couple is less then moment of force)
• Centre of rotaion moved apically away from centre of resistnce (around at apex)
• 3rd order couple + rectangular wire + edgewise Bracket
3. Bodily/translation movement
• Crown & root moves together in same direction
• Pdl loaded on same side  compression all along one side of root
• Ideal force = 100grams (70 - 120g)
• Eg:- protraction & retraction , intrusion & extrusion
• Put pressure at cor or put force on crown bucally & lingually
• Mc/Mf = 1 (Mc=Mf)
• Centre of rotation moved infentily away from centre of resistance
• There is no rotation

4. Root torque
• Root moving, crown doesn’t
• Ideal uprighting forces  75g
• Using couples & rectangular wires
• Mc/Mf > 1 (moment of couple greater then moment of force)
5. Rotation
• Rotation at its long axis
• It would compress the area same as we will see in tipping
• Ideal force = 50g
• Mc/Mf  does not exist
• Centre of rotation is at centre of reistance

6. Extrusion
• Pulling a tooth gently out of the socket
• Ideal force = 50g

7. Intrusion
• Pushing tooth into the socket
• Gentle forces are applied down the long axis of tooth
Force duration
• Threshold for tooth movement is 4-8 hrs
• This is why patients need to wear appliances
for hrs/day
• Appliances need patient compliance
1. Continious force
• Forces stays fairly constant (always constant force)  ideal spring
• It declines little then again is reactivated by the doctor
• Light wires, fixed appliances (braces)
• Frontal resorption

2. Interupted
• Forces slowly declines to zero
• Elastic chain  in 24 hrs 50% force is lost
• Fixed appliances

3. Intermittent forces
• Forces abruptly declines to zero
• When patients takes the applainces out the forces become zero, then
again put in the forces are back to normal
• Aligners, rubber bands, frankel, headgears, expanders, chin-cups
 Regional acceleratory phenomenon
• To fasten movement
• Regional  inflammation at both cut site & adjacent bone
• Acceleratory  intensified bone resposne due to aggitated
inflammatory mediators
• This phenomenon relies on the fact that if we can agitate the the
inflammatory process by making the cuts at bones where the
inflammation is going on to fasten that process

• Regional  inflammation at the both cut sites & adjacent bone

• Acceleratory  intensified bone response due to aggitated
inflammatory mediators
Procedures
• Propel  making holes
• Wilckodontics  full thickness flap with selective alevolar
corticotomy then use bone graft close that & immediately aplly
orthodontic forces
 Deleterious
effects of
orthodontic
tooth movement
• Mobility  widened pdls
• Pain  necrosis & remodelling of pdl
• Inflammation  poor OH
• Root resporption  heavy forces, trauma, bruxism
• Delayed tooth movement
• Allergic reaction

• Active periodontitis , brusxism  avoid ortho before correcting

these
1. Pain
• Due to heavy forces mostly  necrotic area = pain
• Prevent by using lighter forces
If due to light forces
• To relieve  chew a sugar free gum or plastic wayfer (increase blood flow)
If due to heavy forces
• Acetoaminophen

2. Inflammation reaction
• Poor oral hygiene  most common
• Latex & nickel allergy
• Patch test to diagnose
• 2-3 bracket first for 2 weeks if u feel he is allergy (follow-up & see)
• Ceramic brackets, plastic brackets, zirconia & composite brackets, aligners
• Tma wires (beta titanium), composite wires, esthetic wires
3. Mobility
• Avoid situation which causes this problem  go for mild forces
• Gic blocks on other teeth for the problemetic tooth to stablize

4. Pulp affected
• Longer extreme movement, excessive trauma  concern for vitality loss
• Refer to operative
• Treat any cavity or carious lesion
• History of trauma & examination, vitalities test

5. Root resorption
• Heavy force
• Large defects
• Apicl defects
• Genetic
• Single root
• Traum, bruxism, heavy mastication
Types of root resoprtion
1. Moderate generalized root resoprtion
• Associated with orthodontic forces  excessive
• Prolonged treatment duration
• Continious repeated forces
• Most common  upper anteriors
• ¼ root resorption

2. Severe generalized root resorption

• Unknow etiology
• Thyroid deficiency pts & asthamtic pts
• To prevent  thyroid supplements
• More then ¼

3. Severe localized
• Associated with orthodontic forces  excessicve
• Prolonged treatment duration
• Affects upper centrals & laterals & lower  1st molars

Intrusion  root resorption

Phases of tooth movement
1. Intial
• Apply force = immediate movement of tooth in its socket
Due to
• Tooth moving in pdl space
• Alveolar bone bending
2. Lag phase
• Little or no tooth movement
• Longer duration in case we apply extreme phase
3. Post lag phase
• Removal of hylanized are = movement
Periodontium
• Surrounds tooth
Basic structure of pdl
• Pdl space  0.5mm
• Fibers run at right angle to the long access of the tooth
• Undifferentiatied cells  inactive before forces apply
Cells in pdl
• Fibroblast  destroy and produce fibers
• Osteoblast
• Osteoclas
• Cementoblast
• Cementoclast
• Nerve endings  proprioception
• We study what is happening at the cellular and molecular level
when we apply orthodontic forces

Transduction
• Conversion of mechanical energy to biological signal for
remodelling response is called transduction
Theories
• Mechano-chemical hypothesis
• Bio-electric
• Pressure tension theory / blood flow theory
1. Mechano-chemical hypothesis
• Change in solubility of hydrooxyapetite crystal due to physical
stress on bone, which causes remodelling
• Physical stress = change in solubility of crystals – remodelling
• Not widely accepted hypothesis
2. Bioelectric
• Orthodontic forces = flexing & bending of alevolar bone = electric signal generates = alter metabolism
of bones
Types of electric signals
a) Piezoelectricity
• Obsereved in crystalline material
• Deformation of crystal structures causes electrons to be displaced form one part to another =
generating electric current
• Bone & collagen has piezoelectric propery
Features
• Quick decay rate  force applied it immediatly turns to zero even if the foce is continiously applied
• Reverse piezoelectricity

b) Streaming potential
• Electrokinatic effects that arises when the electric double layer overlying a charged surface is displaced
as interestial fluid moves
• Ions in fluids surroning the living bone interact with the electric fields generated when bone in bent
• These currents of smal voltage are called streaming potential
• Long decay period
c) Bio-electric potential
• Orthodontic force  bending  bone surface becomes electrically charged  concave surfave (-ve),
convex (+ve)  remodelling
3. Tension pressure theory
• Force = tissue trauma = 1st messenger relases (helps in cellular
differentiation)
• 1st messenger binds to the cell surface receptors = activates extra-
cellular signals
• Extra-cellular signals converted to  intra-cellular signals
• Intracellular signals cause release of 2nd messengers after 4hrs of time by
converting  Atp to CAMP & causing ca channels to open to relase ca
• Camp & ca activates protein kinase enzyme
• Protein kinase enzyme causes  phosphorylation of cells = cells
differentiation = activation of osteoblast & osteoclast  remodelling 
movement

Primary messeneger  force

1st messenger  PGE, pth, substance p, vasoactive peptides
2nd messenger  Camp, ca
Mechanical
principles
Centre of resistance
• Fixed point where if u apply force then the entire tooth will have a
translatory motion (move in a linear motion )
• A force with a line of action passing through centre of resistance, it will
produce translation
• Depends on length of root, number & morphology also depends on alveolar
height
• Bodily movement  crown & root both
• For free floating object  COR = COM
• COR  occlusal  root resorption
• COR  apical  periodontal compromise

On single rooted teeth

• Point will b on the long axis of tooth, somwhere between 1/3 or 1 half of root
Multi-rooted teeth
• 1-2mm apical to the furcation / furcation area
Centre of mass
• Point where all the mass of that object is concentrated

Centre of rotation
• Unfixed point around which the tooth rotates

Force
• Linear vector with magnitude & direction
• Point of force application is crucial
• Push or pull

Moment (Mf)
• Tendency of force to rotate body on a specific axis
• Measured at from some distance from COR
• Moment = force x direction

Couple (Mc)
• Pair of equal & opposite non-collinear forces
• Pure rotation
• Require 2 point contact
• Eg :- 1st order (mesio-distal rotation), 2nd order (mesio-distal angulation), 3rd order (bucco-lingual
Anchorage
• Resistance to unwanted movement
• Based on newtons 3rd law
• For every desired tooth movement there is equal & opposite
undesired movement
• Light force has less anchorgae toll
• Heavy force has more anchorage toll = more chances of
undesirable movements

• We see root surface area before planning any anchorage

(more root surface area more will be the anchorage )
Reciprocal anchorage
• Tooth moving in opposite direction equally (due equal amount of
pdl & root surface area)
• 50:50
• Diastema closure

Group a
• When u want retract ur incisors more as compare to posterior
• 75% tooth movement of anterior & 25% posterior (anterior peche
molar agey)
• Class 2 div1

Group b
Group c
• 75% tooth movement of posterior & 25% anterior (molar agey &
anterior peche)
• Class 3
• Opposite to group A

Absoulute anchorage
• U don’t take anchorage from the dentition
• Anchorage from skeletal
• Headgear, screws in bone
Reinforced anchorage
• Add up another tooth to that tooth from where u r exterting force
• Headgear  for anchorage
• Eg :- class 2 div 1 u extracted upper 4 and u want to retract 3 so u take
anchorage from 6 but the 6 alone is not enough u retract 3, then u add 7
&/or 5 to retract the 3 (add 6 & 7 by ligation wire = co-ligation)

Skeletal anchorage
• TADS  temporary anchorage device (don’t want osteointegration)
• Plates
• Screws
• Earliest to place  age 11 (when bone is mature enough)
Used for
• Distalizing molars
Stationary anchorage
• Crown tipping first then root uprighting is done
• We allow bodily movement with tipping of anterior (the bodiliy
tooth movement is resisted due to less amount of force)

Cortical anchorage
• Anchorage from cortical bone
• Lock root in bone and do the retraction
• Disadvantage  root resorption
Maximum anchorage
• Not more then ¼ of the extraction space should be lost by
forward movement of anchorage teeth
Moderate anchorage
• Anchor teeth can be permitted to move forward into ¼ to ½ of
extraction space
Minimum anchorage
• More then half extraction space can be lost by anchor teeth
moving mesially
 Drug effects on
orthodontic tooth
movement
1. Drugs which enhance tooth movement
• Vit d
• PGE2 inj into pdl  increase diferentiation of osteoclasts = more
resortion (tooth movement in day) (painfull not done nowadays)

Drugs which inhibit tooth movement

1. PG inhibitors
• Nsaids  chronic user we refer them to doctor to switch or
alernatively stop drugs
• Corticosteriods 
2. Bisphosphonates
Nsaids
1. Aspirin
2. Ibbrufen
3. Indomethacin
Exceptional
• Acetoaminophen

• Other drugs
Bisphosphonates
• Given in osteoporosis patients
• Post menopause women have increased osteoclastic mediated
bone resorption resulting in osteoporosis
• We give bisphosphonates to these patients to stop this (binds to
hydrooxyapetite crystals & blocks osteclastic activity)
• This drug accumulates in the bone surface & core  eleminates
faster at surface if drug stopped (3months ) (6months -1yr from
core)
Treatment
• Consult physician and switch to estorgen therapy
Procedures to enhance movement
1. Corticotomy
• Posterior cross bite in adult patients can be coreected by this
procedure
2. Modified corticotomy
3. Vibration-acceledent  frequency is 30hertz & applied in
mouth for 20mins x 2times/day
4. Phototherapy biolux  wavelength of 800-850 nanometer
for 20mins, 97% light is wasted only 3% is used to
activate undifferentiated cells
5. Theraputic ultrasound
Ortho wires &
brackets
• Wire does all the work for moving
• Bracket is just the handle

1. Arch wires
• Started with  gold, platinum, indium & silver
• In 1930  stainless stell wires came
• 1970  chromium alloys arrived
• 1980  tma (beta titanium) (fininshing stage)
Properties of wire
Phases
1. Activation
• Loading, amount of force applied to engage the wire into bracket
slot

2. Deactivation
• Unloading, Amount of forces wires apply to tooth to get into its
orignal place
 Stress stain curve
• Tells/explains the behaviour of any elastic material
Stress
• internal distribution of the forces = force/unit areas
• Measured in pounds/square inch or megapascal

Strain
• internal distortion produced by the load = deflection/unit length

Stress is proportional to strain

1. Strength
• Loading  how easily it will break
• Unloading  how much force wire can deliver
• Strength = stiffness x range

Represented by these

Proportional limit
• highest point where stress & strain are in linear relationship
• No deformation  come back to original

Yield strength/point
• when stress/load is applied and it crosses proportional limit there comes a point where u
see minimal/some permanent distortion but only .1%

Ultimate tensile strength

• point beyond the yield strength, maximun elastic load that the wire can tolerate but
when force is released it will never go back to its orignal condition
2. Stiffness
• Loading  how flexible it is
• Unloading  how much force wire will deliver as it comes backs to
its orignal shape

• More vertical graph / higher slope  more stiff wire

• More horizontal graph / lower slope  more flexible wire / springy

Vertical slope in graph

• Stiffer/ rigid = high modulus of elasticity

Horizontal curve
• Felxible/less stiff, springer object (rubber band)
3. Range
• Loading  how far it can deflect while maintaining its elasticity
before plastic deformity
• Unloading how far & for how long will it remain active
• On force deflection curve

Springback
• Wire defelcted beyond yeild point but it will come back to its
orginal shape
4. Resilence
• Capacity in a matertial to store energy, comibnation of strength &
springiness (rubber stretched & when leave it, it has energy to
come back to its orignal place)
• Below strain-stress curve up to porportional limit

5. Formability
• ability to go under plastic deformity before breakage / maximum
load a wire can handle before breaking
• How much permanenet deformity it can handle before breaking
• Under strain-stress cruve from yield strength to failure point
6. Modulus of elasticity/young modulus
• Describes relative stiffness/rigidity of wire, linear realtionship of
stress & strain
 Properties of ideal wire
• Hight strength
• Low stiffness
• High range
• High formability
• Friction free
• Corrosion free
• Biocompatible
• Cheap
• Esthetic
• Should be soldered & weldable
 Material &
geometry of wire
Increasing strenth & stiffness
• NiTi < TMA < S.S
• NITI  weakest & most felxible
• S.S  storngest & stiffest

Diameter  Increasing
• Increase strength
• Increase stiffness
• Decrease range

Length  increasing
• Decrease strength
• Decrease stiffness
• Increase range

Rectangular wire
• Stronger & stiffer then round

Beam
1. Stainless steel arch wire
• Also know as 18-8
• First invented by angles in 1930
• No range  once bent will deform
• Annealing  softens when heating
• Hardens when apply cold
Composition
• 18% is chromiun
• 8% is nickel
• 71% is iron
Uses
• For space closure & finishing
Properties
• Low cost
• Good fromabilty
• Good corrosion resistance  due to chromium
• Can be soldered & welded
Types
1. Super grade
• When we don’t need bending in stainless steel wire
• Good ultimate tensile strength
• Only for space closure by sliding mechanism
2. Regular grade
• Loops mechanics

Space closure is done by 2 mechanisms

1. Friction  sliding (friction will be created)
2. Friction-less  loops mechanics (only possible with S.S
wire)
2. Cobalt chromium
• Also know as rocky mountain arch wire
• Developed as a eligiloy
• Not used nowadays

Properties
• Expensives
• Softens by cold
• Hardens by heat

Composition
• Cobalt 40-45 %
• Chromium 15-22%
• Nickle for strength
Disadvantages
• Disappeared during end of 20th centurary
• Additional cost
3. Nickel titanium
• Important wire used in 1st stage of comprehensive treatment
Used
• Crowded, malaligned teeth
Composition
• 52% nickle
• 41% titanium  more friction due to titanium
• 2% cobalt
Properties
• Good springiness
• Good range
• Good resilence
• Shape memory
• Good range
• Poor formabilty
• Not be soldered or welded
Types
1. Austenitic
• first stage due to good springiness
• Stable at high temp & low stress
• Superelasticity
2. Martenitic
• most commonly used in 3rd stage(finishing stage)
• Stable at low temp & high stress

Both types can change to eachother (smooth transition) by

changing temp & stress
Stress increases = austenitic  martenitic (stress induced)
Temp increase = martenitic  austenitic (thermal induced)
4. Beta titanium (tma)
Uses
• Finishing/3rd stage & intermediate stage (rectangular wires)
• Has properties which lies between SS & Nickel titanium wire
• Combination of strength, springiness & formability
Composition
• High titanium  71%  more friction due to titanum
Properties
• More coefficient of friction  that why not used during sliding

Never comes in round  comes in square or rectangular

For root movement we use  square of rectangular wires
Cross section of wire
• Round  initial & intermediate stage, crowding, leveling the arch
& to open/close space
• Square  final stage, postion crown & root in correct relationship
• Rectangular  final stage, postion crown & root in correct
relationship
• Multi-stranded  used before invention of nickel titanium, still
used in retainers
Wire sequence

• During first stage of comprehensive treatment

1. Nickel titanium wire
• 0.012
• 0.014
• 0.016  no crowding start with this
• 0.018
• 16 x 22
• 17 x 25
During 2nd stage
2. Stainless steel
• 0.012
• 0.014
• 0.016
• 0.018
• 16 x 22
• 17 x 25

During last stage

3. SS or beta titanium
• 16 x 22
• 17 x 25
Brackets
• Angles made the brackets & wire system but they alone could not
do the tooth movement
• So he introduced the band system (1st, 2nd & 3rd order bands for
tooth movement)

Adrews
• He incorporated this band system into the brackets
• As bending was hard, time consuming & hard for patient
1st order bend
• In & out order band
• Facio-lingual bends
• Bending was compensated by increasing/decreasing the thickness of base of
brackets by andrews

2nd order bend

• Mesio-distal root movement
• Also known as artistic band
• Andrews compensated this by angulating the bracket system
• U need square/rectangular wire for root movement in bracket system (we can
use round and give bends to do this movement)

3rd order bend

• Bucco-lingual root movement
• Also known as torque band
 Preadjusted edgewise brackets
• Each bracket have its on prescription for each tooth
• Each brackets has a prescribed  base thickness, tip & torque
build in
• brackets must be positioned  in centre of facial surface of its
clinical crown
Types of bracket
1. Metal
• Unesthetic
• Made of  S.S

2. Ceramic
• Esthetic
• Prone to fracture
• Increased friction  while trying to put wire

3. Self ligating
• Built-in dorr locks for archwire
• Expensisve
• No need for ligation
Bands
• Kind of bracket system with a ligating system incorporated into it
• No need of ligatures as the tube is present for wire to go in
• Can be upper & lower
• Placed usally on 1st molar (can be placed on 2nd molars as well

Molar bands has 3 tubes

• First for head gear (no this tube in lower bands)
• Second slot for arch wire
• Third for auxillary wire (lies gingivally)
• Hook  always gingivally facing & distal facing (attach power chains
here )

Indication
• Heavy intermittent forces against the attachment (when using headgear)
• Teeth that will need both labial & lingual attachment
Steps of banding
1. Seperation (breaking contact
• Elasmeric separtors  not given in too tight contacts between
teeth, goes occlusally then we pull gingivally, can leave for 7-
20days, radiolucent (in lost in pdl space then cant find
radiographically)
• Brass  goe below the contact point, loosen after 7-10 days
• We use seperator pliers

2. Fitting of band
• Select size on cast then do
• Instruments used  band pusher & band seater

3. Cementation
Orthodontic
treatment
phases
Phase 1
• Early treatment rendered during mixed dentition
a) Improve oral environment
b) Correct problems that are easier to fix early
c) Reduce complexity of treatment in the permanent dentition
Transverse
1. Posterior cross-bite
• Treat if there is functional shift
• Associated with mandibular shift
• Treat age  6 – 9
• Treat asap  as transvers dimension is first to stop growth
• Palatal expansion  Quad helix, Haas, Hyrax
• Usally  RPE used
• Expander activated 2 times / day
• After activation  expander in mouth for 3-6months (retention)

• 0.25mm = 1 turn
Antero-posterior
1. Anterior cross-bite
a) Involve  one or few teeth
Which can cause
• Wear
• Gingival strain
Treatment
• 2 x 4 or 2 x 6, active retainer with finger spring

b) Full underbite
• Due to skeletal class 3
• Treatment  reverse pull headgear, chin-cup

• Ant crossbite in muliple primary maxillary teeth  inidcation of skeletal

growth problems / developing class 3
• Children with class 3 tendency will have edge – edge in primary and will
2. Severe overjet
• Increased trauma
• Psycho-social concern
Treatment
• 2 x 4 , headgear
Vertical
1. Anterior open bite
Causes
a) Thumb sucking
• Narrow maxilla + posterior crossbite
• Proclined max incisors
• Retroclined mand incisors

b) Tongue thrusting
• Pts postion tongue anteriorly during swallowing
• Proclined both upper & lower incisors + generalized spacing

• Maxillary constriction occurs due to  increased pressure on

buccinator from sucking

Treatment
Thumb-sucking
• Common till age 3
Depends on
• Intensity
• Time / day
• Duration

Causes
• Ant open bite
• Maxillary constriction
• Increased overjet
• Post cross bite

• Intervention at age  5-6 if habit still there

Appliance
• Blue grass
2. Palatal impingment
Due to
• Deep bite
Symptoms
• Pain / discomfort
• Damage to ginigval attachment / soft tissue
Treatment
• Maxillary bite plane  protects top of mouth, intrude lower ant
teeth
Alignment &
symmetry
1. Impacted teeth
• Common in ortho is canine impaction
• Need opg for this

Karols rule
• Canine not past midline of lateral  90% chances of eruption
• Canine past midline of lateral  64% chances of eruption

2. moderate crowding

• We donnot extract primary teeth to correct minor crowding

• If more then 4mm of crowding
Treatment
• Lip bumper  retracts lips & let lower incisors lean forward
• Lower lingual holding arch  once all lower incisors have erupted (to hold
3. Severe crowding
• Crowding  more than 8mm
• Do at the time of lateral eruptions
Treatment
• Serial extraction  c- d- 4

Contrainidcation
• Signification skeletal class 2 & class 3
• Midl to meoderate crowding
Comprehensive
treatment &
appliances
• Types of ortho
 Growth
modification
• Successful only during peirod of growth

Maxilla Mandible

- -
prognathic Retrognathic prognathic Retrognathic

- -
Reverse pull Functional
Headgear Chin-cup
headgear appliance
1. Headgear
• During pre-pubertal phase

Worn
• 12-14 hrs / day

Types
a) High / occipital
• Retrain maxillary growth forward  skeletal effect
• Force vector 
• Intrudes & distalizes upper molars  dental effect
• Best for class 2 open bite cases

b) Low / cervical pull

• Neck strap
• Retrain maxillary growth forward  skeletal effect
• Force vector  downward
• Extrudes & distalizes upper molars  dental effect
c) j-hook shaped
• For retraction of canine & incisors
• Extra-oral anchorage
• In maximum anchorage cases
• J-hook  engaged into the loop in the arch wire by laterals or
canines
• Dento-alveolar affect only

2. Reverse pull headgear / face-mask

• Stimulate  maxillary growth forward

• Protraction  upper incisors
• Retraction  lower incisors
• Clockwise rotation of mandible
• Best for class3 pt with deficient maxilla
3. Chin-cup
• Restrains mandibular growth forward
• Ineffective in humans
• Clockwise rotation of mandible
• Class 3 mandibular excess pts

4. Functional appliances
• Used before pubertal growth spurt
• Class 2  mandibular deficiency
• Bionator
• Activator
• Herbst appliance
• Clark twin block
Functional
appliances
• These are the devices that are used to alter patients functional environment in an
attempt to influcence & permanently change the surronding hard tissue
• Target is to achieve balanced profile  orthognathic
• These applaince work by  using functional forces of muscle of mastication & facial
expression to bring skeletal & dental changes mostly in AP direction
• Given in cvm 3  beacue of peak mandibular growth

How does appliance work

• Maxillary incisors  retroclination
• Mandibular incisors  proclination
• Guidance of eruption of posterior teeth (distal in maxilla & mesial in mandible)
• Maxillary restrain
• Mandibular forward growth
• Glenoid fossa remodeling

Aims
• Correction of overjet & over bite
1. Bionator

• Low angle (reduced lower facial height)

• Deep bite
• Simplest & most durabale
• Removable
• Passive tooth borne
• In deficient mandible
• Block of plastic b/w teeth guides the pt into advancement
of pt
• Class 2 div 1
• Also called cut down activator
2. Activator

• Removable
• Uncomfortable
• First apliance to be developed
• Lingual flanges contact lingual mucosa by lower molars & usually
extend deeper then bionator
3. CTB (Clark twin block)

• Two-piece appliance
• Removable
• Fixed  cemented on  molars / premolars
• Inclines  force pt to advance mandible in order to close
• Pros  provides more positive mandibular changes (accelerate bone growth at condyle)
• Active tooth borne
• Have springs & screws  active part
• High angle patient & normal angle
• If deep curve of spee  trim the bite block (posterior eruption in growing, extrusion of lower
anterior in adults)

Component
• Labial bow
• Adams clasp
• Jack screw
• Posterior acrylic capping
• Ramps  30degress to each other  force pt to advance mandible to close mouth
4. MARA (mandibular anterior repositioning appliance)
• Fixed
• Advance mandibile when closing
Pros
• Less bulky
• More durable
• More stable than herbst
Cons
• Less mandibular advancement than CTB & herbst

5. Herbst
• Fixed
• Piston and tube device
• Passively push mandibile forward (no pt compliance needed)
Dental change
• Upper distal & intrusive force
• Lower mesial & intrusive force
• Proclination of lower incisors
• Retroclination of upper incisors
 Other class 2 correctors
1. Forsus
• Fixed
• Push rod spring
• More dental affect  upper distal & intrusion, lower mesil & intrusion
Pros
• No need for compliance
• More maxillary restriction
Cons
• Requires heavy upper & lower arch wires

2. Pendulum
• Fixed
• Distalization applaince
• Banded to upper 1st molars  ditalization & derotation
• Pandex appliance  Added jackscrew
Pros
• No need for compliance
Cons
3. Frankel
• Hyperactive mentalis or abnormal musculature
• Removable
• Only tissue borne appliance
 Palatal
expansion
• Widen maxillary base by expanding mid-palatal suture
• Correcting the mal-occlusion of transverse plane
Indication
• Maxillary constriction
• Posterior cross bite
• Mild crowding
• Distal molar movement
• To aid maxillary protraction

Development of palate ( from 6th week – 12th week)

1. Primary palate
• Develops from two median nasal prominces = intermaxillary segment (4 incisors also)

2. Secondary palate
• Develops in hard & soft palate posterior to the incisive foramen
• Develop from lateral palatine shelf (oriented into superio-inferior plane with tongue in
between )
• Lateral palatine shelfs elongate and fuses & tongue moves inferiorly
• On 9th week lateral palatine shelf fuses with primary palate & nasal septum in ap direction
Intermaxillary suture
• Intermaxillary suture fiber = type 3 collagen
• Mid palatine suture ossification happens from 15-19yr ( till 16yr in
female & 18yr in male )
• Closure progresses more rapidly in oral then in nasal part
• Closure  posterior part first
Classification of expansion
1. Orthodontic/dental
2. Orthopedic/skeletal
3. Passive
4. Surgically assisted rapid palatal expansion (SARPE)

Also classified as
5. Rapid  (0.5mm/day) (2-3 turns/day) (midline diastema)
6. Semi-rapid  (0.25mm/day) (1 turn/day)
7. Slow  (1mm/week) (1 turn/alternate day) (5-10lbs)
Device classification
8. RME devices
9. Slow expansion devices
1. Orthodontic / dental
• Expansion produced is dentoalveolar in nature
• Lateral tipping of crown & lingual tipping of roots
• Wide palatal base & lingually inclined dento-alveolar process = dental crossbite
• Finger spring, removable expansion plate

2. Orthopedic / skeletal
• The changes produced are skeletal in nature rather than tipping of teeth
• Results in seperation of mid palatal suture
• Narrow palatal vault & bucally inclined dento-alveolar process = skeletal crossbite
• Eg :- rapid maxillary expansion
• Bone deposited in the area of expanison  3-6months

3. Passive
• Shielding of forces from buccal & labial musculature (no active component)
• Expansion happens due to Intrinsic forces of tongue
• Aids in eruption of posterior tooth more bucally
• Appliance used  lip bumper & Frankel FR 2 (only tissue borne appliance)
Phenomenon of active stabilization
• Tongue pressure is more than buccal pressure but the pdl pressure supports the buccal pressure
Co – cr
Centric occlusion
• Bite of convinience
• Occurs with the teeth in a position of maximum inter-cuspation

Centric relation
• Position of mandible in relation to maxilla
• Condyle is relaxed & is in its terminal hinge axis (uppermost &
foremost with in glenoid fossa)
• Musculo-skeletal stable position

• CO-CR should be coincident

 CR-CO discrepency
CO-CR discrepancy
• Midline shift in  CO, unilateral crossbite
• No midline shift in  CR & bilateral constriction will be there
• We treat patient in CR

Functional shift
• Premature contact on closure which shifts mandible to one side
• Usually when we have narrow arches
EG
• premature contact of decidious canine in decidious dentiton
• Premature contact of lateral incisors in permanent dentition

• Unilateral cross bite = in bimaxillary constricted maxilla with functional

Expansion needed

• Measure maxillary inter-molar width ( MB cusp tip to MB cusp tip )

• Measure mandibular inter-molar width ( buccal groove –o buccal
groove )

MAND – MAX = EXPANSION NEEDED ( NORMAL DIFFERENCE 1.5MM)

• We add 2-3mm more for overcorrection ( to prevent relapse)
• To prevent relapse we use same appliance as retainer without
activating for 3-6months

Appliances used in differences

• 4mm or less = quad helix, arch wires, removable plate
• 5-12mm = fixed mid palatal expanders, hyrax,
• More than 12mm= jack-screw + surgery
RME / RAPID PALATAL EXPANSION
• Introduced by andrew haas
• 2 turns daily = 0.5mm expansion
• 2-3 weeks = 10mm expansion
• Rpe  creates 10-20 lbs pressure across suture

Indication
• Transverse discrepancy >4mm
• Maxillary molars buccally inclined  (compensation for narrow arch )
(true max constriction)
• Facilitate maxillary protraction in Class III cases by disrupting circum-
maxillary sutures
Contra-indicated
• Individuals past growth spurt
• Recession on buccal aspect of molars
Effects of RME
1. On dental
• Posterior teeth used as handles to transmit forces to maxilla
• Posterior teeth tip buccally
• Appearance of midline diastema, which is half of the distance by
which the screw is activated Closes spontaneously within 6
months due to trans-septal fibers traction
2. Skeletal
Maxillary
• Palatal processes separate in a triangular or wedge-shaped manner
• Maximum opening seen anteriorly
• Maximum opening towards the oral cavity with progressively less towards
the nasal aspect
Mandibular
• Mandible rotates downwards and backwards due to the downward
movement of the maxillary posterior teeth in a buccal direction Palatal
cusps of maxillary posterior teeth occlude with lingual inclines of buccal
cusps of mandibular posterior teeth = open the bite
• occlusal coverage if want to prevent  bonded expanders
Nasal cavity
• RME increases the intra-nasal space as outer walls of nasal cavity move
apart
• Improvement in nasal airflow occurs
• In young children may distort nose due to paranasal swelling and hump
Palatal expanders
1. Schwarz
2. W-arch
3. Quad helix
4. Hyrax
5. Haas
6. Transpalatal arch
1. Schwarz
• Removable
• Jackscrew expander
• Mostly dental tipping
• Only for mild dental crossbite
• Quick relapse if not worn (even one day)

2. W-arch
• Fixed
• Banded on molars
• Delivers a few 100 grams of force  slow expansion
• 1/3 skeeltal expansion
• 2/3 dental tipping
• More effective
• More comfortable
• More efficient then schwarz
3. QUAD-HELIX
• Fixed
• Like w-arch
• Four helical loops
• Capable of applying force more anterior or posterior depending on how it is activated 
Differential expansion
• Activate anterior  posterior expansion (vice-versa)
• If left for long time  leave imprint on dorsal surface of tongue
• More dental expansion 1:6

4. Hyrax expander
• Fixed
• Tooth-borne appliance
• Makes use of Hyrax screw
• 1 turn/day  100newtons of force
Pros
• Effective skeletal expansion
Cons
• Poor hygiene
• Bulky & difficult to place
5. Haas
• Fixed
• Tooth and tissue borne appliance
• Transmits forces to teeth as well as palatal shelves
• Has 2 big acrylic pads which contact palatal mucosa
• Rigid wire framework soldered to 1st premolar and molar bands
buccally & palatally
Pros
• More skeletal expansion
Cons
• Harder to clean

6. TPA (trans-palatal arch)

• Usually used for transverse anchorage (holding it steady)
Mixed dentiton
appliance
1. Nance
2. Lower lingual holding arch
3. Lip bumper
1. Nance appliance
• Upper arch
• Space maintainer or anchorage
• Maintain  A-P position for upper molars (space maintainer)

2. Lower lingual holding arch (LLHA)

• Space maintainer or anchorage
• Hold open leeway space

3. Lip bumber
• Lower arch
• Acrylic pad  agianst lower lip
• Wire into buccal tubes of molars
• Transmits lower lip pressure to molars  tipping them distally
• Relieves lower lip pressure from incisors  let them procline / tip forward
 Permanent
dentition applaince
1. Aligners
2. Braces
1. Aligners
• Clear & removable
• Series of trays are manufactured according to a priscription & worn by pt in
sequence
• Bonded attachements are often required to aid in specific tooth movement

2. Braces
• Fixed
• Earliest can be used  eruption of 1st permanent molars
• Ideal for comprehensive case  late mixed dentiton or permanent dentition
Steps
• Enamel prophylaxsis / cleaning  pumice removes pellicle & enhance wettability
• Etch  micro-pores  for micromechanical bonding
• Prime  conditions enamel & chemically bonds to resin which is placed onto
bracket
• Bracket positioning  centre of the crown, cure adhesive resin
Ortho planning
 What to do ?
Extraction Non-extraction
• Sever crowding • Mild crowding or spacing
• Minimal overbite or openbite • Deep bite
• Full protrusive lips • Flat retrusive lips
• Acute naso-labial angle • Obtuse naso-labial angle
• Anterior recession or minimal
attached gingival tissue
• Camoflage
 Stages of
comprhensive
treatment
1. Alignement & leveling
• Straigtening teeth
• Curve of spee leveleing
• Improve over bite

2. A-P correction & space closure

• Molar relationship
• Space closure

3. Finishing & detailing

• Correct root tipping
Adult treatment
• No growth modification
• More likely to request cermaic, lingual, invisible braces
• Correct periodontal health before ortho treatment
• Steel ligatures retain less plaque then elastomeric ligatures
Retention
• Retention is needed to prevent relapse
Causes of relapse
1. Elastic recoil
• Teeth return to its original position
• Takes time  for bone to mature and soft tissue to adjust

2. Differential jaw growth

• Growth of mandible in late life can cause relapse
1. Elastic recoil
• Allow time for reorganization of soft tissue
• PDL fibers  3 - 4 months (full time retention )
• Gingival fibers  4 - 6 months (night time wearing)
• Supracrestal fibers  1yr (night time wearing)

Supracrestal fibrotomy
• Severing supracrestal gingival fibers
• Done in severe rotation cases (rotated max lat incisors)
2. Differential jaw growth
• Due to late mandibular growth
• Comprehsnive treatment  age 12 (18-30month treatment
duration)
• Late  AP (end at mid teenage) & vertical growth (late teens or
early 20s) can cause relapse

• Moving teeth excessively  disrupting tissue equilibrium =

relapse
Appliances
1. Hawley retainer (upper)
• Most common
• Acrylic plate  connects all, can build ant bite plate for overbite
correction
• Labial bow  incisor retention
• Adams clasp  molar retention

2. Hawley retainer (lower)

• Wrap around – clip-on retainer
• Acrylic  lingual
• Labial bow / plastic clip-on bar reinforced with wire  from 3-3
3. Vacuum formed
• Clear – transparent
• Separation in posterior teeth may develop

4. Lingual bonded retainers

Indicated
• Moved lower incisors forward  2mm
• Diastema of upper incisors
• Flexible wire  bonded to each tooth
• Rigid wire  only two teeth (usually lower canines or upper
centrals)
• Mandibular bonded  canine to canine
• Palatal bonded  usually not used, indicated in diastema
Relapse of class
2
Overcorrection
• 1-2mm of occlusal realtionship during finishing --> specially
when elastics were used
• The more severe the class 2 = more relapse
• Younger the pt was during debond = more relapse
• Can cosnider  headgear + bionator + full time retention
Relapse of class
3
Overcorrection
• 1-2mm of occlusal realtionship during finishing  specially when
elastics were used
• Continious mNdibular growth is very likely & extremely difficult to
control
• Surgical correction after growth has fully expressed itself
Deep bite
relapse
• Prevent  over-eruption of lower incisors
• Upper hawlay + anterior bite plane
Open bite
relapse
• Prevent  incisors intrusion
• Prevent  molar extrusion
• Hawlay + posterior bite block
• Vacuum formed with thickend plastic over posterior teeth  jaw
sepration
 Surgical
orthodontics
Orthognathic surgery is indicated
• When orthodontics alone can not work
• For severe skeletal discrepency
• Class 3, open bite, asymmetry
Antero-Posterior
correction
1. Lefort 1
Maxillary advancement
• To correct class 3
• Overcorrection
• Bring maxilla forward

Maxillary setback
• Bring maxilla backward
• To correct class 2

2. BSSO (bisagital split osteotomy)

• Cuts through mandibile through one side or both avoiding IAN to reposition corpus of
body of mandible

Mandibile advancement
• To correct class 2
Mandible setback
 Vertical
correction
1. Lefort 1
Maxillary superior repositioning
• For open bite
• To shorten face
• Move maxilla up causes mandibile to rotate to close even more

Maxillary inferior repositioning

• To correct deep bite
• To lengthen face
• Move maxilla down causes mandibile to rotate to open even more
Transverse
correction
1. Sarpe (surgical assisted rapid palatal expansion)
• Maxillary expansion
• Done when suture not closed
• If closed then cut it open & traction of maxilla

2. Maxillary constriction
3. Mandibular expansion (mandibular symphysis distraction
osteogenesis)
4. Mandibular constriction
Genioplasty
1. Sliding genioplasty
• Moving chin in all three direction
• Submental cut
• Less chance of relapse to most
Envelops of
discrepency
• Describes the amount of change that can be achieved
1. Orthodontically moving teeth
• Ideal values we can move teeth
2. Changing the growth of jaws
3. Surgically repositioning the jaw
 Post op
complications
1. BSSO
• Damage to IAN  parasthesia
• Condylar sag  relapse (more with osteotomy with distraction
osteogenesis)
• Swelling
• Infection
• Bleeding

2. General anesthesia
• Alectasis  collapse of portion of tongue, fever
• Pneumotosis intestenalis  air in intestines, fever
Pediatric
dentistry
 Tooth
development &
eruption
 Odontogenesis

1. Inititation
• 6 weeks in utro
• Oral epithelium  outer layer , mouting covering
• Dental lamina  thickening in the oral epithelium, it is first evidence of
forming, budding tooth
• Ectomesenchyme  signal oral epithelium to proliferate into dental
lamina

• Oral epithelium & dental lamina  ectodermal origin

• Ectomesenchyme  ectodrmal  neural crest
2. Bud stage
• 8 week in utro
• Dental lamina  proliferate & invade underlying mesenchyme &
forms buds
• Buds  called dental placodes
• Mesenchyme starts condensing under buds  condensing
mesenchyme

• All primary teeth & permanent molars only  arise from dental lamina
• Permanent canine, incisors & premolars  arise from there
predecessor (secondary buds)

• Excessive budding  extra tooth

• No budding  missing tooth
3. Cap stage
• 9 weeks in utro
• Bud proliferates more
• Each dental placode changes to  enamel organ (enamal organ creates enamel)

Layers of enamel organ

• OEE (outer enamel epithelium) outer cell layer
• IEE (inner enamel epithelium)  inner cell layer
• Stellate reticulum  cells b/w OEE & IEE
• Enamel knots  areas of focal thickening in IEE (cusp tips) (also signaling
center)

• Condensed mesenchyme aggregate & form  dental papilla

• Dental papilla  dentine & pulp
• Dental follicle  sac which surrounds enamel organ & dental papilla
4. Bell stage
• 11 weeks in utro
• Two phases here

a) Histo-differentiation
• Transformation into distinct cell type
• IEE  ameloblast (tall columnar)
• Dental papilla  odontoblast (tall columnar)
• Defects here  amelogenesis & dentinogenesis imperfecta

b) morpho-differentiation
• Size & shape of crown determined here
• Defects  shape & size abnormalities  peg lateral, macrodontia
5. Apposition
• 14 weeks in utro
• Odontoblast  deposit dentine matrix (collagen)
• Dentine matrix signals ameloblast to secrete  enamel matrix
(amelogenin)
• Cervial loop then extends / elongates  junction where IEE & OEE
meet)
• Extension is called  HERS (hertwigs epithelial root sheath)
• HERS stimulate odontoblast to secrete  radicular dentine
• HERS disintegrate  leaves behinde some clusters called
epithelial rests of malassez

• IEE + OEE  REE (reduced enamel epithelium)  junctional

epithelium
6. Maturation
• Also known as calcification / mineralization
• 14+ weeks in utero
• Longest stage
• Deposition of enamel & dentine
• Calcification beings at  tips & edge & move cervically
• Takes 2 yrs for primary tooth crown
• Takes 4-5 yrs for permanent tooth crown

• Defects  enamel hypomineralization, fluorosis (14 week – 8 yrs ),

tetracycline staining (14 week – 8 yrs )
Eruption
In Months

NXI
• Rule of 4:4
• 4 teeth every 4 months
• Starting with 7 month with 4 teeth erupted
In years 10yrs
1st premolars MAIN
• 6 yrs 10.5  upper 2nd premolar TEETH IN FEMALE ERUPT EARLY
2-3 RULE (2/3 ROOT
1st molars DEVELOPMED)
11 yrs
Lower central
Upper canine
Lower 2nd premolat
• 7 yrs Lower 2nd molar
Upper central
Lower lateral 12 yrs
Upper 2nd molar
8 yrs 17 yrs
Upper lateral 3rd molars

9 yrs
Developmental
disturbances
1. Abnormalities of morpho-differentiation
• Anomalies in size, shape, number
2. Abnormalities of histo-differentiation
• Anomalies in structure

• Dental follicle cells  osteoblasts & fibroblasts PDL

• IEE ameloblast
• Dental papilla cell odontoblasts
• Epithelial rests of malassez cementoblasts
• Dental lamina remains (epithelial pearls) gives rise to
supernumery tooth, odontomes, eruption cyst
Anomalies of number
1. Anodontia
• No/absence of teeth
Types
• Complete  all teeth missing
• Partial/hypodontia  one/more teeth missing
• Pseudo  teeth absent clinically due to impaction or late eruption
• False  teeth exfoliated or extracted

Congeintally missing permanent tooth

• Thirdmolars
• 2nd mandibular Premolars
• Maxillary lateral incisors
• Maxillary 2nd premolar
• 2nd premolar missing  close space with extraction therapy &
make symmetrical
• Lateral incisor  canine subsitution or prosthetic

Commonly missing primary tooth

• Primary Maxillary lateral  conginitally missing

Most common primary ankylosed tooth

• Primary lower 2nd molar
2. Hypodontia
• Lack of development of  1-5 teeth
• Common in permanent teeth (females)
• Maxillary lateral incisor, mandibular 2nd molar
• Third molars not included
2. Downs syndrome
• It is a condition in which a child is born with an extra copy of their 21st
chromosome — hence its other name, trisomy 21. This causes physical
and mental developmental delays and disabilities
3. Crouzans syndrome
• Craniosynostosis  premature fusion of skull bones
• Bulging eyes, underdeveloped under jaw
• Increased distance between orbits
5. Ellis-van-creveld syndrome
• Disorder of bone growth  results in dwarfism
• Extra fingers and toes
• Malformed finger nails and toe nails
• Heart defects
• Weyers acrofacial dystosis  caused by defects in same gene (Weyers
acrofacial dysostosis is a disorder that affects the development of the teeth,
nails)

6. Orol facial digital syndrome

3. Oligodontia
• Missing  6 or more teeth
• Third molars do not count

Syndromes associated
1. Hypohidrotic ectodermal dysplasia
• Rare (x-linked) (congenital absence of ectodermal structures)
• Small and pointed teeth (vampire like)
• Absence of sweat glands  hyperthermia
• Sparse hair and scalp, Promoinent fore-head, thick lips & a
flattened bridge of nose
Most common missing teeth
• Third molars  2nd mand premolars  max laterals

Primary max laterals

• Most common missing toot in kids
4. Hyperdontia
• Supernumerary teeth (extra teeth)
• 3% population
• Usually single (common in permanent teeth) (females)(maxilla)
• Develops in  anterior and molar region of maxilla, pre-molar region
of mandible

Causes
1. Continued proliferation of primary/permanent dental lamina
2. Second tooth bud
3. Splitting of a regular tooth bud

Classification
• Shape
Shape
• Conical (vampire jesa)
• Tuberculate/ barrel shapped
• Supplemental  normal tooth shape and size

Position
• Mesio-dens  extra teeth on anterior region, b/w maxillary central
incisors (most common)
• Para-molar  situated buccaly/palatally around molar (maxillary
molar usually buccal side ) ( 2nd most common)
• Disto-molar  distal to 3rd molar
Clinical implications
• Esthetics is affected
• Malpositioning of teeth
• Area of plaque and calculus retention

Sets of dentition
1. Diphyodent
• 2 sets of teeth
• Mammals, humans

2. Polyphydont
• Many sets
• Sharks & crocodiles
Syndromes associated

1. cleido-cranial dysplasia
• Genetic, affects bones and teeth of people
• More fragile bone (face, spine, skull, collarbones, legs)
• Collarbone may be absent

2. Clept lip/palate
3. Gardeners syndrome/Familial adenomatous polyposis (FAP)
• Caused by mutation in apc gene
• Colo-rectal polyps, tumors (benign & malignant)
• Osteomas of jaw
• Skin cysts and fibromas
• Abnormal root formation
• Impacted teeth other than third

4. oro-facial digital syndrome

Anomalies of size
1. Micro-dontia
• Teeth smaller then normal
• Bell stage defect
Types
• Generalized all teeth due to  pituitary dwarfism, ectodermal
dysplasia, downs syndrome

• Localized  one teeth  maxillary lateral incisors most common

(peg laterals) (autosomal dominant trait)
• 2nd most common  maxillary 3rd molar
2. Macro-dontia
• Teeth larger then normal
• Bell stage defect
Types
• Generalized  due to pituitary gigantism, pineal hyperplasia with
hyper-insulism, rabson mendenhall

• Localized  hemifacial hyperplasia/hypertrophy , common in

mandibular 3rd molar
3. Double teeth
• Two teeth appeared joined together
• Crown, root or both
• United by enamel, cementum, dentine & pulp chamber
• Common in primary teeth  incisors & canine
Etiology
• Unknown
• Trauma, crowding of teeth
1. Gemination
• Bud divide to two  2 crowns, 1 root & 1 canal
• Affects anterior teeth
• Cap stage
• Normal tooth count when abnormal tooth counted as one
 normal count
Causes
• Single tooth bud divide into two teeth/ partial division or twinning
of single tooth germ
2. Fusion
• Two developing teeth join together to form one  2 tooth
germs
• Cap stage
• Common in primary teeth  anterior
• Missing teeth when abnormal teeth counted as one  one
less than normal
Fusion before calcification  all component of teeth fuse
Fusion after/ later stage  2 separate crown & fused roots
Pattern of dentition
1. Hypsodontia
• Tall crown
• Cows

2. Brachydontia
• Short crowns
• Dogs, cats, humans
Anomalies shape of
teeth
1. Dilaceration
• Curving or agulation of tooth roots
• Tooth severly bent along its long axis
• Causes  trauma to primary tooth  causing bent in permanent
tooth
Clinical significance
• Difficult extraction
• Root canal filling hard
2. Taurodontism
• Bull like tooth
• Furcation moves apically down
• Affects multi-rooted teeth
• Enlarged pulp chamber radiographically (increased apical-
occlusal height)

Causes
• Failure of hertwigs root sheath to invaginate at horizontal level
• Klinefelter syndrome (mardon ma larki jese alamat) (x chromosome in
male)
• Poly x-syndrome (extra x chromosome in female)(taller than normal,
learning difficulties, delayed development of speech & language skills)
Linked to
• Type 4 amelogenesis imperfecta
4. Dens evaginatus
• Developmental anomaly  extra cusp (contains all
dentine, enamel, pulp)
• In incisors  talons cusp
• In lower premolars  leongs premolar
• Cusp like supernumerary focal enamel protrusion on
occlusal/lingual surface of crown
Pathogenesis
• Proliferation of area of IEE & odontogenic mesenchyme into
dental organ during early tooth development
• Cap stage
5. Dens invaginatus/ dens in dente/ tooth with in a tooth
• Exaggeration/accentuation of lingual pit
• Common in permanent maxillary lateral incisor
• Bilateral
• Predisposes tooth to early caries and pulpitis  via tunne
• Prophylactic filling of pit recommended
• Invagination IEE
• Need xray to diagnose
Anomalies of
structure
Disturbance in
enamel
Development of enamel

1. Secretory stage  amleoblasts produce matrix (amelogenin,

enamelin, ameloblastin, tuftelin )
• Any disturbance here  deficient matrix production = hypoplastic
enamel
• Pits and groves on enamel surface  clinically
• It a quantitative defect

2. Maturation stage calcification of matrix

• Disturbance here  deficient mineral deposition
• Soft hypomineralized enamel  white/opaque pigegmented buff
and orange & brown quickly chipped and worn off
• It a qualitative defect
Extent of enamel defects depends on
1. Intensity of causative factor
2. Duration of the factors presence
3. Time at which factors occurs during crown development

Ateiology
4. Local
• Infection, trauma, radiotherapy, idiopathic

2. General

Environmental/ systemic
• Pre-natal infections (rebella, syphillis), maternal disease, excess fluoride
• Post-natal severe childhood infections, chronic disease, nutritional deficiency, cancer (chemo)
• Neo-natal hemolytic disease of newborn, hypocalcemia, premature/prolonged labour

Genetic
• Teeth affected only amelogenisis imperfecta
• Teeth affected in association with generalized defects  ectodermal dysplasia syndrome, downs
syndrome
1. Enamel hypoplasia
• Undereveloped enamel
• Less then normal number of cell
• Failure in apposition stage  enamel matrix formation
• Normal quality but deficient quantity
• In children with hypoparathyroidism

a) Turners hypoplasia
• Peri-apical infection or truma to primary tooth  inflammation  messes up
ameloblast of developing permanent tooth
• Facial of incisors & premolars

b) Congenital syphillis
• Permanent incisors screw driver appearance (mesial and distal side tapers)
hutchinsons incisors  hypoplastic notch
• Permanent 1st molar  globular mass on occlusal surfaces mulberry
2. Enamel hypocalcification
• Abnormal mineralization  white spots
• Failure in maturation stage
• Normal quantitiy but defective quality
• Chalky teeth  yellow – brown
3. Amelogenisis imperfecta

• Disorder of enamel formation intrinsic alteration of enamel

• Affects both dentition
• Heterogenous group of heridetery disorder
• Mutation in enamel proteins enamelin & amelogenin
• Normal pulp & dentine  no / thin enamel
• During bell stage
• In radiograph  u will see teeth similar to crown pre

Gentic disorder & inherited as

• Autosomal dominant (common)
• Autosomal recessive
• X-linked dominent

Tretament
Types (not for inbde )
1. Hypoplastic
2. Hypocalcified
3. Hypomineralized/hypomaturation
1. Hypoplastic type
• Insufficient matrix
• Insufficient amout of enamel
• Less than normal thickness
• Thin and glossy enamel (hard)
• Abnormal contours and absent interproximal contacts

Appearances
a) Rough form
• Localized areas of hypoplastic randomly distributed
Produces
• roughness and piting (generalized)
• Irregular vertical grooving & wrinkling

b) Smooth form
• Whole enamel defected
• Sharp needle like cusps
2. Hypocalcified type
• Common
• Noraml teeth, shape, size, thickness
• Soft chalky consistency of enamel (enamel easyily chipped away
leaving dentine exposed)
• Readily lost by abrasion and attrition
• Teeth worn down to gum level
• Dentine easily stained

3. Hypomaturation type
• Normal thickness on eruption but soon after exposure  opaque,
brownish-yellow to white apperance
• Soft enamel & attrition
• Snow capped appearance (incisal third and occlusal third)
Defects in
dentine
Aetiology
• Mostly genetic
• Some environemental/systemic distturbances affection calcium
metabolism or calcification
Local causes
• Trauma = turner teeth/hypoplasia
General
• Dentinogenesis imperfecta
• Dentine dysplasia
• Regiional ondotodysplasia
• Environmental/systemic
1. Dentinogenesis imperfecta
• Both dentitions
• Male & female
• Mutation in  sialo-phospho protein gene (dspp)
• Autosomal dominant disorder
• Intrinsic alteration of dentine
• Bell stage

Clinical features
• Opalescent  On eruption teeth has normal contour but an opalescent amber appearance
• Short roots
• Tulip/ bell shaped crown
• Obliterated pulp  no pulp cavity
• Bulbous crown due to  constricted DEJ
• Blue sclera
• Greyish to brown appearance
• Dentine soft
• Enamel fracture due to less dentine support
• Absent scalloping b/w DEJ
Microscopically
• Few and large irregular dentinal tubules
• Smooth DEJ  no scalloping
• Increased water content, decreased mineral content
• Decreased caries

Treatment
• Full crown  esthetics
Types
Type 1
• syndrome associated (osteogenesis imperfecta)(involves
bone)(teeth and other systems involved)
• Primary dentition severly affected
• Opalescent teeth
• Mutation in gene that encode collagen type 1
• Blue sclera of eyes

Radiographically
• short, blunt roots with obliteration by dentine
Type 2
• most common(not associated with any syndrome)(only involves
teeth)
• Mutation in dspp gene
• Both dentitions
Radiographically short, blunt roots with obliteration by dentine

Type 3  in specific race (region around bradywine in southern

maryland america)
• Decidious teeth (multiple pulpal exposures)
• Related to type 2
• Rare
Radiographically  thin dentine(thin dentine shell teeth), root
canals & pulp chambers extremely large
2. Dentine dysplasia
• Autosomal dominant (rare)
• Interinsic alteration of dentine
• All teeth  both dentition

Types

a) Type 1/ radicular dentine dysplasia

• Root less
• Normal color and shape of crown (both dentition)(crown with
dysplastic dentine with calcified bodies)
• Obliterate pulp
• Sometimes fragments of residual pulp horizontal lucencies (chevrons)
• Peri-apical lesions
• Short roots
b) Type 2

• Change in color of primary tooth  opalescent

• No change in color of permanent dentition  normal
• Large coronal pulps  thistle tube apperance/ chevron
shaped)
• Varient of dentino-genesis imperfecta
• Mutation in sialo-phospho-protein
3. Regional odontodysplasia/ ghost teeth

• Rare
• Both dentitions
• Abnormalities of dentine + enamel + dental follicle
• Affects ameloblast + odontoblanst + cementoblast
• Aetiology  unknown

Clinically
• Irregular teeth shape with hypoplastic enamel
• Thinner dentine
• Pulp stones
• Short roots and wide-open apices
• Enlarged pulp chambers
Radiographically
• Less radio-opacity of teeth with no difference b/w enamel and
dentine
• Pulp stones
• Thin enamel & denitne
• Poor contrast
• Short root open apices

Treatment
• Let them erupt  bring alveolar bone
• Extract affected teeth
 Difference
Amelgenisis imperfecta Dentinogenesis imperfecta
• Disorder of enamel formation • Autosomal dominant disorder
• Affects both dentition • Both dentitions
• Mutation in enamel protein • Male & female
anamelin & amelogenin
• Mutation in  sialo-phospho
• Autosomal dominant (common) protein gene (dspp)
Clinically Clinically
• smaller-than-normal teeth
• Opalescent
• yellow or brown discoloration of the
teeth • Bluish-grey, brownish, yellowish
• teeth that are prone to damage • Dentine soft
and breakage • Enamel fracture due to less
• sensitive teeth dentine support
• Thin enamel • Absent scalloping b/w DEJ
• Enamel lost by abrasion & attrition • Tulip/ bell shaped crown
 Detine dysplasia Dentinogenesis imperfecta
• Autosomal dominant (rare) • Autosomal dominant disorder
• Root less • Both dentitions
• Normal color and shape of • Male & female
crown (both dentition)(crown • Mutation in  sialo-phospho
with dysplastic dentine with protein gene (dspp)
calcified bodies)
Clinically
• Obliterate pulp
• Opalescent
• Sometimes fragments of
residual pulp horizontal • Bluish-grey, brownish, yellowish
lucencies (chevrons) • Dentine soft
• Peri-apical lesions • Enamel fracture due to less
• Short roots dentine support
• Premature tooth loss • Absent scalloping b/w DEJ
• Tulip/ bell shaped crown
4. Concrescene
• Acquired disorder
• Roots of one or more teeth united by cementum only
• Permenant dentition (maxillary 2nd and 3rd molar)
• Inference with extraction or eruption

Etiology
• Trauma
• Crowding
• Hypercementosis (excess production of cementum)

Pathogenesis
• Trauma to jaw  loss of interdental bone  roots of neighbouring teeth come closer
and join due to cementum

Clinical significance
• Extraction of two teeth when single was intented
5. Enamel pearls
• Droplet of enamel on the roots
• Chunk of enamel  blocking attachment of sharpys fibers
• Can be on Furacation of roots
Maxillary permanent molars  only in molars
• Can not come off scaling
• Periodontal pocket
• Symptomless  1-3mm radiopaque round
• May lead to root caries, pulpitis, external resorption
6. Supernumerary roots
• Extra roots
• Common in mandibular canine, premolar & molars(3rd)
• Rare in maxillary anterior and mandibular incisors
Disturbance in
cementum
Cementum
• Calcified substance (attaches tooth to alveolar bone by anchoring
PDL)
• Covers roots
• Avascular
• Cementoblasts
• Cellular & acellular
1. Hypercementosis
• Excessive cementum deposition
• Bulbous roots
• No pain
Associated with
• Anklyosis
• Concrescene
Causes
• Periapical inflammation
• Mechanical
• Functionless and enerupted teeth
• Pagets disease of bone
2. Hypocementosis
• Lack of cementum in tooth
• Uncommon
Seen in
• Cleido-cranial dysplasia
• Hypophosphatia
Abnormalties of
dental pulp
1. Pulp calcification
• Calcified masses of tissue present in pulp chamber & roots of teeth
• Increase with age
• Can be microscopic or large
• Aetiology unknown
classification
1. Diffuse or linear
• Found in root canals parallel to vessels
2. Nodular (stones)
• Found in pulp chamber (denticles)
Types
• True denticles composed of dentine and lined by odontoblasts
• False denticles  formed from degrading cells which mineralize (no
tubular structure)
3. Free
• Surrounded by pulp tissue
4. Attached
Resorption
1. Physiological
• Occurs naturally as shedding of decidious teeth
• Normal developmental process
Pathological
 External
• Initiated in periodontium affecting the external root surface
• Starts at root level
Inflammatory resorption
• Peri-apical inflammation
• Reimplantation/transplantation of teeth
Pressure/mechanical
• Orthodontics
• Pressure by cyst or tumor
Idopathic
• Burrowing type of resorption
• Common  cervical area
Internal
• Dentine & pulpal wall begins to resorb centrally within the root
canal
• Associated with  pulpitis
• Clinically  pink spot on teeth when coronal dentine is resorped
Discoloration of
teeth
Discoloration of teeth
1. Exogenous/extrinsic stains
• Stains of the surface of teeth which can be removed by
abrassives
Causes
• Bettel nut, tobacco
• Chromogenic bacteria brown, black, green, orange stains
(orange stains mostly in children)(brown and black seen on
cervical zone of teeth)

2. Endogenous/intrinsic stains
• Dicoloration of teeth resulting from deposits of systemically
circulating substance during development
2. Changes in color due change in structure
• flurosis
• Amelogenisis imperfecta
• Caries
• Dentinogenesis imperfecta, dentine dysplasia type 2
• Enamel opacities
3. Diffusion of pigments into dental tissue after formation
• Extrinsic stains
• Restorative material (amalgam)
• Pulp necrosis products
4. Pigments incorporated during teeth formation
• Bile pigments  green/brown color of teeth (congenital hyperbilirubinia)
• Porphyrins teeth red fluoresence under UV light (congenital porphyriaporphyrin not
metabolized properly)
• Tetracyclin newly erupted teeth yellow by the time oxidies then grey &brown
(tetracylin can cross placenta)(binds to ca & gets deposited in teeth/bone)(both
dentitions)
• Minocyctine hydrochloride  synthetic derivative of tetracyclin(stains roots of adult
Non-bacterial loss of tooth
structure
1. Resorption
2. Tooth wear
Attrition
• Tooth loss due to tooth to tooth contact
• Rate of attrition more in dentine than enamel
Physiological
• With age (constant pattern)
• Incisal edge of incisors  occlusal surface of molars  palatal cusp of maxillary
teeth  buccal cusp of mandibular teeth
Pathological
• Abnormal occlusion  developmental, extraction
• Bruxism  grinding teeth & jaw clenching
• Bettel nut/ tobacco chewing
• Abnormal tooth structure  amelogenesis & dentinogenesis imperfecta

Attrition  exposure of dentinal tubules formation of reactionary

dentineformation of translucent zoneformation of dead tracts  hypersentivity
Abrasion
• Pathological wearing of tooth surface by friction of foreign body which is
independent of occlusion
• Maxillary teeth more involved
• More pronounced on labial cervical region of incisors, canines and premolar
• Right hand side people left teeth involved (vice-versa)
• Wedge shaped lesions
Tooth brush abrasion
• Common
• Seen on exposed surfaces of root
• Due to horizontal brushing
• Gum recession

• Habitual abrasion pipe smokers

• Occupational abrasion  pen,pencil (object held b/w teeth)
• Ritual abrasion  mostly seen in African tribes
Erosion
• Loss of tooth surface due to chemical contact
Dietry erosion
• Acidic drinks and citrus fruits
• Gingival third of teeth involved
• Common  labial surface of max incisors
• Clinically  shallow broad concavities with polished surfaces
Occupational erosion
• Seen in workers in contact with acid (lead battery makers)
• Incisal third of the incisors (labial)
Regurgitation erosion
• Due to vomiting and stomach contents regurgitation (generalized tooth loss of lingual
surface of maxillary tooth)
• Palatal surfaces of maxillary teeth
• Associated with anorexia nervosa & bulimia nervosa
Idopathic
• Saliva of these patients have high citric acid and mucin content
Primary teeth
anatomy
watch video
• Thinner enamel
• Bigger pulp
• Whiter
• Occlusally directed enamel rods
• Cervical buldge  at primary 1st molar (cervical ridge)
• Divergent roots
• Small or absent root trunk
Primary teeth
treatment
Amalgam for primary teeth
• Cavity prep
• 1.5 mm depth
• Extend into susceptible pits & fissure
Sock prepartion
• Rounded line angles
• Smooth flat pulpal floor
• 90 degree cavosurface margin
• Isthmus  1/3 inter-cuspal width
Composite preparation
• More conservative
• Require dry, isolated field
• Common area of failure  gingival margin
S.S crown
• For extenssive caries  passed axial line angles
• 1 mm occlusal reduction
• Seat from lingual to buccal
• Cervical bulge provides retention
• Never used for permanet restoration
Strip crown
• For primary incisors with proximal caries
• Good choice  if adquate tooth remaining for bonding & for
easthetics
• Celluloid crown form with one hole  lets composite flow
• Caries decides crown prep
• 1mm incisal reduction
Endodontic size
& symptoms for
primary teeth
• Pain & sensitivity
• Mobility
• Abscess / fistula
• Furcation radiolucency = primary pulpal necrosis
• Root resorption  patholoigcal vs physiological
Indirect capping
• Procedure where in the deepest layer of remaining affected carious
dentine is covered with the layer of biocompatible material in order to
prevent pulp exposure & further trauma to the pulp
Objective
• To preserve the vitality of pulp by completely removing the carious
infected dentine & place material to enable affected dentine

Indication
• Deep carious lesion
• No history of pain
• On signs of irreversible pulpitis
• Excessive tooth removal  pulp visible through remaining thin dentin
layer (pink red)
• No exposure
• Normal lamina dura & pdl
• No radiolucecny peri-apically
Contrainidcation
• Severe pain – Irreversible pulitis
• Exposure
• Mobilty
• Negative to pulp test
• Break in lamina dura
• Periapical radiolucency

Material
• Calcium hydroxide
• RMGIC
1. La

2. Isolation

3. Step wise excavation

• Caries removed in increments in two or three appointments over
fews months – year
• Every time carious excavated  followed by gic base & temporary
restoration
• This approach avoids the unwanted exposure
• Remove carious lesion in increments & properly
• Caoh2  temporary filling material
4. Wait for 3-8 weeks
5. Asymptomatic  go for pulp capping
1. La
2. Dubber dam
3. Carious removal
4. Caoh2
5. Rmgic
6. Filling
Direct capping
• Procedure in which exposed vital pulp is covered with a
protective dressing or base placed directly over the site of
exposure in attempt to preserve pulp vitality

Objective
• Create new dentine in area of exposure & subsequent healing

Material used
• Calcium hydroxide  may cause internal root resoprtion in
primary teeth

Causes of exposure
• Accidental exposure
 Indication Contraindication

• Asymptomatic • Severe tooth ache at night

• 0.5mm or small (pin-point • Size larger then 0.5mm
lesion) • Tooth mobility
• Hemorrhage easily controlled • Excessive uncontrolled
• Exposure occurred is clean & hemorrhage
not contaminated • Serous exudate
• Atraumatic exposure • Swelling/fistula
 Procedure

1. Pulp exposure
2. Anesthetize & dubber dam
3. Irrigation  saline or distalled water
4. Hemostatis  6% naoh

Two techiques can be used from here

5. Caoh2
6. Mta
Caoh2 technique
• Place  CaOH2 on the exposure site
• Over then RMGIC filling
• Then final restoration  composite/amalagam

MTA technique
• We have 2 approaches
a) Place MTA  RMGIC  restoration
b) Place MTA  moist cotton pellet  unbounded coposite (interim
filling)  after 5-10days call patient  remove everything  final
restoration
Pulpotomy
• Complete removal of coronal portion of dental pulp followed by
placement of suitable medicament to preserve pulp vitality
• Mostly done in primary teeth

Objective
• Remove coronal inflammed pulp
• Maintain tooth vitality  radicular pulp

Indication
• Carious lesion  involving coronal pulp only
• Mechanical exposure
• Reversible pulpitis
Contraindication
• Irreversible pulpitis
• Fistula
• Swelling
• Uncontrolled bleeding
• Periapical / furcation radiolucency
• Mobility
• Root resorption

Types
1. Vital
a) Devitalization / mummification
b) Preservation / minimal devitalization
2. Non vital
• Also called mortal pulpotomy
• Material used  beechwood cresol
• Not imp for inbde
Devitalization
1. Single sitting 
2. Two stage 

Preservation
• Material used  zoe, ferric sulphate, glutaraldehyde

Regenrative
• Material used  Caoh2, mta, bmp, collagen, freeze dried bone,
osteogenic protien
Single visit
1. La
2. Rubber dam
3. Carious removed
4. Deroofing of chamber
5. Remove coronal pulp  spoon excavator
6. Cleaned with saline  to remove debris
7. Dry Cotton pellet placed  hemostasis
8. Diluted formacresol dipped in cotton pellet placed  5 minutes
9. Dry cotton pellet placed over this  to avoid contact of formocresol to
other tissues
10.Remove formacresol  check for brownish discoloration (pulp fixation)
11.Zoe placed  and called for next appointment after week
12.Asymptomatic tooth  filling (ZOE )
13.Crown placement  ss crown
2 visit
1. La
2. Rubber dam
3. Carious removed
4. Deroofing of chamber
5. Paraform paste placed with cotton pellet
6. Tooth sealed for couple weeks
• In mean time formaldehyde gas is produced inside  going to coronal & radicular pulp 
fixation
2nd visit
1. La
2. Rubber dam
3. Temporary filling removed
4. Cotton pellet removed
5. Clean with saline
6. Antiseptic paste
7. Permanent restoration
8. Crown ss
Fromacresol
• Prevents tissue autolysis
• Fromacresol  used to prevent decompostion of dead
bodies

Disadvantage
• Cytogenic  toxic to other tissue
• Mutagenic  cancer
• Carcinogenic
• Systemic distribution

Ferric sulfate
• Hemostasis
•
Pulpectomy
• Bascially rct  For primary teeth
• Obturation  ZOE
• CI  1st primary molars due to multiple accesory canals (not
successful)

• Hardest tooth to save with endo  primary 1st molar

• Best tooth to save with endo for space maintainer 
primary 2nd molar
Extraction
• First primary molar mostly  necrotic
• Unrestorable
• Mobile
• Root resoprtion

Exception
• 2nd primary molar with mild – moderate root resorption in
young
• Saved by endo therapy  then used as space maintianer
 Pulpectomy

Pulpotomy
 Space
management
1. Primate space
• It’s a feature of primary dentition
• Physiological space present between teeth
• Most noticeable space
• Present between b & c in upper arch  mesial to canine
• Between c & d in lower arch  distal to canine
• Best utilized in lower
• Lost up till the age of 6  with eruption of 1st permanent molar

2. Leeway space
• Difference between the sum of the mesiodistal crown widths of the primary
canines and molars & the permanent canines and premolars
• Upper arch  1.5 for inbde
• Lower arch  2.5 for inbde (sabse zyada 2nd primary molar se ati
hai)
• By 11-12yrs this space is lost  with exfoliation of E & eruption of
3. Interdental spaces
• Present between incisors
• These spacing are required for proper alignment of permanent
incisors
• Naturally occurring during transition from primary to
permanent  due to growth & expansion of dental arche
• Age  7 – 11
 Timing
Space management
• proactive
• Manage & hold leeway space before primary teeth are lost

Space maintainence
• Reactive
• We maintain space after premature loss of primary tooth

Space regaining
• Retroactive
• After loss of space
• Regain  max of 3mm
Primary incisors loss a & b
• Not a big deal
• Not common
• Ma cause localized space lose
Use
• Kiddie partial  speech, easthetics
 Loss of Primary canine c
• Cause lingual collapse of incisors  loss arch length
Tx
• Lower lingual holding arch  wait till lower incisors erupt
• Nance appliance

Arch length
• Distace from the contact poinnt b/w central incisors to the mesial
contact point of permanent 1st molar
 Primary 1st molar loss d
Tx
• Band & loop  crown or band on permanet 1st molar or primary
2nd molar e
• Lingual holding arch
• Nance
 Primary 2nd molar loss e
Tx
• Distal shoe  from d to unerupted 1st molar
• Lingual arch or nance  if permanent 1st moalr erupted
Eruption timing
variation
1. Lower 2nd permanent molar erupts ahead of 2nd premolar
• It would utilizie leeway space & no space left for premolar
• Use space maintianer  lingual arch

2. Upper canine ahead / alongside 1st premolar

• Canine forced labially
• Vampire fang

3. Asymmtery b/w right & left side

• 6 months is normal
• Extract primary contralaterla if early exfoliation  to keep midline
Amount of root
development
• No space maintainer need if  bone bone b/w primary &
permanent
• Eruption movement begin  crown completion
• Tooth pierces bone 2/3 root developed
• Tooth pierces gingiva  ¾ root developed

Rule of 7
• Primary molar lost before age 7  delayed premolar
eruption
• Primary molar erupt after age 7  accelerated premolar
eruption
Space closure
• Occurs within first 6 months of tooth loss
• Tipping  not bodily movement
• Active eruption of neighbouring tooth  increase in space lost
Ecoptic eruption
 Central incisors
Lingual eruption
• Resolved own its own
• Not resolved if  over retained primary incisors

Lateral eruption
• Due to early exfoliation of primary laterals
• Extract contralater primary latera  to avoid midline deviation
 Premolars
Distal eruption
• Common in mandibular 2nd premolar where it resorpt only distal
root of primary second molar = retained primary 2nd molar

Buccal / lingual eruption

• Common
• Extraction primary molar if it is not ready to exfoliate in few
weeks
 Molars
• Permanent 1st molars

Mesial eruption
• Get impacted under distal aspect of of primary 2nd molar
• Common
• Maxillary 1st molar
• Common in maxilla
Tx
• Spacer  minor 1mm enamel ledge  minor issue
• Halterman appliance  distalize 6 and correct path  major issue
Ankylosed teeth
 Primary molars
• 1 % african american
• 4 % caucasians
• More common in mandible
• Es more common then Ds

Diagnosis
• Submerged  infra-occlusion
• No mobility
• Hollow sound / metallic sound when tapped
• Radiograph  loss of pdl

Treatment
• No treatment
Peadatric soft
tissue
Healthy gingiva features
 Ginigvitis
• Verey common children and adolscent
• 70 % children  age 7
• Plaque  gingivitis  periodontitis
• Pariental participation unitl age 8 is recommeded
• Peak  puberty (swelled id papilla in anteriors)
 Acute necrotizing
ulcerative gingivitis
(ANUG)
• Microbial disease occurs in impaired host
• Starts at inter-dental papilla
• Fusospirochetal gingivitis
• Commonly happens in adults  15 – 35 YRS
• Can happen in kids also
• also known as  vincent infection, vincent angina, trench
mouth

Etiology
• Bacteria  fusi-form, spirochaetal, prevotella intermedia
• Stress
• Local predisposing factors  gingivits, ppd, smoking
• Impaired host response
• Nutritional deficiency
Clinical signs
• Necrosis and sloughing
• Fetid odour
• Metallic foul taste
• Grey Pseudomembrane slough ( when removed gingiva
will be smooth, red, shiny)
• Destruction of ID papillae  blunted papilla
• Punched out lesion (crater like)
• Extreme senstivity to touch
• Pasty saliva
• Local lymphadenopathy
• Spontaneous bleeding
Histopathology
• Surface epithelium destroyed replaced by fibrin meshwork
• Underlying ulcerative cells
• Edematous epithelium
• C.T  hyperemic, engorged capillaries, pmns

Treatment
• Debridement
• Removal of pseudo membrane
• Warm water rinses with hydrogen peroxide
• Cholerhexidine mouthwash
• Metronidazole
• Brufen
 Reduced
attached gingiva
(RAG)
• Best type of gingiva  attached gingiva
• Good for oral hygiene  with better brushing
• Less sensitive
• Reduced  band less then 2mm wide

Causes
• Labial eruption path of tooth
• Recession
• Proclined incisors
• Orthodontics

Treatment
• Free gingival graft  widen kertininzed tissue
Eruption cyst
• Common in children
• Common in incisors & mandibular 1st molars
Clincally
• Bump on crest of the alveolar ridge where tooth should be
Radiograph
• Confirm the diagnosis
Treatment
• Nothing
• Symptomatic  simple surgical excision
High frenum
• Attached high up alveolar ridge
• Associated with gingival recession
• Diastema

Treatment
• Close space first
• Then frenectomy  if this done first there will be  scar
tissue  rebound
 Localized
Aggresive
periodontitis
• Also called juvenile periodontitis
• Effects adults and young  healthy
• With little/no plaque
• No systemic diseases
• Genetic predisposition
• Multifactorial
Clinically
• 1st permanenet molar & permanent incisors
• Before puberty
• Destruction with minimal plaque
• 3-4 times faster bone loss than chronic
• Mobility
• Vertical bone loss  arch shaped
• A.actinomycetemcomitans
• Robust immune response  increase in serum antibodies

Treatment
• Surgical inervation
• Antibiotics
Primary features
• Rapid loss of attachment and tooth supporting bone
• Individual is healthy
• Familial aggregation / genetic
Secondary features
• Inconsistency of the low amounts of present etiological
factors(i.e., plaque) and the observed pronounced tissue
destruction
• Strong colonization by Aggregatibacter actinomycetemcomitans
and, in some populations Porphyromonas Gingivalis
• Hyper-responsive macrophages
• Abnormalities of neutrophil function
• Self-limiting disease
 Generalized
Aggresive
periodontitis
Generalized
• More teeth involved
• Younger then 30yrs  12 -2 5
• More plaque & calculus
• Interproximal attachment loss
• Mobility
• No systemic disease
• Period of destruction and period of quit
• P.gingivalis, p.intermedia, ekinella  dominate
Treatment
• Tetracyline
• Amoxcilin
• Chlorehexidine
• Follow ups every 3-4weeks
Diagnosis
• Probing
• history
 Prepubertal
periodontitis
• Involves  primary molars
• Common in  african amercian
Treatment
• Debridement
• Antibiotics
 Systemic
pathology
1. Achondroplasia

• No cartilage growth = dwarfism (peter dinklage games of thrones)

• Caused by mutation in FGFR-3 gene on chromosome 4
• Associated with abnormality in endochondral ossification = lengthening of bone
inhibited causing  disproportinate short stature
• 80% mutation are de-novo (new)
• 20% inherited

Symptoms
• Large head + short arms & legs + small maxilla + deficient cranial base +
underdeveloped mandible
• Short proximal limbs
• Large head
• Common  class 3
• Delayed eruption & exfoliation
• Short fingers & toes
2. Gigantism
• Excessive height growth
• Excess pubertal growth hromones
• Excessive secretion  somatotrope cells ( ant pituatary)
Symptoms
• Enlarged tongue
• Mandibular  prgonathism
• Longer roots
• Excessive height growth
3. gingivo-stomatitis
• HSV – 1

Symptoms
• Sores of mouth & gingiva
• Acute / primary form  involves kid under age of 3
Prodormal symptoms --> 1-2 days before presentation of ulcers/ sore mouth
• Fever
• Malaise
• Headache
• Dysphagia
• Vomiting
• Lymphadenopathy

Treatment
• Symptomatic
4. Coxsackie virus
• Causes apthous ulcers  whiteyellow ulcers with red surronding

Triggers
• Stress
• Menstrual cycle
• Hormonal changes
• Allergies

Symptoms
• Ulcers
• Buring sensation
• Pain  decrease in 7-10 days
• Heals  1- 3 weeks
• Recurrent Apthmous minor  less then 2 mm in diameter, last = 2 weeks
• Recurrent Apthmous major  10mm in diameter, laste = more then 2 weeks, heal with scarring
• Recurrent herpetic form  clusters of ulcers
• Frequent reccurence  screen for diabetes / bechets syndrome

Treatment
5. Cretinism
• Severe hypothyroidism

Signs & symptoms

• Defective mental & physical development
• Dwarf
• Curved spine
• Pendulous abdomen
• distorted limbs
• Harsh & scanty hair
• Under developed mandible
• Over developed maxilla
• Enlarged tongue
• Delayed eruption on teeth
• Retianed primary teeth
Cranio-facial
anomalies
1. Cleft palate
• Occurs in 6-8 week in utro
• Isolated clefts  common in female
• Impaired speech & swallowing
• Inability for soft palate to close the air flow into the naso-pharynx

2. Cleft lip
• 5-6th week in utero
• More common in males
• More on left side then right
Classes of CL
• Class 1  unilateral notching of vermillion not extending to lip
• Class 2  same as class 1 but extending into lip not the floor of the nose
• Class 3 class 2 + extending into the floor of nose
• Class 4  bilateral
Timing of treatment of CL – CP
• CL repair  10 weeks after birth
• CP repair  9-18 months after birth
• Pharyngeal flap or pharyngealplasty  3-5 yrs or later depends on
speech development
• Alevolar reconstruction  6-9 yrs depends on dental development
• Cleft orthognathic surgery  14-16 in girls, 16-18 in boys
• Celft rhinoplasty  depends on skeletal maturity
• CL revision  after 5 yrs of age anytime
3. Pierre robin syndrome
• Collagen gene 2A1 mutation
• Hypermobility of joints
• Mitral valve prolapse
• Micrognathia  glossoptosis  CP  breathing & feeding
problems

4. Treacher collin syndrome n

• Also called  mandibulofacial dystosis
• Mutation  5q32 gene
• Notches eyelids
• Downslanting of eyes
• Mid face deficiency
•
5. Downs syndrome
• Trisomy 21
• Low caries but high periodontic issue
• Delayed physical & mental development
• Delayed eruption
• Short & stocky stature
• Broad & flat face with slanting eyes & short nose
• Ears are small and low set
• Heart defects are common
Omas
1. Hemangioma
• Most comon benign tmor of infant
• Due to proliferation of blood vessels
• Appears  1- 2 weeks after birth
• More common in girls
• Site  lips, tongue & buccal mucosa
• Self treated or can be surgically removed

2. Lymphangioma
• well circumcised mass of lymphatic vessels
• Most in neck & axilla
• Red-blue translucent masses  spongy
• Treatment  excisonal biopsy
3. Neurofibroma
• Firm & encapsualted
• Proliferation of schwann cells
• Site tongue, buccal mucosa, vestibule & palate
• Multiple lesions  consider  neuro fibromatosis ( von-reckling
hausens)
Bumps
1. Measles
• Called  rubella paramyxovirus
• 1-2 weeks incubation
Symptoms
• Fever
• Cough
• Rash
• Kopliks spots  intra orally
• Highly contagious
Treatment
• Suportive
2. German measles
• Called  rubella benign viral disease
Symptoms
• Red bump
• Swolled lymph nodes
• Mild fever
• Enamel defects
Treatment
• Supportive
3. Small pox
• Acute viral disease
Symptoms
• High fever
• Nausea
• Vomiting
• Chill
• Headache
• Ulcerated or vesicular lesion s
Types
• Variola major  severe & common form
• Variola minor  less severe, less common

Treatment
4. Mumps
• Acute & contagious
• Swelling of parotid gland
• Replication  upper respiratory tract
• Spread  respiratiory secretions, saliva, fomites
• Incubation time  12-25 days
• Vaccinate  MMR (measles, mumps, rubella)
Dental trauma
 Traumatic dental injuries
1. Minor injuries  ellis class 1 & class 2
• Concussion
• Craze line
• Enamel fracture
• Enamel & dentine fracture

2. Moderate  ellis class 3 & 4

• Subluxation
• Enamel, dentine & pulp fracture

3. Major  ellis class 5 & 6

• Luxation  intrusion, extrusion, lateral luxation
• Avulsion
• Alevolar fracture
Dental trauma in children
• Common in  boys
• Maxiilary teeth more common
• Increased overjet  more then 6mm = higher trauma
chances
 Medical history
1. Coagulation disorders

2. Tetnus coverage
• Active immunization  tetnus, diptheria & pertusis  1st yr
• Booster  1.5, 3 & 6 ys  then every 4-5 yrs

3. Rule out head injury

• Neurological assessemnt  drowsiness, amnesia, vison

4. Radiograph
• At incident
• Follow up  1, 2 & 6 months
1. Concussion
• No displacement
• No pdl tear  sour pdl
• No mobility
• Tooth tender
• High chances of pulpal necrosis for permanent tooth with closed apices

2. Subluxation
• Ripped pdl
• Bleeding around collar  sulcular hemorrhage

Treatment for both (primary teeth)

• No treatment  no splint
• Soft diet
• Ohi
• Follow up
3. Intrusion
• Of primary teeth
• Into the socket
• Primary teeth  positioned labial to the permanent successors

• May damage developing permanent

• Hypoplasia  during apposition
• Hypocalcification  during calcification
• Dilaceration  during root development

Treatment
• No treatment
• Spontaneously re-erupt
4. Extrusion
• Of primary tooth
• Out of socket little
• Greater luxation  greater damage to vasculature  necrosis

Treatment
• Extrution more then 3mm  extract + space maintainer
• If pt seen before formation of apical clot  felxible splint for 1-2
weeks + endo treatment
• Follow -up
5. Avulsion
• Primary tooth out of socket
• Reimplantation of primary tooth  poor prognosis
• Reimplantation of permanent tooth  good prognosis
• Time outside mouth less then 30min  reimplant + flexible splint +
endo + antibiotics + soft diet
• Time outside mouth more then 30min  extract + space
maintainer

• Primary teeth  should not be reimplanted (accoridng to book)

Storage for permanent tooth in order

• Viaspan  hank solution  cold milk  saliva  saline  water
• Never use cholhexadine on tooth out of socket  damage
6. Crown fracture
• Enamel  smooth
• Enamel + dentine  restore
• Enamel + dentine + pulp  pulpotomy if vital, pulpectmy if non
vital, extract if pathological root resoprtion

7. Root fracture
• Apical half  no treatment
• Coronal half  rigid splint or extract + space maintainer
Pediatric mandibualr fracture
• Should be treated conservatively
• Presnts as  greenstick or incomplete fracture
• Common in boys
• Conylar fracture incidence  decrease with growing age
• Body & agle fracture  increase with age

a) Non surgical treatment

b) Surgical treatment
• Interdental wiring  2-3 weeks
• Occlusal splints with circum-mandibualr wires 2-3 weeks
• Drop wires & circum-mandibualr wires
• Sututre with or without splint
 Mouth guards
• To prevent injuries

1. Stock
• Available at sports, stores
• Pre made 1 size

2. Mouth formed
• Available at sports, stores
a) Boil & bite form
• Boil in hot water to soften & insert in mouth and molded to teeth
• Never use with braces  melts elastic ligatures
b) Shell
• Firm outer shell
• Inner ethyl metha-acrylate

3. Custom fabricated
• Impression taken by dentist
a) Vaccume formed  suck down on cast model
Root resoprtion
1. Internal
• Odontoblastic layer in pulp damagedd

2. External
• Cementoblastic layer in pdl damaged
a) Surface  normal pdl
b) Replacement  ankylosis, increased risk with long term splint
c) Inflammatory  granulation tissue, radiolucency
d) Cervical  biological width area, pink spot
e) Apical  orthodontic forces
 Child abuse & neglect
• Occurs in all levels  0-3 yrs most commonly
1. Physical  intentional injuries
2. Emotional  denial of affection, isolation
3. Neglect  negligence of basic needs of child

• Dentist are required by law to report suspected child abuse and

neglect, even if there is no proof
Child behaviour
1. Cooperative
• Communicative
• Willing
• Excited
• Minimal apprehension

2. Potential cooperative
• Capabale of appropriate behaviour but are disruptive in dental setting

• Defiant  any age, spoiled & stubborn, does. Not like being advised by adults
• Uncontrolled  3-6 yrs, tantrum
• Timid / avoidant  3-6 yrs, hide behind parents, may deteriorate to
uncontrolled
• Tense cooperative  7 or older, white knuckler, want to behave but very
nervous
• Whining  continious, but no tears
• Fearful / anxuious  scared
3. Uncooperative
• No communication
• No willing
• No comprehening

• Eg : - infants, 2yrs old, disabled

 Frankl rating scale

1  defiinetly negative (refusal / distress)

2  negative resistance (uncooperative, reluctant)
3  positive acceptance (co-operative, reserved)
4  definitely positive  (interested / enjoyed)
 Anticipatory guidance
• Age – appropriate counselling to pt & parents focused on
prevention
• First dental visit  by age 1
 Familiarization
• No treatment dental visit
• Emphasis on dental setting and instruments
 Functional inquiry
• Questionairre or interview
• Allows to learn chief complaint and estimate behaviour
 Knee – Knee exam
• For infants  less then 2 yrs old
• Clinician & parent in knee - knee position
• Child head in dentist lap
• Child legs in parent lap
Five domain of peadatric pt management
1. Physical domain
• Papoose board
• Belt, tape

2. Pharmalogical domain
• Anesthesia, Nitious oxide, sedatives

3. Reward oriented
• Reinforcement

4. Aversive domain
• Punishment

5. Linguistic management
 Behaviour shaping
• Slowly develop behaviour by reinforceing successive
approximations to a desired goal
• Ask pt to open wide  pt opens a little bit  still positive
reinforcement
• Reinforcement should be immediate & specific to the
desired behaviour
 Aversive conditioning
• Punish with the purpose of extinguishing or improving negative
behaviour
• Not for  timid & tense cooperative
• Voice control  speak in firm tone

Hand-over-mouth technique
• Hand overe pts mouth to gain attention of uncontrolled
 Attention-deficit/hyperactivity disorder
(ADHD)
• AD  unattentive
• HD  hyperactive
• More common in boys
• 3-6 yrs age

Common psychostimulant medication

• Methylphenidate (ritalin)
• Attomoxetine (strattera)
• Amphetamine (adderall)
• All three have same side effects
 Autism
• Condition related to brain development that impacs how the
person perceives & socalizes with others

Spectreum refers to wide range of symptoms

1. Repetitive behaviour
• Body movement
• Same questions

2. Heightened sense of light and sound

• Sound from suction and motors, handpiece
• Light from cahi
Local anesthesia
in children
• 4.4 mg / kg  maximum dose in children
• IAN  all lower teeth
• PSA  upper primary molars
• ASA  upper primary anterior
Nitrous sedation
in children
• MAC (minimum alveolar concentration)  conc required to rendeer 50% of pt
immobile
• MAC of nitrious is  105%
• Common side-effect  nausea

Protocol
• Fill bag with O2 & place the hood on pts nose  flow rate 4-6l/min
• Increase nitrous conc in 10% concentration till  30%

Diffusion hypoxia
• Lungs fill with nitrous after stopping it
• We stop nitrous & givem 100% O2 for 3-5mins to clear nitrous from lungs after

Contra-indication
• Less then 2 yrrs old
• Uncooperative
• Wheezing (mild-moderate asthma not a CI)
 Four plateus of 1st stages anesthesia
1. Parasthesia
• Tingling
• Over – with in few mins

2. Vasomotor
• Warm
• Over – with in few mins

3. Drift
• Floating
• Target anaesthesia of nitrous sedation
• Last longer  hours
• Desired levels of sedation

4. Dream
• Eyes closed
• Jaw sag
Fluroide for
children
• Prescription only
• For children with caries risk living in non-fluroidated area
Age
• Less then 3  fluoride drops
• More then 3  lozenges & tablets
• More then 6  mouthwash, 0.02% naF / weekly, 0.05% naF / daily
Recommendation
• Birth – 6 months  no fluroide
• 6 months - 3 yrs  0.25mg (less then 0.3 ppm)
• 3 – 6 yrs  0.5 mg (less then 0.3 ppm), 0.25mg (0-3-0.6 ppm)
• 6 – 16 yrs  0.1mg (less then 0.3 ppm), 0.5 mg (0-3-0.6 ppm)

Facts
• Public water b fluroidated when  levels below 0.7 mg /l
• 20-40mg / day fluroide  inhibit phosphotase
• 40-70mg / day  heartburn & pain in extremeties
• Calcium therapy  to treat fluroide toxicity
• Topical fluroide does not causes  fluorosis
• Greates fluroide conc  outermost layer of enamel
• Proximal & smooth surface beneifit most from fluroide
• Fluoride excreted by kidney in form of urine & sweat  3mg / day
 Fluoride toxicity
• Adult lethal lose  4-5g
• Child lethal dose  15mg/kg
• Odontogenic manifestation  fluorosis

Symptoms
• Nausea
• Vomiting
• Hypersalivation
• Abdominal pain
• Diarrhea
• Acute  cardiac failure & respiratory paralysis

Treatment
• Syrup of IPECAC  induce vomiting
Natal & neonatal
teeth
Natal teeth
• Present at birth
• Mandibular incisor region
• Little root formation  attached to soft tissue
• Treatment  extraction due to fear of aspiration

Neonatal
• Erupts with-in first 30days
• Mandibular incisor region
• Both natal & neo-natal have  hypocalcified enamel matrix

Riga-fede disease
• Baby tooth causing uleration on the ventral part of tongue
• May cause nusring problems
Early childhood
caries (ECC)
• Also called baby childhood syndrome
• Ramapnt decay
• Any dmft before age  6
• Breastfeeding before bed should be stopped  after eruption of
first primary teeth
• General involvement  maxilaary anteriors
• Constipation  fruit juice  ecc
• Ear infection  antibiotics  ecc

Recommdation
• Children should drink from cup by age 1
• Smear toothpaste  before age 2
• Pea toothpaste  age 2 -5
• First dental visit  age 1
High risk for caries
 Behaviour
guidance
techniques
1. Pre-visit imginary
• Provide positive context for dental visit
• Inidcated  all pts

2. Direct observations
• Watch video or observe cooperative pt undergoing dental treatment
• Goal is to provide  ideal role model
• Indication  all pts

3. Distraction
• Distracting / divert attention from something unpleasant
• Shaking cheek while giving injesction
• Tv, earbuds, vr, video games
• Indication  all pts
4. tell-show-do
• Tell  verbal explanation
• Show  demonstrate on model
• Do  execution
• Goal is to familarize & desensitize
• Indication  all pts, autistic, adhd

5. Systemic desensitization
• Gradually expose to the components of in multiple dental visits
• Indication  fear & anxiety, autism
6. Sensory adapted dental environment (SADE)
• Adaptation made to dental clinic for calming effect
• Dim light, light music
• Indication  fear & anxiety, autism

7. Animal assisted therapy (AAT)

• Trained animal in healthcare setting to improve interactions
• Inidcation  fear & anxiety
• Contra-indication  fear of animal, animal allergy, lack of interest
8. Picture exchange communication system (PECS)
• Pt shares a picture card to express a request or a thought
• Many picture cards
• Indication  non-communicative, autistic

9. Voice control
• Delibrately change in voice
• To gain attention & compliance
• Indication  avoidant & defiant behaviour
• Contraindication  hearing impairement, non-communicative

10.hand over mouth technique

• Indication  none
11.Protective stablisation
• Restrictions of movement
• Required informed consent
• Passive  papoose board (not in respiratory distress)
• Active  another person
• Indication  uncontrolled behaviour with urgent care
• Contraidication  respiratory compromise, non-urgent care

12.Treatment deferal
• Not urgent differ
• SDF  silver diamine fluroide
• ITR  interim theruaptic restoration
• Indication  uncontrolled behaviour with non-urgent
Sedation
 • Fear & anxiety •
Indication • • Fear & anxiety Fear & anxiety
Gag , shcn • Extremely Uncooperative
• Uncooperative
• La not affective •
• shcn Shcn
• Long procedure • Substancial dental needs
CI • Very young less then 3
• Elective care
• • Cooperative
Non-communicative • ASA 3 or higher
• • ASA 3 or higher
Respiratory compromise
• • Porphyria  sunglight sensitivity
Sickel cell
• • Heaptic insuffiency
Bleomycin (cancer AB)
Periodontology
Periodontium
• Alveolar bone
• PDL
• Cementum
• Gingiva
 not bound

Normal peridontium
 bound  Keratinized

 Non- Kertinized & non bound

 Gingiva
• Parts of masticatory mucosa which covers the alvolar process &
surrond the cervix part of the tooth

Composed of
• C.T
• Epithelium

Epithelium divvided histologically into three

• Oral epithelium  continious with epithelian lining of attached
gingiva, keratinized
• Sulcular epithelium  non keratinized
• Junctional epithelium  attached to tooh by hemidesmosomes,
non keratinized
Gingival fibers / supra-crestal connective tissue fibers
• Composed of type 1 collagen
• Support gingiva & attach it to the tooth & alveolar bone
• Gingival fibers are continuous with periodontal fibers

Designated by their orientation

• Dento-gingival
• Dento-periosteal
• Circular
• Alveolo-gingival
• Transeptal

Stippling
• Irregular surface texture resembling orange peel  attached gingiva
• Not visible until age 6
• Normal color  coral pink
• Contour
• Consistency / tone
• Texture
 Junctional epithelium
• Collar – like band of stratified squamous non-keratinized epithelium
near sulcus & apical end
• Near sulcus  10-29 cells thick
• Near apical  2-3 cells thick
• 0.25-1.35 mm long

Biological width
• Connective tissue attachment + junctional epithelium attachment
to cementum
• 2.04mm
• Ct 1.04mm
 GCF
• Gingival cervicular fluid
• Contains variety of enzymes & cells  desquamating epithelium
& neutrophils

• Increased in gcf  first detectable sign of inflammtion

• Once inflammation  gcf now considered exudate
 Periodontal disease
• Main factor / initiating factor  plaque / biofilm

• Peridontal health  no inflammation + no pdl & bone destruction

• Gingivitis  inflammation + no pdl & bone destruction
• Periodontitis  inflammation + pdl & bone destruction (CAL)
Pathogenesis
1. Microbial challenge  presented by sub-microbial plaque
(Lipopolysaccharides, antigens)
2. Upregulated host immune resposne  inflammation (cytokines,
MMPS, prostaglandins) (gingivitis)
3. Tissue destruction  periodontitis
 Examination

1. Tooth exam
• Abrastion, erosion, attrition, abfraction, hypersensitivity

2. Periodontal exam
• Probing depth (PPD)  gingival margin - base of pocket
• Clinical attachment loss (CAL)  CEJ – base of pocket
• Bleeding on probing (BoP)  Best measure of inflamation
• Recession  cej to ginigval margin
• Alveolar bone loss  radiograph
• Supuration  pus from pocket (neutrophils in pocket)
• Mobility  pdl support loss
• Furcation

• CAL = PPD + RECESSION

3. Oral examination
• Home care how much brushing & flossing  plaque & calculus
• Inflammtion  reddnes, sweling, bop
• Destruction of peridontal tissue ppd, cal, furcation, mobility,
aveolar destruction
 Miller classification for mobility
• Class 0  normal physiological
• Class 1  slighlty more then normal
• Class 2  moderalty more  less then 1mm bucco-lingual
• Class 3  severely more  more then 1mm bucco-lingual & can
vertical depress in socket

Grading
• Grade 1  horizontal mobility less then 1mm
• Grade 2  horizontal mobility more then 1mm
• Grade 3  horizontal mobility more then 2mm & or vertical
mobility
 Furcation
Factors that can predispose tooth to furcation
• Short trunk  from cej to furcation
• Short root
• Narrow inter radicular dimension  b/w roots
• Cervical enamel projection

Hamps classification (by nabers probe)

• Class 0 no furcation
• Class 1 horizontal furrcation less then 3mm
• Class 2 horizontal furrcation more then 3mm
• Class 3 through & through
 Glikman furcation classification
• Class 1  pocket formation, flute, incipient
• Class 2  pocket formation into the furca, clu de sac
• Class 3 through & through (but coverd by soft tissue, can not
visualize)
• Class 4  through & through & u can visulaize
 Alveolar bone loss
• Normal distance from cej to crest  2mm
• Crest should be parallel to the line connecting CEJ of adjacnet
tooth
Horizontal
• parallel to the line connecting CEJs
Vertical
• Angular
• Classified by the number of bony bones remaining

• Bone height best measured  bitewing

 Infra-bony defects
4 wall defect
• Extraction sockets
• All walls presents
• Circumferential defect

3 wall defect
• Trough
• 3 walls present one not
• Angualr bone loss

2 wall defect
• Crater defect
• Only 2 walls left
• Most common
• Occurs between 2 teeth
• Loss of interseptal bone

1 wall defect
• Only 1 wall left
 Miller classification for recession
• Determines likelihood of regaining tooth coverage

Class 1  marginal tissue recession not extending to mucogingival junction, no loss of interdental
bone or tissue
100% likelhood of root coverage

Class 2  marginal tissue recession extending to mucogingival junction or beyond, no loss of

interdental bone or tissue
100% likelhood of root coverage

Class 3 marginal tissue recession extending to mucogingival junction or beyond, loss of

interdental bone or tissue,tooth rotation prevents root coverage
Partial root coverage

Class 4  marginal tissue recession extending to mucogingival junction or beyond, loss of

interdental bone or tissue, severe rotation prevents root coverage or not anticipated
 Gingivitis
• Color  increased blood flow = redness
• Contous  swelling  inflammation  exduate /edema
• Consistency  chronic gingivits leads to fibrosis

Three stages of disease in developing gingivitis

1. Transient / incipeint
• With in 2-4 days after cessation of oral hygiene
• PMNs
• Sloughed epithelium & bacteria found in sulcus

2. Developing stage
• Collagen destruction
• IGg
• Lymphocytes

3. Chronic stage
• Plasma cells
Inflammation
Intial lesion
• 2-4 days after plaque accumulation
• Vascular changes  dilated capillaries & increased blood flow
• Pmns predominantly
• Increased gcf
Early lesion
• 4-7 days
• Proliferation of capillaries and the increased formation of capillary
loops between rete pegs or ridge
• Predominant  lymphocytes (t-cells )
• Clinically  erythema, BOP
• Collagen destruction also increases. Main fibers that are affected
are Circular and dento-gingival fibers
• Activation of MMPs (Matrix metalloproteinases)also related to
Established lesion
• Predominance of plasma cells and B lymphocytes
• In conjunction with the creation of a small gingival pocket lined
with a pocket epithelium
• 2-3 weeks after plaque accumulation
• The blood vessels become engorged and congested
• Along with extravasation of erythrocytes and breakdown of Hb
Resulting in localized anoxemia which imparts bluish hue over
reddened gingiva
• Collagenolytic activity increased
Advanced lesion/phase of periodontal breakdown
• The extension of the lesion into alveolar bone
• Dominant cells  plasma cells
• Clinically  loss to attachment and alveolar bone
 Plaque induced gingival disease
• Most common
• Interaction between microbial plaque + host interaction = inflammation

1. Moodified by systemic factors

• endocrine changes  puberty, pregnency, diabetes
• Blood dyscraisis  leukemia

2. Modified by medication
a) DIGE
• ca blockers (diltiazam, nifedipine, verapamil, felodipine, amlodipine)
• Dilantin (phenytoin)
• Cyclosporin
3. Modified by malnutrition
• Vit c deficieny (scurvy)
 Non-plaque induced gingival disease
• Less induced
1. In resposne to infection
• Bacterial  neisseria gonorrhoeae, treptonema pallidum
• Viral  herpes
• Fungal  candidiasis

2. In response to allergy
• Foods
• Restorative material
• Toothpaste  sodium lauryl sulphate

3. In response to trauma
• Factitiious  unintetional
• Iatrogenic  doctor caused
• Accidental  burns
 Periodontal disease severity
Slight
• Cal  1-2mm
Moderate
• Cal  3-4mm
Severe
• Cal  more then 5mm

Periodontal disease distribution

• 6 site  B-M, BF, MIDDLE, L-M, L-F, MIDDLE (for each tooth )
• Total no of teeth x 6 = total site in mouth
Localized
• 30% or less sites
Generalized
 Periodontal disease tyoe
Chronic Aggressive
• Most common • Less common
• Clinically not healthy  smoker • Clinically healthy
diabetes • Fast & aggressive
• Slower & progressive bone • Familial aggregation
destruction
• Microbial deposit are not
• Microbial deposit are concistent concistent with extent of
with extent of destruction destruction
• Modified by systemic disease • Localized  molar & incisor
• In old pts • In young pts
 ANUG ANUP
Etiology Etiology
• Mixed fusiform-spirochete bacteria
• Bacteria  fusi-form & (biofilm)
spirochaetal • Stress
• Stress Predisposing host factors
Predisposing factors • Poor oral hygiene
• gingivits, ppd, smoking • Pre-existing periodontal disease
• gingivits, ppd, smoking
• Impaired host response
• Impaired host response
• Nutritional deficiency • Nutritional deficiency
• Aids • Aids
Symptoms Symptoms
• Pseudomemebrane
• Pseudomemebrane
• Fetid odor & taste
• Fetid odor & taste • Blunted papillae
• Blunted papillae • Pasty saliva
3. Acute necrotizing ulcerative gingivitis (ANUG)

• Microbial disease occurs in impaired host

• Starts at inter-dental papilla
• Fusospirochetal gingivitis
Etiology
• Bacteria  fusi-form & spirochaetal
• Stress
• Local predisposing factors  gingivits, ppd, smoking
• Impaired host response
• Nutritional deficiency
• Aids
Clinical signs
• Necrosis and sloughing
• Fetid odour
• Metallic foul taste
• Grey Pseudomembrane slough ( when removed gingiva will be smooth, red,
shiny)
• Destruction of ID papillae
• Punched out lesion (crater like)
• Extreme senstivity to touch
• Pasty saliva
• Local lymphadenopathy
• Spontaneous bleeding
Histopathology
• Surface epithelium destroyed replaced by fibrin meshwork
• Underlying ulcerative cells
• Edematous epithelium
Treatment
• History
• Removal of pseudo membrane
• Warm water rinses with hydrogen peroxide
• Cholerhexidine mouthwash
• Metronidazole
• Brufen
• Three visits
First visit
1. History
• Systemic disease (diabetes, hiv)
• Drugs (medications)
• Habits (smoking, pan etc)
• Diet
• Slepping patterns
• Dental history (brushing habits, hygiene)
• Psycho-social history (stress, living conditions)
2. History of acute disease (kabse, kesa dard hai etc)
3. Examination general
4. Oral examination
• Pseudo membrane
• Halitosis
• Pockets
• Periodontal disease
• Resortaion, ill fitting denture, plaque, calculus
Management
• Isolate the involved area
• Topical anesthesia with cotton (remove pseudomembrane)
• Cleaning area with warm water
• Supragingival scaling (not subgingival due to inflammtion)
• No any surgerys unless emergencies
• Antibiotics  systemic involvement (lymphadenopathy & systemic signs)
Instructions
• Avoid tobacco & smoking
• Warm water rinses with 3% hydrogen peroxide or with 0.12% cholohexadine twice daily (inflammtion
reduction)
• Get good rest (avoid exertion)
• Ultra-Soft tooth brush with simple toothpaste (no mint etc) or with water (cholerhexadine
mouthwashes)
• Analgesics  ibuprofen
• Hydration

• Amoxcillin 500mg every 6hrs for 10 days

If amoxcillin sensitive
• Erythromycin 500mg every 6hrs or metronidazole 500mg twice daily for 7 days
Second visit
• After 2-3 days
1. Re-evaluation
• All the signs and symptoms
• Pain mostly gone/less
• Overall improved conditions
2. Erythematous gingival margins without any
pseudomembrane
3. Scaling
• Scaling
• Gently remove calculus after decress in gingival enlargement
4. Same instructions as before
Third visit
• After 5 days
1. Evaluated for symptoms
• Mostly symptom free
• Some erythema may b present
• Slight pain on touching
2. Patient instrutions
• Control of biofilm
• Maintain oral hygiene
• Counselling on habibts & nutritions
• Hydrogen peroxide rinses discontinued but cholorahexdine
continued for addition 2-3 weeks
• Scaling & root planning repeated if necessary
Followups
• 4-6 weeks
Pindborg stages
1  id papilla affected
2  marginal also affected, complete loss of papilla
3  attach gingiva involved
4  bone exposed
Horning & cohen
1  tip of id
2  necrosis of entire id
3  marginal ginva affected
4  attached gingiva
5  extending to buccal and labial mucosa
6  exposing bone
7  involving cheek
Listgarten
zone 1  bacterial zone
Zone 2  neutrophil rich zone
Zone 3  necrotic zone
4. Acute nectrotizing ulcerative periodontitis (ANUP)

• Extension of an nug to peridontal tissues leading to attachment loss

and bone loss
Etiology
• Mixed fusiform-spirochete bacteria (biofilm)

Predisposing host factors

• Poor oral hygiene
• Pre-existing periodontal disease
• Smoking
• Viral infections
• Immunocompromised status
• Psychosocial stress
Clinically
• Necrosis & ulceration of coronal portion of interdental papillae
and gingival margin
• Red and painful gingival margin
• Severe attachment loss and bone loss
• Deep interdental osseous craters
• Oral malodour
• Fever
• Malaise
• Lymphadenopathy
• No pockets are found  because of necrosis of junctional
epithelium & also marginal epithelium & C.T resulting in gingival
recession (so no pockets formed)
(For a pocket to form JE must move apically )
Nup in hiv
• Will show linear gingival erythema
• Rapid bone and attachement loss
• Necrosis of bone

Treatment of nup
• Oral hygiene
• Scaling and root planning
• Antiplaque agents
• Antibiotics
• Screening for hiv
 Aids
• Hiv
• Targets  cd4 helper cells
• Macrophages also affected

HIVgingivitis
• Linear marginal gingival erythema
• Gingivitis may become more generalized & is resistant to conventional
therapy

HIV periodontitis
• Rapid destruction of gingiva  ulceration & craters
• Widespread necrosis  affecting soft & hard tissue  sequestration of
alveolar bone
 Periodotnal abscess

• Acute pain  contstant, severe & dull throbbing

• Thermal changes no effect on discomfort
• Rapid onset  increase with the mobility of tooth

Treatment
• Curretage via sulcus
• Flap surgery
• Incision & drainage
 New
Classification
system
 New AAP periodontal classification
1. Peridontal health and gingival disease & conditions
2. Periodontitis
3. Peri-implant disease & conditions
4. Periodontal manifestation of systemic disease & developmental
& acquired conditions
Peridontal health and gingival disease & conditions
• Periodontal health  gingivitis  periodontitis

1. Periodontal health
• Healthy, soft hard tissue surronding tissue
• Some inflammation is considered in this category
• Bop  less then 10% of sites
• PD  3mm or below
• Intact periodium  no loss of periodontal tissue
• Reduced periodontium  previous loss of bone/tissue, currently
not undergoing loss / stable (hard brushing, crown lengthening)
2. Gingivitis
• Redness
• Erythema
• Swelling
• BOP  10% or more on sites
• Pd  3mm or less
• Stable periodontium  no loss
3. Periodontitis
• Loss of support tissues  due to microbial associated host response
• Associated with  deeper probing depth
• Loss of interproximal attachment

Staging
• Determined by severity & extent of disease at presentation

• Severity  determined primarly by ID CAL at the worst site

Stage 1  1-2 mm
Stage 2 3-4mm
Stage 3 & 4  more then 5mm
• Other method cans be used  radiographic bone loss &
tooth loss due to periodontitis
• Complexity  base on probing depth, nature of bone loss,
furcation
Stage 1  pd less then 4mm , horizontal bone loss
Stage 2  5mm or less, horizontal bone loss
Stage 3  more then 6mm, vertical bone loss, furcation
Stage 4  more then 6mm, occlusal trauma, bite collapse

Some special factors to consider

• Vertical bone loss more then 3mm  stage 3 / 4
• Furcation involvement class 2 / 3  stage 3 / 4
• Less then 20 teeth remaining  stage 4
• Extent & distribution  based on percentage of severity &
complexitiy
Localized  less then 30% involved
Generalized  more then 30%
Molar / incisors pattern  localized aggressive periodontitis
Due to
periodontitis

Decide stage with most severe 1

 Grading
• Determined by thye rate of progression, response to therapy &
overall assessment of risk
• Based on longitudional observation
• Dynamic measurement
• Measured from to a – c & slow to rapid
• Measure in period of 5 years

• RATE OF CAL / BONE LOSS

• DIABETES
• SMOKING
 SLOW MODERATE
RAPID

CAL or RBL  in period of 5 yrs (progression of disease slow or rapid)

RBL %  in comparasion to age (progression of disease slow or rapid)
C-Reactive protein (MARKER OF INFLAMMATION)  MORE THE CRP = MORE
 PERI-DISEASE
• Peri-implant health  peri-implant mucositis  peri-implantitis

Risk factors
• Smoking
• Diabetes
• Poor oral hygiene
• Poor compliance with supportive treatment
• Excess cement
• Lack of keratinzed tissue aroun implant
• Previous periodontitis in natural teeth (peri-implantitis)
1. Peri-implant health
• Absence of inflammation & BOP
• Not possible to deteremine healthy probing depth but  5mm or
less considered normal
• Health is possible around implants with normal or reduced bone
support

2. peri-implant mucositis
• Inflammation & BOP
• Increased probing depth then base line
• No progressive marinal bone loss around implant
3. peri-implantitis
• Inflammation & BOP
• Increased probing depth then base line
• Progressive marinal peri-implant bone loss  3mm or more
Plaque
 Dental plaque
1. Supragingival
• Above ginigval margins
• Aerobic bacteria  due to readily available OXYGEN
• Attached  gram +ve
• Non attached  gram -ve

2. Subgingival
• Below ginigval margin
• Anaerobic bacteria  due to no available OXYGEN
• Tooth  gram +ve
• Apical & epithelium  gram -ve
 Composition
1. Organic
• Polysaccharide
• Porteins
• Glyco proteins
• Lipids

2. In-organic
• Calcium
• Phosphorus
• Sodium
• Potassium fluroide

• Supra-gingival plaque  saliva

 Development of dental plaque
1. Formation of pellicle
• Forms with-in seconds
• All surface in oral cavity are coated with layer of a organic material acquired pellicle
• It consisit of more than 180 peptides, proline rich proteins & glyco-proteins
• Provide attachment site for bacteria

2. Adhesion & Attachment

• With-in minutes
• Initial attachment due to  weak reversible van der waals & electrostatic forces
• Firm attachment  strong irreversible interactions b/w adhesin molecules & host pellicle
receptors
• Specific bacteria comes and attach to pellicle surface
• Primary colonizer provide sites for secondary colonizers to bind

3. Colonization and plaque maturation

• With 24-48 hrs
• Primary colonizers provide receptors for secondary colonizers to attach  This process is
called co-adhesion
Qurom sensing
• Communication between bacteria
• They secrete signaling molecules (auto-inducers)
• Triggers response such as a change in expression of specific
genes once they reach a critical threshold
• Growth of bacteria
• Resitance to antibiotics
• Two types of signaling molecules in dental plaque
1. Peptides
2. Al-2
Interaction b/w biofilm bacteria
• Can be benficial
• Can be dangerous eg:- s.oligofermentans can convert lactic acid
produced by s.mutans into h2o2 which can kill s.mutans

Resistance
• Biofilm bacteria are 100—1500 times more resistanbt to antibiotics
due to
o Slower growth rate in biofilm
o Biofil matrix
o Enzymes  B-lactamases, formaldehyde (trapped & concentrated in
E.C matrix)
o Pumps
Mode of resistance
• Conjugation, transformation, plasmid transfer & transponce transfer
 Complexes
Early/primary colonizers
• Gram +ve facultative (aerobics)

Yellow complex
• streptococcus  facultativr
• S-mutans  coronal caries
• S. salivaris  on tongue

Purple complex
• actinomyces odontolyticus  healthy ginigva, root caries, facultative

• Pseudomonas, staph  implant

Secondary colonizers
Green complex
• elkenella conodens, aa serotype a

Orange complex
• fusobacteria, prevotella intermedia, campylobacter rectus

Red complex
• p.gingivalis, tannerella forsythus, T denticola
• Associated with BOP & deeper pockets
Plaque Hypothesis

Most accepted
Bacteria + other factors
(diabetes)
 Aggregatibacter actinomycetemcomitans
( A.actinomycetemcomitans )
• Aggressive periodontitis
• Non-motile gram –ve rod
• Capnophillic  grows well in CO2
• Lukotoxins  kill keukocytes
• Lipopolysaccharide (endotoxin)  cell of of this
• Collagnease
• Protease  cleaves IgG
 P.Gingivalis
• Chronic periodontitis
• Non-motile gram –ve rod
• Fimbria  important for adherence
• Capsule
• Gingipain  protease that cleaves host proteins
• Collagenase
• Hemolysin
 T.Denticola
• Cause  ANUG / ANUP
• Motile fram –ve spirochete
• Penetrate epithelium & connective tissue
• Protease that degrade  collagen, IG, complement factor
 T.Forsythea
• Non-motile gram –ve rod
• Protease  cleaves complemnt factors & IG
 P.Intermedia
• Pregnency gingivitis
• Non motile, gram –ve rod
• Become darkly pigmented when grown on blood agar plates
 C.Rectus

• Motile gram –ve

• Polar flagellum
 F.Nucleatum
• Bridge b/w primary & secondary colonizers
• Non motile gram –ve rod
• Iduce apoptosis of leukocyte & relase tissue damageing
substance from leukocytes
Local factors
1. Calculus
• Mineralized dental plaque
• Wont cause caries
• Form with-in 1-14 days
Types
1. Supraginigval
• White / yellow
• Saliva  mineralization
• Near duct opening  lingual surface of mand ant, buccal surface
of max molars

2. Sub-gingival
• Dark / brown
• GCF  mineralization
2. Materia alba
• Soft cheese like food debris
• Unorganized bacteria
• Easily displaced with water

3. Malocclusions
• Contribute to plaque retention
• Rotation or mal positioned teeth

4. Faulty restoration
• Over hang
• Open margin
• Open contacts
• Over contoured  much worst for gingival health then under-
5. Subgingival margins
• Plaque accumulate
• Giginval recession & inflammation
• Deep pockets

6. Appliances
• Removable
• Fixed  more
• Oral jewelry  pocket, bone loss, recession

7. Self implicted injury

• Aggressive horizontal brushing
• Nail bite
 Extrinsic stains
• Esthetic concern  primarly
• Orange  ant, poor oh
• Brown  dark colored drinks (coffee, tea, coca-cola) , poor oh
• Dark brown & black  tobacco
• Yellow brown  chlorhexadine & stanneous fluoride
• Black  thin lines on cervical third, healthy teeth, due to iron
• Green – Yellow  ant teeth, poor oh, chromogenic bacteria
• Bluish green  metallic dust exposure
Pathogensis
1. Neutrophils
• 1st line of defence
• Controlling bacterial challenge and destroying periodontal tissue
• Migrate from subepithelial plexus to gingival pocket by chemotaxis
• They do phagocytosis & kill them by biological bleach
• Biological bleach = myeloperoxide + oxygen radicals
• MMP-8 (Neutrophil collagenase)  destruction of peridontal tissue
• Predominant cells  in peridodontal pocket
• Most common in exudate of  acute periodontal abscess

• Mmp 8  inhibited by  tetracycline

Neutrophils abnormalities
• Defective chemotaxsis  aggressive periodontitis
• Neutropenia
• Chediak-higashi syndrome
• Papillon lefevre syndrome
2. Macrophages
• Anitgen presenting cells (APCs)
• Like monocyte & dendritic cells
• Regulare immune response by relasing  cytokine IL-8

3. Mast cells
• Cause vasular  permiability & dialation
• Produce  IgE

4. Lymphocytes
• B cells become plasma cells & make  antibodies
• T helper (CD4) cell helps in communication
• T-cytotoxic cell (CD8) kills intracellular antigens
• N-K cells are T-cells that  recognize & kill tumor & virally infected
 Pro-inflammatory mediators
1. IL-1  bone resoprtion
2. IL-6
3. TNF-a  macrophage activation
4. PGE2
5. MMP  collagen destrution (released by neutrophils)
 Anti-inflammatory mediators
1. IL-4
2. IL-10
3. Timps
 Pathogenesis of gingivitis
Stage 1
• Initial lesion  2-4 days
• Neutrophils , increased gcf

Stage 2
• Early lesion  4-7 days
Reversible
• T-lymphocytes, increased collagen loss
• BOP

Stage 3
• Established lesion 14-21 days
• B-lymphocytes, mature plasma cells, collagen loss
• Change in  color, contour, consistency

Stage 4
• Advanced lesion
 Phases of acute inflammation
1. Vascular phase
• Initially  vasocontriction (temporary)
• Folled by  vasodialation
• Increased vascular permeability

2. Cellular phase
• Leukocytes  PMNs predominant
• Macrophages appear late

• Cell involved in acute inflammation  mast cells, basophils,

platelets
Treatment
planning
Short term goal
• Reduce gingival inflammation
• Confort & esthetics

Long term goal

• Eliminate pain
• Arrest soft & hard tissue destruction
• Establish occlusal stability & fuction
• Reduce teeth loss
• Prevent disease recurrence
• Function & health
 Preliminary phase  0

• Treat emergencies  endodontic / periodontitc abscess

• Extract hopeless teeth
 Phase 1 / non- surgical phase
Plaque control & pt education
• Diet control
• Caries control
• Prophylaxsis, scaling & root planning, OHI,
• Correct restorative irritations  overhang,
• Local & systemic antibiotics

Periodontal re-evaluation
• Done after 4-8 weeks of phase 1 treatment
• For allowing healing & formation of JE
 Phase 2 / surgical phase
Reduce or eliminate peridontal pockets
• Correct soft & hard tiiseu defects
• Regenerate periodontal tissue
• Implants
• Periodontal therapy
• Endodontic therapy
 Phase 3 restorative phase
• Not reached until periodontal disease is controlled
• Fixed & removable prosthesis
• Final restorations
 Phase 4 maintainence phase
Supportive periodontal therapy
• Periodoic ongoing evaluation of pts OH
• Periodoic ongoing evaluation of periodontal tissues
• Periodntal maintainence is performed in a conitinium with phase
2 & 3 every 3 months for the first year
 Risk elemenets
1. Risk factors
• Associated with disease
• Smoking, diabetes, pathogenic bacteria, plaque

2. Risk determinent
• Unchangable background characteristics
• Increase likehood of disease
• Age , genetics, gender, socio-economic status

3. Risk indicator
• Not causally associated with disease
• Point higher disease
• Stress, osteoporosis, HIV /AIDS, infrequent dental visits

4. Risk marker / predictor

• Quantatative association with disease
• Previous hsitory
Prognosis
• Prediction of the outcome of the disease
• Prognosis for individual teeth must be considered in context of
entire dentition

Clincial factors
• Age  young with same disease as older has worst prognosis
• Disease severity  CAL (most imp in determining the
prognosis)
• Plaque control  poor OH
• Patient compliance
• Vertical bone loss  better prognosis with regenerative therapy (3
wall defect)
Systemic factors
• Smoking
• Diabetes  uncontrolled  worse
• Parkinsons  unable to maintian OH

Local factors
• Plaque
• Calculus
• Sub-gingival restorations  plaque retention

Anatomic factors

Prosthetic & restorative factors

Instruments in
scaling & root
planning
Sickel scaler
• For supra-gingival calculus
• Two cutting edges
• Pointed tip
• Triangular  cross section
 Curretes
• For sub-gingival calculus
• Rounded tip

1. Universal
• Used in any area of mouth
• Two cutting edges
• Semi-circle  cross section

2. Gracys
• One cutting edge
• Semi-circle  cross section
• For specific areas
• Gracy  1-2 3-4  anteriors
• Gracy  5-6  anterior & premolars
• Gracy  7-8 9-10  posterior facial & lingual surface
• Gracy  11-12  posterior mesial
Ultra-sonic scalers
• For tenacious calculus

Contra-indicated
• Pace-makers
• Infectious disease  spread by aerosols
• Respiratory disease risk

Types
• Magneostricitve  elliptical pattern
• Piezoelectric  linear pattern

Functions of scaler
• Lavage  flush with water
• Cavitation  air bubbles collapse and release energy to flush out debris
• Vibration mechanically remove deposits & debris
• Acoustic turbulance  agitation observed in fluids by mechanical vibrations that
 Strokes

Exploratory  light feeling strokes, probe & explorers (ppd & cal)

Scaling  short storng pull

Root planning  light-moderate pull stroke for final smoothing

Ultrasonics  light-intermittent stroke, tip parallel to root surface in

constant motion

Inserteing currete in pocket  0 degree angulation b/w tooth &

blade (close)
Scaling & root planning  angle should be 45-90 degree (open-
 Prophy cup & brush
• Prophylaxis for the pt
• Remove supragingival plaque
Cup
• Flexes on the slight pressure to the contours of teeth & pocket
access
Brush
• Enables better access to  groves & interproximal areas
Prophy jet
• Delivers slurry of water & biocarbonate to remove
extrinsic stains
Surgical therapy
 Gingival surgery (1)
• Only involving gingiva
• Above mucogingival junction
• Healing by secondary healing / intention

1. Gingivectomy
To eliminate
• Suprabony pockets
• Gingival enlargement

2. gingivoplasty
• Excision To reshape tissue deformity
• Esthetic issue
3. Distal wedge
• To reduce pocket distal to terminal molar
• Maxilla  full thickness flap + parallel incisions
• Mandible  full thickness flap + V-shaped incisions
 Muco-gingival surgery (2)
Free gingival graft
• Widen band of keratinized tissue
• Keratined tissue  stronger, good hygiene
• Happens below or apical  gingival margin
• Ideal thickness  1 – 1.5
• Common donor site  palate

Connective tissue graft

• Root coverage
• For recessed tooth
• Happens above or coronal  gingival margin
• Common donor site  palate
Frenectomy
• Removal of frenum

Frenotomy
• Incision of frenum

Vestibuloplasty
• Deepen the vestibule
• Make incision in base of vestibule
 Osseous surgery (3)
• Architecture = bony defects

1. Postive architecture
• Interproximal bone coronal to radiculur
• Interprximal higher then radicular
• This is most desired

2. Flat architecture
• Interpoximal bone at same level of radicular
• Same height

3. Negative architecture
• Interradicular bone apical to the radicular bone
Ostectomy
• Removal of supporting bone  alevolar bone
• Aggresive

Osteotomy
• Removal of non-supporting bone
• Reduce bone away from the tooth
• After osteotomy there remains peaks of bones at the line angle
called  widow peaks
• Widow peaks predisposes to  periodontal pocket in that area
 Healing after surgery
1. Regeneration
• Complete restoration of architecture & function

2. Repair
• Not complete restoration of architecture & fucntion
• Heal by scar or formation of long JE

3. Reattachment
• Reunion of epithelia & C.T to the root surface afgter incision or injury

4. New attachment
• Embedding of new pdl fibers in the new cementum that have been
previosuly deprived by of its original attachment
 Periodontal regeneration (4)
• Also formerly know as  guided tissue regeneration (GTR)
• Regenrate  bone, PDL, cementum
• Pdl regeenration  coronal movement

Barrier membrane
• Is the tank  protects tissue
• Prevent soft tissue downgrowth  epithelial cells
• Permits hard tissue ingrowth
• Membranes  ePTFE,

Bone graft
• Damage
• Regenerative missing bone
• Osteo-inductive, osteo-conductive , osteogenic

Biologic agent
• Healer
Wound healing
• These cells populate the wound area
Epithelia cells  1
C.T cells  2
PDL cells  3
Bone  4

• Soft tissue grow faster then bone & pdl

• So if it gets space it will occupy before bone
Direct root surface treatment
• Chelating agents expose collagen fibrils through demineralization
& may improve ne attachment  EDTA & citric acid
 Periodontal pack
• Contains  ZOE
• Leave in place for 1 week
• Pack do not enhance healing
Used
• Protect surgical wound
• Prevent tissue displacemnt
• Prevent Post op bleeding
• Minimize discomfort
 Bone graft materials
1. Autograft
• From your self
• Cortical bone graft
• Cancellous  (jaw bone--> chin, max tuberosity, iliac crest, tibia)
• Best  has all three qualities  osteo-conductive, osteo-inductive & osteo-
genic

2. Allograft
• Another human  cadaver
• Next best  osteo-conductive & inductive

3. Xenograft
• From another species / animal  cow, pig

4. Alloplast
Osteoconductive
• Scaffold  forming physical scaffold
Osteo-inductive
• Converting progenitor cells to osteoblast
Osteo-genic
• Make bone
1 & 2 wall defect
• Ossecous resection (ostectomy)
• To recontour bone to restore positive architecture
• Hemiseptal  1 wall
• Crater  2 wall

3 & 4 wall defect

• Regeneration
• Better blood supply & cell source proximity
• Deep narrow 3 wall defect  ideal for regenerating infrabony defects
• Trough  3 wall

Hamp class 2 furcation

• Ideal for regenerating furcation defects

Miller class 1
• With thick gingival biotype
• Wide keratinized tissue
Flap design
 Classification
Tissue content
• Full thickness
• Partial thickness

Flap placement
• Displaced
• Non-displaced

Papillae management
• Conventional
• Preservative
 Flap design
Rules
• Base should be wider then top  to ensure blood supply
• Incision over healthy bone  avoid bony defects & eminences
• Rounded corners
• Vertical relase at line angle  no mid facial or mid papilla
• Avoid vital structures  nerves, arteries
• Post-operative plaque control  most imp after periodontal
surgery
 Flap thickness
Split / partial thickness/ mucosal
• Ginginva, mucosa, submucosa
• Used for muco-gingival surgery  no need to expose bone

Full thickness / muco-periosteal

• Gingiva, mucosa, periosteum
• Used for osseous surgery & periodontal regeneration  to permit
primary closure, also used in apically positioned flap

• Whenever bone exposed  1mm bone resoprtion &

remodeling
 Full thickness flap
• Mucoperiosteal  mucosa + periosteum
• Good for modifying bone
• Bad for thin bone  chances of dehiscience & fenestration
Horizontal incisions

1. Internal or reverse bevel

• 1mm from gingival margin
• Removes pocket lining but preserves outer gingiva

2. Sulcular / crevicular
• Through base of pocket to alveolar crest

3. Interdental or inter-proximal
• Removes the collar of tissue around the tooth u created with first
2 incision
1. Modified widman flap
• Combination of all three incisions  precise horizontal
incision
• Provides access to subgingival areas for  debridement,
cleaning
• Goal of new attachment
• Not reduction of osseous defects  no osteotectomy
• Atraumatic flap

2. Apically repositioned flap

• Requires additional  vertical relasing incision beyong muco-
gingival junction in order to attain pocket reduction
 Partial thickness flap
• Mucosal tissue
• Leave perisoteum intact for vascular bed for  graft
 Displaced flap
• Displaced
• Placed  coronal, lateral or apical to the original position
• Vertical incision into alevolar mucosa beyond muco-gingival
junction  to increase mobility
• Can not be palatal  they can not b displaced
Non-dispalced flap
• Flap returned back to its original position
Conventional flap
• Split papilla in half
• Needed whrn interdental space is too narrow
• Can lead to formation of black  triangle
• Modfied windman & apically positioned flap (examples)

Papilla preservation flap

• Preserve the papilla
• Oblique cut  lingual line angle of 1 tooth to facial line angle to
adjacent tooth
• Scallop  line angle – line angle on lingual surface
• Scallop  line angle – line angle on facial surface
 Flap examples
1. Coronally placed
• For single or mulitple-tooth recession defect
• Root coverage
• Increase pocket depth

2. Laterally positioned
• Also called pedicle flap / double papilla technique
• For small single- tooth recession defect  most common
• Better color match & less damage
• Root coverage
• No change in pocket depth

3. Apicaly positioned
• Reduce pocket depth
• Expose impaced tooth
• Crown lenghtening
4. Modified widman
• Facilitates surgical debridement
• Does not directly reduce pocket depth
• Eliminate pocket lining  gingival curretage
• Pocket reduction  after healing

5. Undisplaced
• Most common now
• Improve access  to clean
• Remove entire pocket wall  eliminates pocket completely
• Aggressive & less technique sensitive

6. Semilunar
• Cresent shaped
• Conservative
• Apicoectomy
7. Envolope
• Most common in oral srgery
• Quick & easy
• No vertical releasing incisions
• Full thickness non displaced flap

8. Distal wedge
• Distal to terminal molar followind wisdom tooth extraction
• Reduce pocket depth
• Maxilla  parallel
• Mandible  traingle
• No partial flap as it is  full thickness flap
1. Free gingival graft
• Wide band of keratinized tissue
• Donor site  posterior hard palate, partial thickness flap
• Recipient site  partial thickness flap

2. Connective tissue graft

• Root coverage
• Donor site  posterior hard palate, partial thickness flap
• Recipient site  partial thickness flap
Adjuntive
therapy
 Antibiotics (1)
• Decrease number of bacteria in  pocket
• Should be only used as adjunct to mechanical debridement in phase 1
• In aggressive & refractory periodontitis
• Bacteriocidal & bacteriostatic drugs should not be used at same time

Tetracycline
• Concentrate in  GCF
• Doxycyline 1dose / day  improve pt compliance

Most affective against periodontitis

• Amoxcillin (550mg tid) + metronidazole (250mg tid) For 14 days
• Duration is most imp then the dose
• Avoid alcohol with metronidazole
Local delivery antibiotics (LDA)
• When localized recuurent or residual
• Probing depth  more then 5mm
• Inflammation still present following conventional therapys

Drugs
• Arrestin = minocycline
• Atridox = doxycycline
• Perio-chip = chlorhexidine glucanate
 Host modulation therapy (2)
• Down regulate destructive aspects of the host response
• Should be only used as adjunct to mechanical debridement in
phase 1
• In chronic periodontitis

Drugs
NSAIDs
• Inhibits Prostaglandins = inhibits inflammation

Bisphosphanates
• Inhibit osteoclast = not bone resorption
• Side effect  BRONJ (bisphosphonate related osteonecrosis of jaw)
Subantimicrobial dose doxycycline (SDD)
• Inhibits MMPS (released by neutrophils , destroy type 1
collagen of pdls )
• Inhibits  collagenase (inbde question for host modulation
therapy)
• Mostly used only currently approved by FDA & ADA
• 20mg twice/day for 3-9 months (periostat)

Locally administered host modifing agents

• These may also periodontal regeneration
• Emdogain – enamel matrix protein
• PDGF = GEM 21S
 Occlusal correction (3)
• Sometimes root problem is occlusal
• Bad occlusion may progress / fasten the peirodontitis process

Radiographic signs
• Widening of  pdl space
• Thickening of lamina dura
• Angualr bone loss
• Root resorption
• Hypercementosis
1. Traumatic occlusion
• Force of trauma exceeds the repairative capacity of attachment
apparatus
Types
a) Primary occlusal trauma
• Excessive force on normal periodontium

b) Secondary occlusal trauma

• Normal occlusal forces on reduced periodontium

Fremitus  phenomenon
• Vibration of teeth upon closing
Occlusal therapy
• Delayed until or after inflammation has resolved

a) Coronoplasty
• Occlusal adjustments
• Reshaping & recontouring occlusal surface

b) inter-occlusal appliance
• Bite guards
• To distribute forces to all teeth  minimize excessive force on individual
teeth

c) Splinting
• Improve pt comforat & fuction
• By immobilizing excessive mobile teeth
 Furcation correction (4)
• Furcation area  imposible to clean

Furcation correction
1. Furcationplasty
• Move furcation up
• More accessable
• To make it clean

2. Tunneling
• Create the tunnel  increase furcation
• We move tissue apically
3. Root resection
• Cut one root
• Endo treatment + crown
• Easy of clean
• Eg :- distobuccal root is resected in 1st max molar

4. Hemisection / premolarization
• Cut tooth in half
• Make 1 molar to 2 premolars
Prevention &
maintainence
 Toothbrushing
Bass method
• Bristles at 45 degrees at gingival margin
• 0.5mm into the sulcus

Brush
• Soft nylon
• Change every 3months

Trauma from tooth-brush

• Usually occurs in  canine, premolar
• Causes  recession, laceration, v-shaped notches on cervical area
• Dentine abraded  25 times faster then enamel
 Flossing
• Flossing does not prevent cavitys
• Flossing does prevent gum disease
• Don’t forget to
 Water pik
• Home water irrigation system
• Flush out debris & reduce baterial load on gingiva
• No the biofilm on the tooth
 Epidemiology
• Chronic > localized aggressive > generalized aggressive >
refractory
• Chronic most common  african male

Maintenance
• Re-evaluation  4-8 weeks after phase 1 therapy
• Periodontal therapy  every 3 months 1st year
Endodontis
 Pulp biology & tooth pain
Pulp biology
• Contains loose fibrous C.T  with nerves, vessels, lymphatics
• Contains  fibroblast
• Contains  odontoblast (secrete dentine)
• Contains undifferentiated mesenchymal cells
• Pulp is surronded by hard dentine  limits the ability to expand
• Lacks collateral circulation limits its ability to cope with infection

Odontoblast
• Primary dentine  before root completion
• Secondary dentine  after root formation complete

Udifferentiated mesenchymal cells

• Make secondary odontoblast  which makes  tertiary dentine
 Dentine & pulp defence
• Sclerotic dentine  calcification of dentinal tubules in resposne to
caries or ageing
• Reactionary dentine / secondary dentine  reaction to the
minor damage
• Repairative dentine / tertiary dentine  repair for major
damage

• Pulpal necrosis  response to the advancing caries or other

severe damage

• Pulp caping  makes either repairative or rectionary

 Histologic zone of pulp
• From out to in
1. Predentine
2. Odontoblastic layer  all nuclei here
3. Cell free zone of weil  no cells here, nerve bundles here
4. Cell rich zone  nuclei & cells
5. Pulp core
 Fibers in pain
A delta fibers  dentinal pain
• Large myelinated
• Afferent nerve
• Course  coronally through pulp (pulpo-dentinal junction)
• Sharp. Transient  first pain (fast pain)
• Not associated with Cold (dentinal pain)

C fibers  pulpitis pain

• Small unmyelinated
• Afferent nerve
• Course  central pulp
• Dull throbbing  second pain (slow pain)
 Pain sensitization
Hyperalgesia
• Heightened / more resposne to pain
• Inflammatory mediator in pulp  increase pain intensity

Allodynia
• Reduced pain threshold, pain due to stimulus that does not
normally provoke pain
• Sun burn  normally touching skin does not hurt, but when sun
burn tocuhing causes pain

Referred pain
• Peri-auricular pain often refers form mandibular molars, as both
 Endodontic diagnosis
1. Pulpal diagnosis
• Normal pulp
• Reversible pulpitis
• Irreversible symptmatic pulpitis
• Irreversible asymptmatic pulpitis
• Pulpal necrosis
• Previously treated pulp

2. Peri-Apical diagnosis
• Normal apical tissue
• Symptomatic apical periodontitis
• Asymtomatic apical periodontitis
• Acute apical abscess
• Endo lesion  originates in pulp
• Perio lesion  originates in culcus
• Perio-endo lesion  treat endo first then perio
1. Normal pulp
• Asymptomatic
• Mild to moderate transient response to thermal & electrical stimuli

2. Reversible pulpitis
• Symptomatic
• Cold stimulus  quick, sharp, hypersensitive transient response (hyperalgesia)
• No complaints of spontaneous pain
• Caused by  irritant that affects pulp (caries, deep cleaning, deep restoration)
• Symptom, not a disease

3. Symptmatic Irreversible pulpitis

• Symptomatic
• Irreversible pulp damage  even if u remove the irritant
• Characterized  spontanous intermittent / continious pain
• Cold  lingering pain
• Postion change / nocturnal change  pain (bending, lying)
• Radiograph  insufficent
3. Asymptmatic Irreversible pulpitis
• Pulp response Normal
• Histologically  irreversible changes / damage to pulp

4. Pulpal necrosis
• Usually asymptomatic but not always
• Can be partial or total
• Due to long term interuption of blood supply to pulp = necrosis
• Discoloration of crown  treat with rct & internal bleaching
• Common cause  trauma (anterior teeth)

• Necrotic pulp left untreated  toxins spread beyond apical

foramen
•
 Pulp testing
Endo ice
• Dichlorodifluoromethane
• -30 degress
• Chilled pellet applied to middle third of facial surface
• Normal pulp  normal response, non lingering  1-2 SECS AFTER REMOVAL
• Reversible pulpitis  heightend non lingering  1-2 SECS AFTER REMOVAL
• Symptomatic irreversibsle  heightend lingering
• Asymptomatic irreversibsle  normal response
• Pulp necrosis  no response
NO RESPONSE TO THERMAL TEST  NECROSIS, OBLITERATION, IMATURE TOOTH, RECENT
TRAUMA

Electric pulp test (EPT)

• Least reliable
• Indicates if there are  vital sensory fibers in pulp  1-79 VITAL, 80 NESCROSIS
• Does not tell about  vascular supply to pulp
• False +ve - touch gingiva, tooth not dried properly
• False –ve  recent traumatized tooth, calcified canal
1. Normal apical diagnosis
• Asymptomatic
• No TTP
• No pain on palpation
• No radiolucency

2. Symptomatic apical periodontitis

• Painful inflammation around the apex
• TTP +ve  intense throbbing pain
• Localized inflammatory infiltrate with in pdl
• If tooth vital & this issue  simple occlusal adjustments relieve pain
• If tooth necrotic  RCT

3. Asymptomatic apical periodontitis

• Asymptomatic
• Periapical radiolucency  radicular cyst, granuloma
• Confirmation of pulpal necrosis
4. Acute apical abscess
• Rapid swelling
• Severe pain
• Purulent exudate (liquefaction necrosis) aroun apex

5. Chronic apical abscess

• Draining sinus tract  small swelling, pinpoint swelling type
• Without discomfort or little
• Put GP into the tract & take  radiograph
 Periapical diagnosis
1. Percussion
• Taping on the tooth
• Determines Prescence of inflammation in the pdl

2. Palpation
• Feeling on the gums by finger around the apex of the tooth
• Indicates  spread of inflammation from pdl to the overlying
periodontium

3. Radiographs
 Root Canal Treatment
1. Access prep
• Deroof the chamber to access the pulp
• Straigh-line access to orifice & apex
• Conservation of tooth structure
• Occlusal  posterior
• Lingual  anterior
• Burs  round / tapered
• Rubber dam should be placed if possible

• Incisors  triangular (to remove pulp horns, straight line acces, preserve
marginal ridges )
• Canine  ovoid / oval
• Premolars  oval (bucco-lingually)
• Max molars  blunted triangle / rhomboid
 Canals
Maxillary
• Central  triangle  1
• Lateral  ovoid  1
• canine  ovoid  1
• 1st premolar  ovoid / oval  2 (75%) , 1 (20%)
• 2nd premoalr  ovoid / oval  1 (75%), 2(25%)
• 1st molar  rhomboid / blunted traingle  4 (60%), 3(40%)
• 2nd molar rhomboid / blunted traingle  3 (60%), 4(40%)

Mandibular
• Central  triangle /ovoid 1 (95%)
• Lateral  ovoid  1  1 (70%), 2 (30%)
• canine  ovoid  1 (95%)
• 1st premolar  ovoid / oval  1 (80%) , 2(20%)
• 2nd premoalr  ovoid / oval  1 (90%), 2(10%)
• 1st molar  trapexoidal  3 (70%), 4(30%)
 Instruments
1. S.S hand file  0.02 taper (file gets 0.02 thick ervey 1mm u go down)

a) K-files (kerr)
• Twsited square shape
• Watch-winding method
• Cross section  diamond, square, triangular

b) H-file (hedstorm)
• Spiral cone
• Only cuts in retraction (when pulling out)
• Tear drop  cross-section

2. NiTi rotary
3. Gates gilidden drill
• To open orifice

4. Barbed broach
• Entangle & remove

5. Reamer
• Twisted triangle shape
• Clock-wise motion
Color
• Pink  6
• Grey  8
• Purple  10

• White  15, 45
• Yellow  20, 50
• Red  25, 55
• Blue  30, 60
• Green  35, 70
• Black  40, 80
 2. Cleaning & shaping
1. Crown down
• Big to small
• Usually done with rotary
• Start by shaping coronal third by big file
• Poor fit = less friction = more efficiency
• Less chances of instrument breakage

2. Step back
• Small to big
• Usually done with  hand files
• Apical third prepared first
• Good fit = more friction = less efficient
 3. Irrigation & medicament
• With each file irrigation is must
Irrigation solutions
1. Sodium hypochlorite (NaOCl)
• Bleach
• Dissolves organic matter  bacteria

2. Chlorhexadine
• Kill or inhibit the microorganism
• Lack the solevnt action
•
Chelating agent
1. EDTA (ethylenediamine tetra acetic acid)
• Lubrication
• Dissolves inorganic matter  smear layer
• Chelating agent
• Active agent  RC-prep

Intracanal dressing
1. Calcium – hydroxide
• Odor less
• Medicament of choice
• Antibacterial  Cautaring & high ph
Chloroform
• Dissolves gp in retreatment
Endodontic microbiology

a) Primary endodontic infection

• Bacterioides  gram –ve obligate anerobes ( can not live in O2)

b) Failed endodontic treatment

• Enterococcus faecalis  gram +ve facultative anerobe
 4. Obturation
• Filling & sealing the root canal system
• Gutta percha (GP) & sealer  ZOE

Types of obturation
a) Cold lateral  using spreaders & creating space & fill with gp
b) Warm vertical  melting & using plugger
 Surgical endo-treatment
• Persistant infection in apical area
• Retrograde rct

1. Incision & drainage

• Surgical opening in soft tissue to relase exudate & pressure
• Best for localized & fluctuant swelling

2. Trephination
• Surgical opening made into hard tissue to release exudate &
pressure
3. Periapical microsurgery
• Access through bone  at apex
• Retrograde filling  to seal apex
• Coronal seal already done rct + obturation + filling
• Resect 3mm with 0 – 10 degree bevel  root apex = apicoectomy

• Apicoectomy + retrograde seal (instrument with ultrasonic

instrument) = Periapical microsurgery

• Retrograde seal  MTA

 Complications
1. Ledge formation
• Artificial irrgeularity in canal
• Another path other then original path
• NiTi files  less likely to ledge

Causes
• No straight line access
• Longer canals
• Small diameter canal
• Curved canals
• No proper irrigation & lubrication
Treatment
• Use smaller instruments to bypass the canal  renegotiation
2. Instrument seperation
• Breaking into the canal
• Flexible NiTi files  more likely to fracture
• Later the instrument breakage = better the prognosis (due to more
cleaning_
• Apical the breakage = harder the retrieval

Causes
• Excessive force
• Jumping file sizes  directly to big = fracture
• Poor irrigation & lubrication
• Not replacing files  reuse to many time

Treatment
• Retrieval
3. Perforation
a) Coronal perforation
• Through the crown
b) Furcal perforation
• Through the pulpal floor
c) Strip perforation
• Excessive coronal flaring
• Danger zone  mandibular molar in the m esial root on the distal
side (dentine here is too thin  strip perforation)
d) Root perforation
• Lateral root perforation  instrumentation into the ledge =
artificial apical formamen
• More apical root perforation = good prognosis
• Immediate hemorrhage or sudden pain = perforation

Treatment
• Internal repair  MTA
 Truamatic injuries
Trauma protocol
1. Tetanus boster  avulsion only (48hrs)
2. Radiographs
3. Antibiotics  avulsion only
4. Vitality check  pulp test
5. More 
6. Appointments  follow-ups (3 week  3month  6months  1 yrs
1. Uncomplicated fracture
• All fractures of teeth without pulp involvement
• Enamel only  smooth edges
• Enamel + dentine  restore

2. Complicated fracture
• Pulp involvement
• Less than 24hrs  direct pulp capping (DPC)
• More then or equal to 24hrs  partial pulpotomy (cvek)
• More then or equal to 72hrs  complete pulpotomy (ppty)
3. Horizontal root fracture
• Should take  3 PA xray + 1 occlusal xray
• Ideal healing  calcific heal / calcific metamorphosis

Vital tooth  splint asap

• Coronal fracture  rigid spling 6-12 weesk
• Mid root fracture  flexible splint 3 weeks
• Apical fracture  flexible splint for 2 weeks max ( to avoid
ankylosis)

Necrosis  rct
• 25% chances of coronal fracture to necrosis
• Apical fracture necrosis  rare
4. Concussion
• No displacement
• No mobility
• Pdl  sore
Treatment
• Do nothing
• Soft diet
• No biting
• Ohi
5. Subluxation
• No displacemnt
• Mobility present  tooth loose in socket
• Pdl rips & bleed

Treatment
• Flexible splint  1-2 weeks
• Closed apex  6% chances of necrosis
• Open apex  good prognosis
6. Extrusion
• Tooth little out of socket not completely
Treatment
• Open apex  reposition + felxible splint, monitor
• Closed apex  reposition + felxible splint, rct if needed

• 65% chance of necrosis  closed apex

7. Lateral luxation
• Displacement of tooth in any direction except axially
• Usually crown  palatally
• Root  labially
Treatment
• Open apex  reposition + felxible splint, monitor
• Closed apex  reposition + felxible splint, rct if needed

• 80% chance of necrosis  closed apex

8. Intrusion
• Apical displacement of the tooth
• Damages  vessels

Treatment
• Open apex allow to re-erupt
• Closed apex  reposition, flexible splint, rct

• 96% chances of necrosis  closed apex

9. Avulsion / ex-articulation
• Out of socket
• Extra-alevolar dry time (EADT)  time tooth is out os socket & dry
• More the tooth out of socket = worst prognosis

Treatment
• Reimplant asap, flexible splint for 2 weeks

• Closed apex < 60 min EADT  reimplant, splint

• Open apex < 60 min EADT  reimplant, splint, no rct but
apexification at first sign of infected pulp
• Closed apex > 60 min EADTreimplant, splint, rct
• Open apex > 60 min EADT  reimplant / not, splint, rct, implant
Storage media
1. Hank sol
2. Milk
3. Saline
4. Saliva
5. Water  least desirable
10.External resoprtion
• Long term after trauma
• Initiate  periodontium (due to damage to cementoblastic layer)

Types
a) Replacement resorption
• Ankylosis & replacement of pdl with bone
• Can be due to splints

b) Cervical resorption
• Subepithelial sulcular infection from trauma or non vital bleaching
• Initiate at  CEJ
• Appearance  ragged moth eaten appearance
• Clinically  pink spot

c) Inflammatory root resorption

• Bacteria & byproduct from nectrotic pulp travel through dentinal tubules to the periodontium
• Margin are ragged & poorly defined
• Lesion moves - moves with angled radiographs
11.internal resorption
• Initiate  with-in canal (deu to damage to odontoblastic layer)
• Better prognosis & easier treatment then external
• Inflammation due to necrotic pulp from caries or trauma

• Sharp defined margins  which do not move with angled

radiographs
• Lesion at centre of the tooth

Treatment
• Rct
• Flowable obturation material
12.Calcific metamorphosis
• Trauma  induces odontoblast to make more repairitive / tertiary
denitne

Clincally
• Yellow – organge color tooth
• Obliterated canals
• More likely with  open apices, intrusion, severe crown fracture
 Adjuntive therapy
Calcium hydroxide (CaOH2)
• Stimulates secondary odontoblast to repair with  dentinal bridge /
tertiary dentine formation
• High ph  12.5 (cautrizes tissue, kills bacteria)
• Resorpable

Mineral trioxide aggregate (MTA)

• Stimulate cementoblast  to form hard tissue
• Three mineral  calcium, silicon, aluminum
• Bismuth oxide opaccifier (can leak & stain the tooth)
• Long setting time  3 hrs
• Sets in presence of moisture
 Vital pulp therapy
1. Pulp capping

a) Direct
• CaOH2  hard barrier formed with-in 6weeks (REPAIRITIVE DENTINE)
• Directly placed on healthy pulp on the exposure
• Carious / mechanical  Exposure 2mm or less
• Traumatic exposure  less then 24hrs

b) Indirect
• CaOH2, MTA or RMGIC
• When near healthy pulp & thin dentine left
• Deep caries
2. Pulpotomy
• Temporary in permanent tooth as it cause  obliteration, necrosis, = poor
prognosis

a) Partial / CVEK
• Also known as shallow pulpotomy
• Removal of the small portion of the infected coronal pulp
• Truamatic exposure  more then 24hrs
• Carious or mechanical exposure  more then 2mm

b) Complete
• Removal of coronal pulp
• For primary – vital & primary restorable tooth with pulp exposure
(asymptomatic)
• Traumatic exposure  more then 72hrs
• Fromacresol to attain  hemostasis
Buckley formacresol
• 19% formaladehyde
• 35% cresol
• 15% glycerine
• 31% water
• Bacrteriocidal + fixation
• Used  pulpotomy
3. Apexogenesis
• Done in open apex permanent tooth
• Pulpotomy + mta / CaOh 2  close the apex

Contraindication
• Avulsion
• Severe horizontal fracture
• Necrotic teeth
• Non-restorable
 Non vital pulp therapy
1. Pulpectonmy
• Same as rct
• No gp obturation
• Obturation doen with  ZOE

2. b
• Immature permanent tooth  where pulp can not b saved
• Rct
• Then place  MTA / CaOh2  to make apical barrier
 Cracked tooth syndrome
• Pain on  release
• Sensitive to  hot & cold
• Sometime  asymptomatic
• Crack usually extend deep into the dentine & propogate mesio-distal  on marginal
ridges

Diagnosis
• Dyes
• Transillumination  more better then radiographs
• Tooth slooth on each cusp  aids in loaction of the crack
• Common teeth  mandibular 2nd molar  mand 1st molar  maxillary premolar s

Treatment
If normal pulp
• Splint with band & observe or place crown
Diseased pulp
 Vertical root fracture
• Start apically & progress coronally
Occurs
• After cementation of post
• Excessive condensation forces of overprepared canals  (most
common)

Diagnosis
• Isolated probing defect at the site of fracture
• J-shaped / teardrop radiolucency
• Narrow periodontal pocket
• Sinus tract  does not trace to the apex of the root

Treatment
• Single rooted  extract
 Bleaching
1. Vital
a) In office
• Power bleaching
• Hydroperoxide 30 – 35 %
• Hypersensitivity
• Periapical periodontitis
b) At home
• Night guards
• Carbamide peroxide

2. Non vital  also called  intracoronal, internal

a) In office
• Thermo-catalytic bleaching
• Hydroperoxide 30 – 35 %
• Cervical resorption
b) At home
• Walking bleach
• Sodium perborate
Case difficulty
Three things
• Pt consideration
• Diagnostic & treatment consideration
• Other

1. Low
• Uncomplicated
• Favourable results

2. Moderate
• Complicated pre-operative tooth condition
• Achieving favourable results  may b hard to achieve by competent doctor

3. High
• Very Complicated pre-operative tooth condition
Low difficulty  should check all boxes
Moderate  even 1 box check = moderate
High  any boxes checked in high or 3 boxes checked in moderate =
high difficulty case
 Medical class history
Low
• ASA class 1  no systemic disease, generaly healthy pt
• ASA class 2  mild systemic illness without functional restriction eg:-
controlled hypertension

Moderate
• ASA class 3  severe systemic illness but not life threatening

High
• ASA class 4  complex medical hsitory, severe severe illness & is life
threatening

• ASA class 5  less then 24hrs to live (no endo here)

 Anestheisa
Low
• No history of problems with anesthesia

Moderate
• Vasocontrictive intolerance
• CI  to epinephrine
• Eg:- hyperthyroidism , allergy to sulphite, pheochromocytoma

High
• Difficulty achieving and or maintaing anesthesia
 Patient disposition
Low
• Cooperative & compliance

Moderate
• Anxious but coperative

High
• Uncoperative
 Ability to open mouth
Avg mouth opening
• Male  50mm
• Female 45mm

Low
• No limitation

Moderate
• Slight limitation
• Less then 35mm

High
• Significant limitation
 Gag reflux
Low
• None

Moderate
• Occasional

High
• Extreme
 Emergency condition
Low
• Minimum pain or swelling

Moderate
• Moderate pain & swelling

High
• High pain & swellling
 Diagnosis
Low
• Sign & symptoms consistant with recognized pulpal & periapical
condition
• Eg :- irrevrsible pulpitis with symptoimatic apical periodontitis

Moderate
• Extensive differential diagnsosis of the usual sign & symptoms
• Doing many test  differential diagnosis

High
• Confusing sign & symptoms with difficult diagnosis
• Eg:- trigminal neuralgia, fibromyelgia
 Radiographs
• How difficult is it to read radiograph
Low
• Clearly visible canal & apex

Moderate
• High floor of mouth
• Narrow palatal vault
• Tori

High
• Superimposed anatomical structures
• When cbct is required
Tooth type
Low
• Anteriors
• Premolars

Moderate
• 1st molar

High
• 2nd & 3rd molar
Tooth inclination
Low
• Less then 10 degress

Moderate
• 10-30 degress

High
• More then 30 degress

• Exception is molar  tipped mesially = more access

 Rotation
Low
• Slight
• Less then 10 degress

Moderate
• 10-30 degress

High
• More then 30 degress
 Tooth isolation
Low
• Rubber dam placement

Moderate
• Simple pretreatment medication before rubber dam
• Remove calculus
• Hemostasis for bleeding first

High
• Extensive pretreatment medication before rubber dam
• Severe carious & remove it  then determine restorability &
restore it before placing rubber dam
 Crown morphology
Low
• Original
• Normal

Moderate
• Moderate deviation
• Microdontia, taurodontism
• Full coverage restoration
• Carious tooth

High
• Significant deviation
 Canal morphology
Low
• Sligh or no curvature
• Closed apex

Moderate
• Moderate curvature 10-30
• Narrow apex opening  1-1.5mm

High
• Extreme curvature  more then 30  s –shaped
• Extra root 
• Very long tooth
• Open apex

• Mandibular molar extra root lingually  radix entomolaris

 Radiographic apperance of canals
Low
• Visisble & patent canals

Moderate
• Visible but reduced canals
• Pulp stones

High
• Not visible
• Obliterated canals
 Proximity to vital structure
Low
• Apex to vital structure  more then 5mm

Moderate
• Apex to vital structure  3-5mm

High
• Apex to vital structure  less then 3mm
 Resorption
Low
• No resoprtion

Moderate
• Minimal apical resorption

High
• Extensive apical resorption
• Internal or external resorption
 Trauma history
Low
• No history
• Uncomplicated crown fracture
• Ellis 1 & 2

Moderate
• History of fracture
• Complicated crown fracture of mature tooth
• Subluxation
• Ellis 3

High
• Complicated crown fracture of immature tooth  ellis class 3
• Root fracture
• Alveolar fracture
• Intrusion / extrusion
• Avulsion
 Endodontic treatment history
Low
• No previosu history

Moderate
• Previous access without any complication
• No obturation done in 1st appointment
• Obutration done in second  this considered moderate

High
• Previous access with complication  perforation, ledge, sepration
of instrument
• Previous endo treatment  reendo
 Peridontal endodontic condition
Low
• None to moderate periodontal disease
• Perio problem not associated with endo problem

Moderate
• Endo-perio lesions

High
• Severe periodontal disease  CAL
• Cracked teeth syndrome
• Root amputation priro to the endo treatment
Oral pathology
Developmental
condition
1. Cleft lip
• 1 in evrey 1000 births
• Unilateral  80 %
• Bilateral  20%
• Lack of fusion b/w medial nasal process & maxillary process

2. Cleft palate
• 1 in evrey 2000 births
• Failure of fusion b/w palatine shelves

3. Lip pits
• Invaginations commissures or the midline of lower lip
• VAN DER WOUDE syndrome  clefts + pits
4. Fordyces granules
• Ectopic sebaous glands (raised)
• Benign
• No treatment
• Buccal or labial mucosa

5. Leukoedema
• Whiteish or white-grey edematous lesion on the buccal mucosa
• Dessipates when cheek streached
• No treatment

6. Lingual thyroid
• Thyroid tisue mass the the midline bass of tongue
• Located along the embryonic path of throid descent
7. Thyroglossal duct cyst
• Mid line neck swelling
• Located along the embryonic path of throid descent

8. Geographic tongue
• Also known as  benign migratory glossitis or erythema migrans
• Central red islands surronded by white annular rings which change over
time

Association  nutritional deficiency, stress, hormonal imbalance

Symptoms
• Hurt
• Burn
Treatment
• Symptomatic
9. Fissured tongue
• Fold & furrows of the tongue dorsum
• Melkersson rosenthal syndrome  fissured tongue + facial
paralysis + granulomatous cheilitis

10.Angioma
• Tumor composed of vessels & lymph

a) Cherry angioma
• Extremely common
• Benigh
• Pinpoint  red mole
b) Hemangioma
• Congenital focal proliferation of capillaries
• Most undergo involution
• Persistant lesion  excison

c) Lymphangioma
• Congenital focal proliferation of lymph vessels
Oral lymphangioma
• Super rare
• Purple spots on the tongue
Systic hygroma
• When it is on neck

Sturge weber syndrome

• Angiomas of  leptomeninges (pia + archnoid) + skin (along
distribution of trigeminal nerve)
11.Exotosis & tori
• Bony growth
• Buccal exotosis  buccaly
• Palatal tori  on palate

12.dermoid cyst
• Mass in midline
• If above myleohyoid  floor of mouth
• If below mylohyoid  upper neck
• Contains  adnexal structure (hair +sebaceous gland)
• Doughy consistency

13.Branchial cyst
• Lateral neck swelling
• Epithelial cyst with in the lymph node of the neck (all cyst have
14.Oral lymphoepithelial cyst
• Epithelial cyst within the lymphoid tissue of oral mucosa
• Common site  Palatine & lingual tonsils
• Dyspnea, fluctuant yellow nodule

15.Stafne bone defect

• Radiolucency in posterior mandible  below mandibular canal
• Due to lingual concavity of the jaw

16.Nasopalatine duct cyst

• Caused by cystification of canal remainants
• Heart shaped radiolucency in nasopalatine canal
Treatment
18.Globulomaxillary lesion
• Any radiolucecny b/w  maxillary canine & lateral incisors
• No diagnosis
• It is clinical description

19.Traumatic bone cyst

• Also called  simple bone cyst, idiopathic bone cyst
• Pseudo-cyst
• Large radiolucency  scalloped around roots
• No epithelial lining  dead space in teenagers mandible
• Associated  jaw trauma
Diagnosis
• Aspirate
Treatment
Mucosal lesions
 reactive
1. Linea alba
• White line
• Focal hyperkeratosis
• Due to cheek bite

2. Traumatic ulcer
• Very common
• Ulcer  complete break in epithelium (mucosa + submucosa)
• Erosion  incomplete break (mucosa only)

3. Chemical burn
• Whitish sloughing appearance of the tissue
Can be due to
• Asprin
• Hydrogen peroxide
• Silver nitrate
4. Nicotine stomatits
• Inflammation of the sailvary duct in palate
• Pin-point red dots
• Only premalignant if  due to reverse smoking

5. Amalgam tattoo
• Trauamtic implantation of amalgam particles into the mucosa
• Radiograph  tiny radio-opaque particles (floating)
Clinically
• Black, blue or grey macules
6. Smoking associated melanosis
• Chemicals in tobacco stimulate  melanocytes
• Brown diffuse irregular macules
• In anterior mucosa
• Can also be  Related to smokeless tobacco
• Reversible  if quit smoking
7. Melanotic macule
• Benign hyperpigmentation in mucous membrane
• Freckle of mucosa
• Site  lower lip
Peutz-jeghsrs syndrome
• freckle + intestinal polyps

8. Hairy tongue
• Elongated filiform papillae
9. Dentifrice associated sloughing (toothpaste)
• Due to  sodium lauryl sulfate
• Cause  white sloughing of mucosa
• Suggest  toms of Maine, Rembrandt (toothpaste brands)
10.Submucosal hemorrhage
• Extravascular lesion that do not blanch
Types
• Petechiae  1mm (valsalva manuveur, violent cough, fellatio)
• Perpura  larger then patachiae
• Ecchymosis  1cm or bigger bruise
• Hematoma mass of blood with in tissue (due to injection)
Treatment
• Eliminate cause
• None
Mucosal lesions
 infections
Viral
1. Herpes simplex virus (HSV)
a) Primary
• When u get it first time
• Pan oral  anywhere in body
• Self-limiting
• Happens in childhood
• Treatment  symptomatic / pallaitive
• Remains dormant in  trigminal ganglion

b) Recurrent  (only on keratinized tissue)

• Triggers  stress, sunlight, immunosupression
• Keratined tissue  dorsal (up) of tongue, gingiva, lip (vermillion), hard palate

Herpes labialis / recuurent extra-oral herpes

• Fever blisters
• Cold Sore
• Vermillion border  lip
Recuurent intra-oral herpes
• Occurs  attached gingiva , hard palate

Herpetic whitlow
• Site  fingers
• Dentist should not perform anything until it subscides

Herpes gladiotorum
• Site  head
• Wrestlers

Treatment
• Acylovir  during prodromal period
2. varacella zoster virus (VZV)
Primary
• Called  varacella / chicken pox
• In childhood
• Self-limitng
• Dormat  trigeminal ganalion  mimic symptoms of pulpitis

b) Recurrent  shingles
• Shingles  recurrent painful bumps unilaterally
Triggers
• stress, sunlight, immunosupression
• Cylophosphoamine  imunnosupressor  activates VZV

Ramsay hunt syndrome

• Herpes zoster reactivation in geniculate ganglion
• Affects  CN 7 & 8
• Symptoms  facial paralysis, vertigo, deafness
Treatment
3. Coxsackie virus
• Hand, foot & mouth disease
Herpangina
• Posterior oral cavity
• Soft palate, throat & tonsils

4. Measles
• Rubella
• Kopliks spots  buccal mucosa
• Rash
Treatment
• Self limiting & childhood
5. Papilloma
• Also called  wart
• Caused  human papiloma virus (HPV)
• Benign epithelial pedunculated or sessile proliferation on skin or
mucosa
• Dorsam of the tongue

6. Verruca vulgaris
• Cause  HPV
• Common skin wart

7. Condyloma acuminatum
• Cause  HPV 6 & 11
• Genital wart
• Oral warts  after oral sex
Treatment
8. focal epithelial hyperplasia (hecks disease)
• Cause  HPV 13 & 32
• Multiple  dome shaped warts on oral mucosa
Treatment
• Excisison  great prognosis

9. Oral hairy leukoplakia

• Cause  EBV
• White patch on lateral tongue that does not wipe off
• Associated  HIV & burkitts lymphoma
Bacteria
1. Syphilis
• Cause  contact treptonema pallidum (spirochete)

Types
a) Primary
• Chancre

b) Secondary
• Oral mucous patch
• Condyloma latum
• Maculopapular rash

c) Tertiary
• Gumma
• Cns & cv involvement

Congeintal syphillis
• Hutchinsons triad notched incisors, mulberry molars, deafness, ocular
2. Tuberculosis
• Cause  inhalation  mycobacterium tuberculosis
• Oral non healing ulcer (stellate / star shaped )+ lung infection
• Africa  higher incidence
Types
a) Primary
• Ghon complex  bateria surronded in granuloma that undergoes cesation necrosis
+ infected hilar lymph node draining the first lesion)

b) Secondary
• Widespread lung infection  with cavitation

c) Miliary
• Systemic spread

• Hiv pt  high risk of progressive disease

Treatment
3. Gonorrhea
• Cause  niesseria gonorrhea
• Oral pharyngitis  rare

4. Actinomycosis
• Cause  Actinomysis isralei (filamentous)
• Opportunistic
• Chronic & granulomatous
• Sulfar granules in exudate
Types
a) Periapical  jaw infection
b) Cervico-facial  head & neck
Treatment
5. Scarlet fever
• Cause  group A streptococcus (streptococcus pyogenes)
• When strep throat become systemic
• Strawberry tongue  white coated with red inflammaed
fungiform papilla
Treatment
• Penecillin
Fungal
1. Candiasis
• Thrush
Types
• Pseudomemebranous  rub off & red below
• Atrophic  red
• Median rhomboid glossitis  loss of lingual papilla
• Angular cheilitis  corners of mouth
Treatment
• Azoles  flucanoazole
• Statin  nystatin
2. Deep fungal infection
• Found in soil
Types
• Blastomycosis  us northeast, inhaling of spores (after rain)
• Coccidiodomycosis  us south west, vally fever
• Cryptococcosis  us west
• Histoplasmosis  us midwest
 Mucosal lesions
 immunological
1. Apthous ulcers
• Also called  canker sore
• Affects  non-keratinized tissue
• Sites  labial, buccal & alveolar mucosa , floor of mouth, soft palate, ventral tongue
• Etiology  immunological (HUMAN LEUKOCYTE ANTIGEN)

Types
• Minor  less then 10mm in size, heal without scarring
• Major / suttons disease  10mm – 1 & 3 cm  heal with scarring
• Herptiform pinpoint cluster, reccurrent

Bechets syndrome
• Multi-system vasculisits
• Apthous ulcers  mouth & genital
• Inflammation of eye
• Triad  mouth, genital & eyes
Treatment
2. Erythema multiforme
Site
• Lips  most common
• Buccal mucosa
• Tongue
• Labial mucosa
Symptoms
• Erosions, Ulcers, Heamrrhagic crusting of lips
• Taarget lesions on skin
Types
• Minor  herpes simplex virus sensitivity
• Major  drug sensitivity

Stevan – johnson syndorme

3. Angioadema
• Allergic reaction
• Swelling of  lips, face, neck (diffuse)
• Mast cells release  IgE & histamine
Treatment
• Anti-histamine

4. Wegeners granulomatosis
• Allergic reaction  to inhaled substance
• Strawberry gingivitis
Treatment
• Corticosteroid  Prednisone
• Cyclophosphamide
5. Lichen planus
• T-lymphatocytes  destory basal keratinocytes
• Histopathologically  saw tooth rete pegs
Types
• Reticular  wickhams striae, common
• Erosive  wickhams striae with red ulcerations
Treatment
• Corticosteroids
6. Lupus erythematosis
Types
Discoid chronic
• Disc like spot on face
• Oral  erosive lichen planus like lesion

Systemic
• Butterfly rash
• Multiple organ involvement
• Test  ANA (auto-antibody )

Treatment
• Corticosteroids
7. Scleroderma
• Hardening of skin & connective tissue
• Excessive deposition of collagen in tissue

Dental
• Opening mouth  difficult
• PDL space  widening
• Face  tight mask like facies
8. Pemphigus vulgaris
• Autoimmune disorder of skin and mucous membrane
• Igg auto antibodies formed against desmoglein (1&3) in
epidermal cells (desmosomes)
• Should avoid prophy jet & abrasive paste  high pressure
causes ulcers + pain in these pts
Symptoms
• Nikolsky sign +ve (moving bullae here & there)
• Bullae in mouth  into ulcers painful
• Acantholysis
Treatment
• Cortico steroid
9. Bullous pemphigoid
• Chronic autoimmune skin disease of skin causing it to form bullae
(blister)
• Auto antibodies formed against hemidesmosomes antigen
(BPAG1 & BPAG2) (basement membrane)

Symptoms
• Nikolsky sign –ve
• Sub-epidermal bullae
• Pruritic lesions

• Mucous membrane phemopigoid (imp) do it

 Pemphigus vulgaris Bullous pemphigoid
• Age onset  40-60 • Age onset  60-80
• Superficial/intra-epithelial • Deep/sub-epidermal blisters
blisters • Nikolsky sign –ve
• Nikolsky sign +ve • Bullae in mouth rare
• Bullae in mouth • Itchy
• Non itchy • Chronic
• acute • No acantholysis
• Acantholysis • Auto-antibodies against
• Auto-antibodies against hemidesmosomes
desmosome (desmoglein 1 & 3)
 Mucosal
premalignant
lesions
1. Leukoplakia
• White patch  discription not diagnosis
• Does not wipes off
Treatment
• Biopsy

2. Proliferative verrucous leukoplakia

• Recurrent & warty
• Association  HPV 16 & 18
• MALIGNANT TRANSFORMATION  SCC & verrucous carcinoma

3. Erythroplakia
• Red patch  discription not diagnosis
• Does not wipes off
• Higher risk to malignant then leukoplakia
Treatment
4. Acitinic cheilitis
• Also called  solar cheilitis
• Acitinic = solar
• Sun damage  lip damage
• UV-b

5. Smokless tobacco associated lesion

• White mucosal change to the vestibule  due to tobacco
 Mucosal
malignant
lesions
 Cancer types
• Carcinoma  epithelial
• Sarcoma  mesechymal
• Lekeumia  blood
• Lymphatic  lymph

Cancer stages
• Dysplasia  precancer
• Carcioma in situ  all epithelium affected
• Malignant neoplasm  invade past basement membrane
Local invasion C.T
Malignant invasion  Blood & lymph
1. Verrucus carcinoma
• Causes  tobacco & HPV 16 & 18
• Slow growing
Treatment
• Excision

2. Squamous cell carcinoma

Causes
• Onogenees
• Inactivation of tumor supressor gene
• Metastaszie = lung  bone  liver

• Oropharyngeal Squamous cell carcnioma  HPV 16 & 18

• 5 yr survival  50%

Plummer-vinson syndrome
• mucosal atrophy, dysphagia & iron deficiency anemia
• Increased risk of SSC
Treatment
3. Basal cell carcinoma
• Rare metastases
Cause
• Sun damage
Treatment
• Surgery

4. Oral melanoma
• Malignancy of melanocytes
• Sites  palate & gingiva
• Dark purplish lesion

5 yrs survival
• 65 % for skin lesion
 Connective
tissue benign
tumors
• Lumps or bumps
• Into submucosa layer
1. Fibroma
• Casues  chronic trauma, irritation
• Fibrous hyperplasia of oral mucosa
• Very common

2. Gingival hyperplasia
• Enlargerment
Causes
• Medication  CA blocker, phenytoin(anticonvulsion), cyclosporin
(immunosupressor)
Treatment
• Gingvectomy
3. Denture induced fibrous hyperplasia
a) Epulis fissuratum
• Cause  over-extended flange of denture
• Site  vestibule
b) Papillary hyperplasia
• Unclean denture or POOR OH
• Site  palate

4. Traumatic neuroma
• Entangled submuosa mass of neural tissue & scar
• Cause  nerve injury
• Site  mental foramen

Multiple endocrine neuroplasia (MEN2b)

• Multiple neuromas + medullary thyroid cancer +
5. Pyogenic granuloma
• Common
• Hyperplasia of capillaries = red
• Cause  chronic trauma / irritation
• Site  gingiva
• When occur in pregnancy it is called  pregnancy tumor

6. Nodular fasciitis
• Neoplasm of fibroblast
• Easy to irridicate
• Low recurrence / rare
• Treatment  conservative surgical excision (going to be curative for this)

7. Fibromatosis
• Neoplasm of fibroblast
• Hard to irridicate
• High recurrence
8. Granular cell tumor
• Neoplasm of schwann cells (for making myelin)
• Histology  granular cytoplasm
• Pseudoepitheliomatous hyperplasia  mimics SCC
• Site  dorsal tongue
• On gingiva  congenital epulis of the newborn

9. Schwannoma
• Neoplasm of schwann cells
• Histology  acelluar verocay bodies in antoni A tissue (line
of scrimmage)
10.Neurofibroma
• Neoplasm of fibroblast + schwann cells

Neurofibromatosis type 1 / von recklinghausens disease

• Multiple neurofibroma +multiple skin freckles (café au laut spots) +
axillary frechkels (crows sign) + iris freckles (lisch spots)
• Neuroribromas  can transform into  neurofibrosarcoma

11.Leiomyoma
• Tumor of smooth muscle cells

12.Rhabdhomyoma
• Neoplasm of skeletal muscle cells

13.Lipoma
• Neoplasm of fat cell
 Connective
tissue malignant
tumors
1. Fibrosarcoma
• Malignanacy of fibroblast

2. Neurofibrosarcoma
• Malignant tumor of  schwann cells
• Also known as  malignant peripheral nerve sheath tumor

3. Kaposi sarcoma
• Proliferation of endothelial cells
• Cause  HHV -8
• Commonly seen as complication of AIDS
• Purple lesion
4. Leiomyosarcoma
• Tumor of smooth muscle cells

5. Rhabdhomyosarcoma
• Malignancy of skeletal muscle cells

6. Liposarcoma
• Malignanacy of fat cell
• Common in  buccal mucosa
Salivary gland 
reactive
1. Mucous extravasation phenomenon
• Trauma to excretory duct extravasation of mucous into surronding C.T 
inflammation  granulation tissue wall around mucous formed (cyst
like/pseudo cyst)
• Due to  trauma
• Histo  no epithelial lining

a) Mucocele
• Site  lower lip
• 2-3mm blue fluctuant swelling

b) Ranula
• Site  floor of mouth
• Frog belly appearance

Treatment
2. Mucous retention cyst (true cyst)
• Forms due to obstruction of duct  accumulation of mucosu 
swelling
• Mostly affects minor salivory gland of adults
• Causes  sialolith, mucin plug
• Histo  lined by epithelium
• Pain during meal
• Pus
• Floor of mouth, buccal mucosa, lips
3. Necrotizing sialometaplasia
• Rapid expanding ulcerative lesion
• Schemic necrosis  minor salivary gland
• Cause  trauma, anesthesia
Treatment
• Heals on its on  6 – 10 weeks

4. Sinus retention cyst

• Also called  antral cyst
• Blockage of gland in sinus mucosa
• Radiograph  radioopaque done shaped lesion along floor
of sinus
• Treatment  none
5. Sarcoidosis
• Hyperimmune  granulomas
• Trigger  mycobacteria
• Primary pulmonary disease but affects salivary glands & mucosa
• Xerostomia

Lofgrens syndrome
• Erythema nodusum + bilateral hilar lymphadenopathy + arthritis

Heerford syndrome
• Anterior uveitis + parotid gland enlargement + facial palsy +
fever
• Uveoparotidf ever

Treatment
6. Sjogrens syndrome
• Autoimmune
• Lymphocytes mediated
• High caries risk
• Linked with  lymphoma

Types
a) Primary
• Keratoconjuctivitis ( dry eyes ) + xerostomia (dry mouth)
b) Secondary
• Keratoconjuctivitis ( dry eyes ) + xerostomia (dry mouth) +
Rheumatoid arthritis

Treatment
Salivary gland 
benign
• Classified by microscopic

1. Pleomorphic adenoma
• Mixed tumor  epithelial & C.T cells
• Most common
• Firm rubbery swelling
• Site  palate (minor salivary gland), ear (parotid)

2. Monomorphic adenoma
• Composed  single cell types
• Include  basal cell adenoma, canalicular, myoepithelioma,
oncocytic tumor
• Treatment  excision
3. Whartons tumor
• Cells  oncocytes + lymphoid cells
• Site  parotid of older men
Salivary gland 
malignant
1. Muco-epidermoid carcinoma
• Most common
• Comoposed  epithelial + mucous cells
• Presents as an  ulcerated blue/red mass that may be fluctuant
• They commonly resemble mucoceles or vascular lesions
• Location  parotid gland (most common ) minor salivary glands
of the palate (2nd most common)

2. Polomorphous low grade adenocarcinoma (PLGA)

• 2nd most common  minor salivary gland
• Site  palate

3. Adenoid cystic carcinoma

• Cribriform or swiss cheese microscopic pattern
• 5 yr survival 70%, 15yrs 10%
Lymphoid
neoplasm
1. Hodgkins lymphoma
• Rare in oral cavity
• Reed sternberg cells  malignant B-cells (differntiating point
from non hodgkins)
• Treatment  chemo + radio

2. non-hodgkins lymphoma
• B or t cells lymphoma

Burkitts lymphoma
• B-cell lymphoma
• Involves  bone marrow, pain, swelling, tooth mobility, lip
parasthesia, halts root development
Treatment
3. Multiple myleoma
• Also called  plasma cell myeloma
• Radiograph  punched out radiolucency in skull
• Amyloidosis due to accumulation of complex amyloid protien
Treatment
• Chemo
• Poor prognosis
4. Leukemia
• Neoplasm of bone marrow cells  lymphocytes, NK, granulocytes, megakaryocytes
• Can affect  rbc & platelets
Clinical signs
• Bleeding  platelets
• Fatigue  rbc
• Infection  wbc

Classification based on two things

• Myleoid
• Lymphoid

• Acute
• Chronic

From youngest to oldest (it will afect)

• ALL CML  AML  CLL
Odontogenic cyst
• Cyst = cavity lined by epithelium

1. Radicular cyst
• Periapical cyst
• Associated with  non-vital / necrotic tooth
• Radiographic  apical radiolucency

Necrotic pulp causes

• Acute  abscess
• Chronic  granuloma

• Epithelial rests of malassez (ERM) form lining of the cyst

Treatment
• Rct
• Apicoectomy
2. Dentigerous cyst
• Associated with unerupted tooth  canine & 3rd molars
• In kids  eruption cyst
• Attached on the CEJ of the crown
• Accumulation of fluid b/w reduced enamel epithelium & crown
• Origin  REE
Treatment
• Excision of the cyst  source of future odontogenic tumor

3. Lateral periodontal cyst

• Site  mandibular premolar
• Present lateral to the root
• Associated with  vital tooth
• Treatment  excision
4. Gingival cyst of the adult
• Radiograph  no radiolucency
• On the gingival  b/t two teeth
• Area  mand premolars
• Treament  excision

5. Gingival cyst of newborn

• Lateral palate cyst  bohns nodules
• Midline palate  epstein pearl
• Origin  rest of dental lamina
Treatment
• Non
• Go as age
6. Primordial cyst
• Present  where tooth should have formed / be present
• Common  mand 3rd molar region
• Treatment  complete removal

7. Keratocystic odongenic tumor (KCOT)

• Also called  OKC,
• Aggressive & recurrent
• Common  post ascending ramus of mand
• Histo  corrugated parakeratinized epithelium + palisading of basal cells

Gorlin syndrome
• Multiple KCOTS, multiple BCC, calcified falx cerebri, fatal
• Also called  nevoid basal cell carcinoma

Treatment
8. Calcifying odontogenic cyst
• Also called  gorlin cyst
• Rare
• Radiographically  ghost cells (radiodensities)
Odontogenic
tumor
1. Ameloblastoma
• Most common
• Aggressive benign
• Radiographic  Multilocular radiolucency in posteriot
mandible
Treatment
• Wide excision or resection

2. Calcifying epithelial odontogenic tumour

• Also called  pindborg tumour
• Radiolucency  driven snow / white flake radiolucency
• Histo amorphous pink amyloid with concentric calcified
(lisengang rings)
• Treatment  surgical excision  good prognosis
3. Adenomatoid odontogenic tumour (AOT)
• Epithelial duct like spaces & enameloid material
• Site  anterior maxilla over impacted canine
Treatment
• Surgical excision  good prognosis

4. Odontogenic myxoma
• Also called myxofibroma
• Myxomatous C.T (pulp like material with collagen) = slimy
stroma
• Radiograph  messy unclear borders, honeycomb pattern
• Treatment  surgical excision
5. Central odontogenic fibroma (COF)
• Dense collagen with strands of epithelium
Types
• Central  bone, well defined muli-locular radiolucecny
(post mand)
• Peripheral  gum

6. Cementoblastoma
• Radiograph  well circumcised radio-opaque mass
(replacing root)
• Ball of cemetum
• Treatment  surgical excision & extraction
7. Ameloblastic fibroma
• Common  children & teen
• Site  post mandible
• Myxtomatous C.T
• If odontoma present then called  ameloblastic fibro-
odontoma
• Treatment  surgical excision
8. Odontoma
• Opaque lesion composed of dental hard tissues
• Can block eruption  impaction, ectopic Eruption
Types
a) Compound
• Site  anterior
• Bunch of  miniature teeth

b) Complex
• Site  posterior
• Conglomerate mass

Gardners syndorome
Fibro-osseous
lesion
1. Central ossifying fibroma
• Fibroblastic strom with calcified foci in it (like island)
• Similar in appearance & behaviour to  cemetifying fibroma
• Treatment  surgical excsion

Types
• Central  bone, well circumscribed radiolucency with
ossification in center
• Juvenile  aggressive variant, rapid growth in young

Peripheral
• Gum  gingiva exclusively
• Nodular mass  ID papilla small lesion less then 2mm
• Young  10-19yrs old
2. Firbous dysplasia
• Radiograph  ground glass appearance
• Stop growth affter  puberty
• Before puberty  rapid growth & expansion (angle of
mandible)

Mc-cune albright syndrome

• Polyostotic fibrous dysplasia (more then 1 bone) + cutaneous
café au laite spots + endocrine abnormalities (precocious
pubery (early puberty)

Treatment
• Surgical recontouring
• Wait after & do after puberty
3. peri-apical cemto-osseous dysplasia (PCOD)
• Reactive
• Site  apices of mandibular anterior teeth
• Common  middle age balck females
• Teeth are vital
• Radiograph  first lucent then changes to opaque
• Treatment  none

4. Osteoblastoma
• Circumscribed opaque mass of bone & osteoblast
• Site  post mandible
Treatment
• Surgcial excision
Giant cell lesions
1. Central giant cell granuloma (CGCG)
• Composition  fibroblast + gaint cells
• Site  anterior mandible
Types
a) Central
• Bone
• Radiolucency with thin wispy septation

b) Peripheral
• Also called  giant cell epulis
• Site  Gums or edentulous ridge

Signs & symptoms

• Mostly in females
• Cup-like resorption of underlying bone
• Red-purple/blue nodular mass
Treatment
2. Aneurysmal bone cyst
• Pseudocyst
• Composed  blood filled spaces
• Radiographic  multilocular radiolucency
• Site  post mand
• Expansile
• Aspirational biopsy  first first diagnosis
Treatment
• Excision
3. Hyperparathyroidism
• Multiple bony lesions excessive parathyroid hormone
• Looks like CGCG

Brown tumour
• Excess osteoclast activity = radiolucent lesions
• Bone breakdown = elevated alkaline phosphatase

Von recklinghausens disease of bone

• Result of this disease
• Don’t confuse it with (Von recklinghausens neurofibromatosis )
4. Cherubism
• Autosomal dominant
• Clinically  Symmetrical bilateral bony swelling
• Radiographically  Bilateral multilocular radiolucency
• Stops  after puberty

5. Langerhen cell disease

• Also called  histocytosis
• Hsitocytes build-up in certain body parts
• Radiograph  punched out ‘ice cream scoop’ radiolucency =
causing floating teeth
Treatment
• Excision
6. Pagets disease
• Progressive metabolic disturbance of many bones 
abnormal resoprtion & deposition of bone
• Spine, femur, skull & jaws
• Radiograph  cotton wool appearance
• Denture & hats becomes tight
• Old age 50+
• Lion – like face deformity
• Increased inter-dental spacing in maxilla
• Elevated alkaline phosphotase

Treatment
• Bisphosponates
• Calcitonin
 Bone
inflammatory
lesion
1. Acute osteomyelitis
• Causes odontogenic infection & trauma
• Inflammation begins at  medullary space (cancellous
bone ) progress to cortical bone  periosteum  soft tissue

Symptoms
• Pain
• Fever
• Paraesthesia or anesthesia of IAN
• Tooth  not loose (loose tooth due to periodontitis)

Treatment
• Antibiotics
• Drainage
2. Chronic osteomyleits
• Radiograph  diffuse mottled radiolucency
• Sequestra  dead bone

Garre’s osteomyelitis
• Chronic + Proliferative periosteitis (onin layer)

Treatment
• Antibiotics + debridement
3. Focal sclerosing osteomyelitis (condesing osteitis)
• Bone sclerosis due to low grade chronic inflammation
(chronic pulpitis)
• Diffuse dense bone around apex  to wall off infection
• Associated with  pulpitis or pulpal necrosis
Treatment
• Address the cause
• No treatment other then that

4. Diffuse sclerosing osteomyelitis

• Same as obove but  wider
• Cause  jaw fracture
Treatment
• Antibiotics
5. Bisphosphonate related osteo-necrosis of jaw (BRONJ)
• Higher risk with  iv
• Jaw pain
Treatment
• Chlorhexadine
• Antibiotics
• Cconservative surgery
Bone malignanat
lesion
1. Osteosarcoma
• Sarcoma of jaw  new bone is produced by tumour cells
• Radiograph  sunburst pattern
• 5-yrs survival 25-40%
Treatment
• Resection & chemotherapy

2. Chondrosarcoma
• Sarcoma of jaw  new cartilage is produced
• Involves  condyle
• Same as above  presentation & treatment
3. Ewings sarcoma
• Tumour of long bones
• Round cells
• Affects children
• Swelling

4. Metastatic carcinoma (malignancy )

• Pain
• Swelling
• Paraesthesia  lip
• Ill-defined changes noted
• Breast  lungs  kidney  colon  prostate
Hereditary
conditions
1. White spongue nevus
• Autosomal dominant
• Asymptomatic
• White lesion  buccal mucosa
• Not wipeable

2. Epidermolysis bullosa
• Autosomal dominant / recessive
• Causes skin& mucosa to be super fragile  blisters easily
• Looks like  erythema multiforme (not lip crusting)
3. Hereditary hemorrhagic telangiectasia (HHT)
• Autosomal dominant
• Also known as  OLSER-WEBER-RENDU SYNDROME
• Telangiectasia  red macule or papule  dilated or broken
capillaries
• Abnormal capillary formation on  skin, mucosa, viscera
• Association  iron deficiency anaemia
• Epistaxis  imp sign

4. cleido-cranial dysplasia
• Autosomal dominant
• Strangers’ things wala larka (dustin)
• Missing clavicle
•
5. Ectodermal dysplasia
• X-linked  resessive
• Missing teeth
• Pointy teeth
• Missing sweat glands
• Affects  hair, teeth & nails (hypoplastic)
6. Osteopetrosis
• Also called  marble bone, ALBERS- SCHONBERG
DISEASE
• Defect in osteoclastic bone remodelling =
increased bone density
• Stone bone
7. Amelogenesis imperfecta
• Autosomal dominanat, recessive, x-linked
• Intrinsic alteration of enamel
• Affects all teeth in both dentition
• Thin or no enamel
• Normal denitne & pulp
Treatment
• Crowns
8. Dentinogenesis imperfecta
• Both dentitions
• Male & female
• Mutation in  sialo-phospho protein gene (dspp)
• Autosomal dominant disorder
• Intrinsic alteration of dentine
• Bell stage

Clinical features
• Opalescent  On eruption teeth has normal contour but an opalescent amber appearance
• Short roots
• Tulip/ bell shaped crown
• Obliterated pulp  no pulp cavity
• Bulbous crown due to  constricted DEJ
• Blue sclera
• Greyish to brown appearance
• Dentine soft
• Enamel fracture due to less dentine support
• Absent scalloping b/w DEJ
9. Dentine dysplasia
• Autosomal dominant (rare)
• Interinsic alteration of dentine
• All teeth  both dentition

• Short roots or  root less  type 1

• Chevron pulp / piston throttle appearance  type 2

Treatment
• Not good candidate for restoration
• Extraction
10.Regional odontodysplasia/ ghost teeth
• Rare
• Both dentitions
• Abnormalities of dentine + enamel + dental follicle
• Affects ameloblast + odontoblanst + cementoblast
• Aetiology  unknown

Clinically
• Irregular teeth shape with hypoplastic enamel
• Thinner dentine
• Pulp stones
• Short roots and wide-open apices
• Enlarged pulp chambers  Ghost teeth
• Localized to one quadrant
Treatment
• Let them erupt  bring alveolar bone
11.Gemination
• Bud divide to two  2 crowns, 1 root & 1 canal
• Affects anterior teeth
• Cap stage
• Normal tooth count when abnormal tooth counted as one
 normal count
Causes
• Single tooth bud divide into two teeth/ partial division or twinning
of single tooth germ
12.Fusion
• Two developing teeth join together to form one  2 tooth
germs
• Cap stage
• Common in primary teeth  anterior
• Missing teeth when abnormal teeth counted as one  one
less than normal
Fusion before calcification  all component of teeth fuse
Fusion after/ later stage  2 separate crown & fused roots
Oral surgery
 Local anaesthesia
Classification

1. Amides
• Amides have  I + Caine in their names
• Metabolized by  liver
a) Lidocaine
b) Mepvacaine
c) Bupivacaine

2. Esters
• Metabolized  by pseudocholinesterase in plasma
a) Novocaine
b) Procaine
c) Benzocaine
MOA
Type of anestheisa
Complications
 Basic life support

• First step when initiating CPR  establish unresponsiveness

• Time interval from cardiac arrest to 1st defibrillation is the most

importan factor
• For every min delay in defibrillation from time of collapse 
survical declines by 7-10%

• Order of CPR  CAB (compression, airway, breathing)

• Compression  lower half of sternum b/w nipples
• Compression depth  2 inches
• 30 compression + 2 breaths
Cardio-pulmonary resuscitation (CPR)
a) Airway
• Head tilt
• Jaw thrust  if neck trauma suspected

b) Breathing
• Look, listen, feel
If respiration is absent / inadequate  rescue breathing
• Bag valve mask (BVM)
• Ventilation rate  1 breath / 5-6 sec ( 10-12 / min)

c) Circulation
• Check pulse
• If pulse absent  initiate chest compression
• Compression to ventilation ratio  30:2 (100 compression / min)

d) Defibrillation
 Wound healing
Types
1. primary healing / intention
• Closly reapproximate the wound edges
• Lower risk of infection
• No scar
• Eg:- surgical incision

2. Secondary
• Gap b/w wound edges
• Requires larger amount of  epithelial migration, collagen deposition,
contraction & remodeling (granulation tissue)
• Slower healing
• More scar formation
Stages of wound healing
 Indications for extraction
• Grossly carious
• Endo  internal resoprtion
• Perio  mobility & deep pockets
• Crowding most likely extraction = 1st premolars
• Cracked teeth
• Impacted
• Supernumerary
• Pathology
• Questionable teeth should be extracted before the
radiation therapy  to avoid osteo-radio-necrosis
 Contra-indications for extraction
• Uncontrolled diabetes
• Unstable angina
• Leukemia
• End stage renal disease
• Lymphoma
• Heamophila & platelet disorder
• Head & neck radiation  hyperbaric oxygen therapy (before & after
extraction)
• I/V bisphosphonates  BRONJ
• Pericoronitis  treat infection first then extraction
• Pts should wait 6 months after Coronary artery bypass grafting
(CABG) prior to elective extraction

• Acute infection is not a contraindication  remember la & ph

 Facts
1. Maxillary teeth to be extracted first then mandibular
• Posterior  anterior  1st moalr  canine

2. First force applied in extraction

• Apical force

3. irrigation
• Normal saline should be used for irrigation
• Distilled water is hypotonic  cause cell lysis (due to difference in
osmotic gradient)
 Impacted tooth
• Tooth fail to erupt with in specific time
• Mand 3rd molar  max 3rd molars  max canine  mand 2nd premolar
• Impaction  due to = inadequate arch space
• Impacted tooth should e assessed with  SLOB technique or BAMA rule (buccal
always move away)

Classification
1. Soft tissue impaction
• Height of contour of tooth above bone  but covered by soft tissue
• Extraction  easiest

2. Partial bony impaction

• Height of contour of tooth below bone

3. Complete bony impaction

• Tooth completely into the bone
 Classification according to angulation
• Only for 3rds molars
(winters)
• Position of 3rd molar to the long axis of 2nd molar

1. Vertical
• Soft tissue vertical
• Bonny vertical
2. Horizontal
3. mesio-angular  easieest
4. disto-angular  hardest
5. Bucco-lingual
6. Others  inverted, other than these
War lines
Pell & gregory  only for lower 3rd molars
• Relationship of tooth to ascending ramus of mandible and
distal surface of second molar

Class 1
• Mesio-distal diameter of crown is completely ahead of anterior
border of ramus

Class 2
• Tooth positioned in the way that half crown is covered by the
ramus

Class 3
• Depth of third molar in bone

Position a
• Occlusal level of impacted molar is nearly with the occlusal level
of 2nd molar

Position b
• Occlusion of impacted molar on the cervial level of 2nd molar

Position c
• Occlusion of impacted molar below the cervical level
Inidcations for extraction of
impacted tooth
To prevent
• Periodontal disease  pocket of 4mm or more b/w 2nd &
3rd impacted molar
• Pericoronitis
• Caries
• Root resorption
• Odontogenic cyst & tumors
• Fractures of jaw
• Pre orthodontic treatment
 Congenitally missing teeth
• 3rd molars  max laterals  mand 2nd premolars
Complication of
extraction
 Subperiosteal abscess
• Abscess / infection  trapped underneath perisoteal layer
• Due to  necrostic bone or root left after surgical extraction under
flap
Precaution
• irrigate thoroughly
• Remove any bony speckule under soft tissue
 Oroantral communication (OAC)
• Communication b/w oral & sinus
• Common  maxillary 1st molars (palatal root)

Prevention
• Post op radiograph
• Avoid excessive apical force

Diagnosis
• Black hole
• Hollow sound on suction
• Irrigation  weird sensation
•
Treatment

2mm or less
• None / leave it as it is (sinus precaution)

2-6 mm
• Figure of 8 sutures
• Antibiotics
• Anti-histmines
• Analgesics
• Afferent nasal spray (figure of 8)

More then 6mm

Complications
• Sinusitis
• Oro-antral fistula (epithelialization of communication)

Sinus precaution  10-14 days

• Sneeze by opening mouth
• Avoid nose blowing
• Avoid  cigreette & straws
• Nasal decongestants  7-10 days
Follow up  two see two things
• Evident communication
• Sign of sinusitus
 Alveolar osteitis / dry socket
• Disloadgement of clot before socket heals

Etiology
• Increased fibrinolyic activity
• Loss of clot
• Smoking & oral contraceptive

Symptoms
• Extreme pain  1-3 days after extraxction
• Smell / fetid odor
• Bad taste

Treatment
• Irrigation
• Socket medicament (local pain control) collagen plug / gel form (eugenol in it)
 Nerve injury
• Common  mad 3rd molar  (IAN )

Symptoms
• Anesthesia  loss of sensation
• Parasthesia  abnormal sensation (burning, tingling, pricking or
tickling)
• Dysesthesia  pain to normal stimulus
• Parasthesia more than 4 weeks  refer to microneurosurgical
evaluation

Treatment
• Medrol dosepak  methylprednisolone (steroid to treat
inflammation)
Types of injury
1. Neurapraxia
• Mild injury with no axonal damage
• Spongtanous recovery  within 4 weeks

2. Axonotmesis
• Axonal damage but intact  perineural & endoneural sheath
• Wallerian degenration distsl to injury
• Potential for recovery  1-3 months

3. Neurotmesis
• Complete severance of axon with gap in b/w
• No recovery without surgery
 Tooth displacement
• Maxillary 1st & 2nd molar  sinus
• Maxillary 3rd molar  infratemporal fossa
• Mandibular 3rd moalr  submandibular space
• Tooth lost in  oropharynx  send to ER  chest xray
 Instruments
1. Bite block
• Keep mouth open
• Better visualization
• Stablizes mandible

2. Suction tips
Types
• Yankaur  for soft tissue
• Frazier  hard & soft tissue

3. Towel clips
• Holds drapes placed around pt
4. Tissue retractors
Austin
• Right angle
• For small flaps

Minnesota
• Common used
• Offset curved & broad
• Cheek & flap retraction
• 3rd molar extraction

Weider / sweet-heart
• Broad heart shaped  to protact & retract tongue
• Mandibular lingual surgery

Seldin
• Long & flat
• For elevating down to the floor of the mouth
5. Periosteal elevator
Woodson  small & delicate
No # 9 molt  larger

6. Elevators
• Blade, shank & handle
• Grip  palm grip (pointer finger near the blade)
• Used  disrupt pdl, luxate, expand bone

a) Straight
• No # 301
• Principle  lever
• Blade has Concave surface  should be towards the tooth to be
b) Triangular / cryers
• 2nd most common
• Principle  wheel & axle
• Removing roots  left in socket

c) Pick elevator
• Retain  bdr (root tip)
• Principle  wedge
Types
• Crane  heavy version
• Root tip pick  delicate version
7. Extraction forceps
• Beak, hinge & handle

a) Universal
• 150  upper teeth
• 151  lower teeth
• A = premolars
• S = primary

b) Lower cow horn forceps

• No 23
• Lower grously carieous tooth
• Engage into  bifurcation
c) Upper cow horn forceps
• No  88
• Left & right
• Two beaks  towards palatal root
• One beak  towards buccal bifurcation

d) Ash forceps
• No  74
• For  mandibular premolars

e) Upper root forceps

• No  65
8. blades
• For surgical extraction
• Load into  scalpal blade holder
• Load using  hemostat
• Hold blade handle  pen grasp

Types
a) No  15
• Most common
• Intraoral surgery

b) No  11
• Stab incision  incision & drainage

c) No 10
• Large skin incision

d) No  12
• Muco-gingival surgery
9. Irrigation
• With sterile saline
• Prevents heat generation
• Increase efficiceny of bur  lubrication

10.curretes
• Sppon shaped  for scraping soft tissue
• Always currete socket after extraction  to remove soft tissue
11. bone removers
• To remove sharp bones & speckules
Types
a) Rongeur
• To remove inter-radicular bone

b) Osteotome
• Bone chisel
• Flat end tapped with mallet
• Monobevel  to remove tori
• Bibevel  section tooth

c) Bone file
• Smoothing bone before suture
• Stroke  pull stroke

d) Surgical hand-piece
• Do not use air driven handpiece (fast handpiece) = air into socket & soft tissue = air
emphysema
• Straight fissure bur  section teeth
12.Hemostat
• To clamp blood vessels
• Useful for blunt diesection of soft tissue  incision & drainage
• Face of beak  straight

13.Needle holder
• Short strout beaks
• Face of beak cross hatched  for postive grasp

14.Sutures
• Should be placed from movable to non movable tissue
• Simple interupted  most common & easy
• Silk sutures  wiking property  allows bacteria to invade
15.Other forceps

a) Tissue forceps
• To hold tissue
• Toothed  periosteum, muscle, aponeurosis
• Non-toothed  fascia, mucosa, pathological tissue for biopsy

b) Utility forceps
• For picking items
• Preparing packing material
16.Scissors
a) Dean  cutting sutures (curved / angled up)
b) Mayo  cutting fascia & disecting soft tissue
 Simple extraction
Steps
1. Sever the soft tissue attachment
• Loosen  gingival fibers & pdl fibers
• Confirms good anesthesia
• Allows apical placement of the forceps
• Used  Perisoteal elevator

2. Luxate tooth
• Lever  fulcrum in alveolar bone
• Expansion of bone & tearing of pdl
• Find  purchase point
• Used  dental elevator
3. Deliver the tooth
• Slow & controlled force
• Good grip & stability  using finger (tactile sensation)
• Outward motion (buccal / labial)initial movement for
most permanent teeth
• Inward motion ( lingual / palatal) initial movement for
most primary teeth
• Rotary  conical roots (initial movement )
• Apical  applied to every tooth (avoid excessive pressure in
maxillary molar region)
• Used  forceps
• Upper incisors = labial  lingual  rotational
• Upper Canine = apical  labial  lingual  rotational
• Upper 1st premolars = apical  labial  lingual
• Upper 2nd premoalr = apical  labial  lingual  rotational
• Upper molars = apical buccal palatal (more buccal less palatal)
(deliver tooth in buccal direction )

• Lower incisors = labial  lingual  rotational

• Lower Canine = apical  labial  lingual  rotational
• Lower premolar = apical  labial  lingual  rotational
• Lower molars = apical buccal lingual (more buccal less lingual)
()deliver tooth in buccal direction )
 After tooth removal
• Alveoloplasty  if no orthodontics & implant
• Curretage
• Smooth bone
• Irrigate
 Surgical extraction
Flap design
1. Base should be wider then the free margin  ensure adequate
blood supply
2. Incisions over intact bone  not on defects or eminences
3. Rounded corners
4. Vertical relasing  at the line angle  1 or two teeth away from
working tooth, never on facial aspect or splliting papilla
5. Avoid vital structures  vessels, nerves
 Types of mucoperiosteal flaps
• Envelope  no releasing incisions
• Three cornered  1 releasing incision
• Four cornered / trapezoidal  2 releasing incisions

Semilunar incision
• Incison made apical to muco-gingival junction
• Done for apicoectomy
• Apically displaced flap impossibe in maxillary palatal region

Double Y incision
• Incison in midline & two releasing incisions at each en ( double y)
• For palatal tori
Implant
Contra-indication

1. Uncontrolled diabetes
2. Immuno-compromised pts
3. Voulme & height of bone
4. Bisphosphonates
5. Bruxism
6. Smoking  Smoking drastically compromises blood flow at the
implant site, affecting bone healing and consequently implant
stability.
7. Head & neck radiation
8. Cleft palate
9. Adolscent
10.Not place implant after extraction if there is active infection 
wait 8 weeks after extraction of infected tooth
Not contra-indications
Osteopenia
• Reduced bone mass can compromise bone healing, though it is
not as significant a risk as some of the other factors listed.

Osteopetrosis
• While this condition results in denser bone, it does not impact
implant failure as much as other conditions, especially heavy
smoking.
High caries index
• Though caries do not directly affect implants (since implants
can’t be attacked by cariogenic bacteria), the overall oral health
environment can be a concern.
 Types of implant
1. Subperisoteal
• Into perisoteum
• Not into the bone
• No  osteointegration

2. trans-osteal
• Through the bone
• Ant mandible
• Extra-oral approach

3. Endosteal / endosseous
• In the bone
 Implant component
1. Body / fixture
• Axisymmetric
• Drilled into the bone  sequentially enlarge the osteotomy
• Sequentially enlarge osteotomy  reduce heat, maintain axis with free
hand surgery

2. Abutment
a) One –piece
• Combine  abutment + screw into one componenet
• No anti-rotation component

b) two-piece
• Separate  abutment & screw
3. Crown
a) Screw retained
• Screwed with implant
• Screw access hole  into central fossa or cingulam (esthetic prob)
• Better for restrictive restorative space (need less vertical
restorative space)

b) Cement retained
• Crown cemented to the implant
• Cement may go subgingivally  cause = peri-implantitis
 One-piece implant Two-piece implant

• Body & abutment one • Body & abutment separate

componenet • Body drilled into bone
• Drilled together in bone • Abutment after fixture is placed
• Can not correct angle b/w two • Most common
componets
Anti-rotation component
• Prevent rotation of abutment
• Provides stability of the abutment
• In two-piece implant system

1. Internal hex
2. External hex
 Integration
1. Osteointegration
• Direct structural & functional connection b/w ordered living bone
& load bearing surface of artificial implant
• Material  titanium, zirconia (new)

2. fibrousintegration
• Presence of fibrous tissue b/w implant & bone
• Mobility
• Failure of osteointegration
 Stability
1. Primary stability
• When u first place implant how well thw screw pattern hold

2. Secondary stability
• Osteointegration
• Long-term healing of bone to the titanium
• Osteointeegration  starts around or after 4th week
 Bone quailty
Type 1
• Dense cortical  good primary stability (not good secondary stability)
• Anterior  mandible
• Best for implant

Type 2
• Posterior  mandible

Type 3
• Anterior  maxilla

Type 4
• Cancellous bone
• Poor  stability
• Posterior  maxilla
 Implant placement
1mm distance
• Buccal plate & Lingual plate
• Sinus
• Nasal cavity
• Inf border of mandible

1.5 mm
• From natural tooth

2mm
• IAN

3mm
• From implant – implant

5mm
 One stage surgery Two stage surgery

• Place implant & healing screw • Place implant & cover screw
in one visit then cover them with gingiva
• Remove healing abutment in • Next visit  open gums & place
next visit & place final healing abutment
abutment • Poor primary stability
• Good primary stability  we can • Using graft
do this
• Medically compromised
 Impression
• We use impression coping

Impression coping
• Used to transfer angulation & location of the implant to the
master cast

Techniques
• Open tray  hole in tray
• Closed tray 

• Analog  implant replica

 Socket preservation
• Maintain the height & width after extraction
Main
• Atraumatic extraction
• No breaking  buccal or lingual plate
• Irrigate
• Currete  soft tissue & granuloma
• Place graft
• Resorpable collagen membrane
• Primary closure  not important
 Biologic width
• Rough srface of implnat  into the bone ( for
osteointegration)
• Smooth surface of implant / cuff  for soft tissue (gingival
fibers oreinted parallel to the cuff)

• Implant has no  pdls

• No peridontium
 Surgical stent / guide
• Made to guide where to place implant
a) Angulation
b) Location
c) Depth
 Implant success Implant failure

• Immobile • Mobility
• No peri-mplant radiolucency • Peri-mplant radiolucency
• Peri-implant bone loss  more then 0.2
• peri-implant bone loss less mm / year after 1 year
then 0.2 mm / year after 1 • Pain
year • Infection
• No pain • Paraesthesia
• No infection
• No paraesthesia • Gram –ve anerobic rods & filament
• 47 degree for 1min = failure to
osteointegration
• 40 degree for 7 min = failure to
osteointegration
 Implant in edentulous area
1. Edentulous mandible
Tissue-borne removable prosthesis
• Placed over  1-5 implants
• Most common  2-4 implants
Implant borne prosthesis
• Five implants
• Anterior mandible
• Anterior to mental foramen

2. Edentulous maxilla
Parels classification system
• Class 1  missing max teeth  bone height retained
• Class 2  loss of teeth + some alveolar bone
• Class 3  loss of teeth + most of alveolar bone to basal level
Implants Restoration
• 10mm length implants
• 4-8 implants
 Over denture
• An overdenture is a type of denture that fits over a small number of remaining natural teeth
or implants
• These teeth or implants provide additional support and stability compared to conventional
dentures. Overdentures can be particularly beneficial for improving function and comfort.

Where to place implants for an overdenture

1. For a mandibular (lower jaw) overdenture supported by two implants, the ideal implant
locations are
• Canines This position generally provides good retention, reduces anterior forces, and
minimizes denture rotation.
• Premolars This location maximizes anterior-posterior spread and improves vertical and
horizontal retention.
• Lateral incisors  While not mentioned as often, placing implants here can also provide
adequate stability and is a good location if the patient may consider additional implants in the
future.

Where not to place implants:

• Central incisors: Implant placement here does not provide adequate anterior-posterior spread,
and the overdenture would have minimal additional retention or stability compared to a
 Zirconia implants
• Zirconia implants are unlikely to undergo corrosion and exhibit
better wear resistance and improved esthetics compared to
titanium implants.
• Titanium implants have a higher elastic modulus and are more
fracture resistant than zirconia implants
Trauma & orthognathic surgery
Types of fractures
• Greenstick  not completely fractured
• Comminuted  crushed into multiple fragments
• Simple  closed
• Compound  bone exposed with soft tissue
• Pathologic  occurred at weak site due to pre-existing disease
 Mandibular fractures
• Most common  nasal bone
• 2nd most common face fracture  mandible
• Radiograph  panaromic (best evaluated)(gold standard)
• Condylar  angle  symphysis (common fracture in order)
• Treated  open reduction internal fixation (ideally) (ORIF)
• Bilateral mandbular fracture  posteiror displacement of tongue =
airway obstruction

Bang on one side of mandible cause

• Fracture of same side of  angle ( right fall = right fracture)
• Fracture of opposite side  condyle (right fall = left fracture)

• Prolonged immoblization of condylar fracture  cause  ankylosis of tmj

• Maximum immobiliation of condyle  2 weeks followed by mobilizaition with
Classification of mandibular fracture
1. Favourable
• Not displacced by the forces of muscles
2. Unfavourable
• Displaed by the muscular forces
3. Horizontal

Sign & symptoms

• Mal-occlusion
• Step defects
• Mobility of mandibular segment
• Mucosal laceration
• Floor of mouth ecchymosis
 Midface fractures
• Best evaluated  CBCT

Lefort 1
Fracture line
• Transverse fracture running through the maxilla and pterygoid plates at
a level just above the floor of the nose
• Only involves  maxilla

Signs & symptoms

• Floating maxilla
• Horizontal across maxilla
• Malocclusion
• Buccal vestibule ecchymosis (guerins sign)
Lefort 2
• Pyramidal fracture
• Also know as pyramidal fracture / subzygomatic
• Bilateral mostly
• Involves  maxilla & orbit bone

Fracture line
• Starts form the nasal bone (mid level of nasal bone), below
frontonasal suture
• fracture is a pyramidal shaped fracture along the nasal bridge,
involving the inferomedial orbital rim and orbital floor, and
causes separation of the midface from the skull base.
Sign & symptoms
• Swelling & edema of middle face  moon face
• Mobility of maxilla with mobile nasofrontal complex
• Epitaxis  nasal bleeding
• Circum-orbital echymosis  racoons eyes (brusies around
eyes)
• Subconjuctival hemmorrhage  medial aspect of eye
• Chemosis  blister like eyes, irritated (sojan)
• Enopthalmus  posterior displacement of eyeball in orbit
• Anathesia or paraesthesia of cheek
• Lengthening / elongation of face  open bite
• Paresthesia of infra-orbital nerve
Lefort 3
• Complete cranio-facial dysjunction
• Involves  zygomatic arch

Fracture line
• Starts form fronto-nasal suture
• Runs along fronto maxillary suture
• Crossses lacrimal bone
• Crosses ethmoidal bone (along with it cribriform plate) & travels to lesser wing of
sphenoid
• Passes below the optic foramen
• Then it comes to the inferior orbital fissure

From the base of inferior orbital fissure the fracture line gets divided
a) Laterally it divides and runs along the zygomatico-sphenoid suture & seprates
zygomatic & sphenoid bone & runs along the fronto zygomatic suture
b) Backward it travels to the pterygo-maxillary fissuer & fractures ptergoid plate &
Sign & symptoms
• Dish face deformity  lengthening of face
• Mobile  maxilla + nasofrontal + malar complexes
• Tenderness & deformity of zygomatic arch
• Enapthalmos
• Hooding of eye
• Csf rihnorreha
• Anterior open bite
• Mobility of whole facial skeletal
• Lengthening of nasal skeletal
Blow out fracture / orbital floor fracture
• Evaluate for  entrapement of extraocular muscels (inferior
oblique) = diplopia
Late complication
• Enopthalamus
Zygomaticomaxillary complex fracturec(ZMC)

• Also known as tripod fracture (three fracture lines  lateral

orbit, maxillar & zyomatic bone)
• Blow to  malar eminence (cheek bone fracuture)
• Sign  bleeding under conjuctiva

Zygomatic arch fracture

• Isolated or in combination with ZMC

• Trismus if  interfere with coronoid process
• W deformity  submental vertex & ct scan
• For isolated zygomatic arch fracture  gillis approach
• Submental vortex  diagnosis of isolated zygomatic arch
Zygoma articulated with 4 bones
• Frontal
• Temporal
• Maxillary
• Sphenoid
 Trauma surgery
1. Reduction
• Fracture returned tto normal
Types
a) Open reduction
• Surgical exposure
b) Closed
• No surgical exposure

2. Fixation
• Internal  titanium plate on bone
• IMF / intermaxillary fixation  wiring jaws together, arch bars,
elastics
Csf rhinorrhea
• Most common due to frontal bone fracture
• Lefort 3 after that

Clinical signs
• Unilateral clear nasal discharge
• Worsen with tilt ahead or sneeze or cough
• Salty taste leakge
• Not sticky fluid

Daignosis
1. Handerchief test  central ring of blood surronded by clear ring of csf (halo sign)
2. Nasal endoscopy
3. Lab test
• Glucose testing  more glucose in csf then nasal dicharge (blood & csf)
• Beta-transferrin 2  gold standard (only found in csf)
4. Ct scan + contrast dye
Treatment
1. Conservative
• Wait for 7-10 days it resolves own its own
• Reduce the fracture  gap closed
• Precautinary measure  not cough, open mouth during sneeze,
constipation drugs & keep head upward
• Lumbar puncture
2. Surgical
• Craniotomy
Nasal bone fracture / NOE complex
• Could be alone or with combination of nasal+orbital+ethmoidal
Clinical features
• Depressed nasal bridge
• Edema swelling
• Deviated
• Bleeding
• Csf
• Telecanthous
Investigations
1. Radiographs
• From front & side  for purely nasal bone
• C.T scan  if NOE

Treatment
• If the patient comes within few hrs of fracture we can simply reduce the
nasal bone but if he comes after 24hrs or some days then there is edema
1. We wait 5-10 days to edema to subside (not more then 10days as after
14days bone starts healing )
2. Reduction  walsham forcep, finger
• After reduction we place a nasal pack under the bone for stabilty &
bleeding contron using  nasal speculum (remove after 3 days )
1. Immoblization
• Plaster of paris (7-8 layers)
• External nasal splints
 Skeletal discrepencies
• Apertonathic  anterior open bite
• Vertical maxillary excess  long maxilla, gummy smile
• Horizontal transverse discripency  posterior cross bite
• Macrogenia  big chin
• Microgenia  small chin
Orthognathic surgery
• Radiographs  lateral ceph
• Acrylic splint  used intra-operatively

Genioplasty
• Move chin

Lefort 1 osteotomy
• Move maxilla
• For retrognathic maxilla
• Vertical maxillary excess  gummy smile
• Create lefort 1  fracture

Bsso  move mandible

• For retrosive or protrusive mandible
• Condyle position shoul be  not altered
• Two cuts on mandible  above IAN
 Distraction osteogenesis (DO)
• For bone lengthening
• Bone deposition b/w seperated bone by traction

First phase
• Osteotomy  Cut the bone

Second phase
• Apliance mouted to the cut but not activated for 1 week

Third phase
• Distraction phase  0.5-1mm / day
For maxilla
• Lefort 1 osteotomy

For mandible
• BSSR
• IVRO (intra oral vertical ramus osteotomy
• Genioplasty
 Cleft lip & palate surgery
Cleft lip rule  rule of 10
• Child age  10 weeks
• Weight  10lbs
• Hemoglobin (Hb)  10g/dl
Oro-facial pain
 Biopsychosocial model of pain
Axis 1
• Bio
• Nocicpective input from somatic tissue
• Acute pain

Axis 2
• Psycho-social
• Influence of interaction b/w thalamus, cortex & limbic structure
• Chronic pain

• Not just consider the tooth (axis 1) but also consider the person
with pain (axis 2)
 Pain pathway
1. Transduction
• Pain travel from  pns to cns

2. Transmission
• Pain travel from  cns to thalamus & higher cortical sensors

3. Modulation
• Limitation of the flow of pain information

4. Perception
• Human expreince of pain
• Sum of physiological & psychological factors
1. Somatic pain
• Increased stimulus yeilding increased pain
• Pain is directly porpotional to the stimulus
• Musculo-skeletal  tmj, periodontal, muscular (myofascial)
• Visceral  salivary gland & pulp

2. Neuropathic pain
• Pain independent of stimulus intensity
• Damage to pain pathways  trigeminal neuralgia, stroke, trauma
3. Psycogenic pain
• Intrapsychic disturbance
• Conversition reaction
• Psychotic delusion
• Malingering

4. Atypical pain
• Other then these categories
• Pain of unknow cause
• Diagnosis  pending
 Trigeminal neuralgia (TN)
• Also called  tic douloureux

Clinical
• Mostly in women  post menuposal (older then 50)
• Trigger points
• Sharp, stabing, shooting episodic pain  followed by refractory
phase
• Unilateral
• Affects  trigeminal nerve  pain in that area innervated by nerve
Treatment
• Anticonvulsant  carbamazapine
• Surgery  decompression micro-surgery , gama knife
 Typical ondontalgia
• Secondary to deafferentation (removal of afferent pathway)
• Phantom tooth ache  after endo or extraction
 Post herpetic neuralgia
• Sequela / after herpes zooster
Clinally
• Burning
• Shock like
Treatment
• Anticonvulsant
• Antidepressant
• Sympathetic blocks
 Burning mouth syndrome
Clincally
• Women mostly  post menopausal (older then 50)
• Association  type 2 diabetes, mal nutrition, xerostomia
• Burning painful, dry
• Altered taste
 Chronic headache
• Neurovascular pain
a) Migrane
Clinically
• Unilateral  pulsating pain
• Nausea & vomiting
• Photophobia & phonophobia
• Treatment  triptan (selective serotonin receptor agonist)

b) Tension
Clinically
• Bilateral  non pulsating
• Not aggrevated by routine activity

c) Cluster
Clinically
Temporomandibu
lar joint
disorders (TMD)
Tmj anatomy
Tmj blood supply
Best diagnostic aid for TMJ
CBCT
• Best for hard tissues

MRI
• Best for soft tissue
• Good for looking at disc
• Best for evaluating TMJ
 Disc displacement
• Dis displacement often associated with  synovial inflamation

Anterior displacement With reduction

• Click  when articular disc reduces
• Condyle pops over anteriorly displaced disc & pops on the way back to its
fossa
• Disc displace  anteriorly

Anterior displacement Without reduction

• Locked
• Condyle is stuck behind anteriorly displaced disc
• Limited motion  unable to open completely
• Episilateral deviation on opening (towards affected side )
 Internal derangement
• Articular disc in wrong place  anteriorly or posteriorly
• Posterior band of articular disc is anteriorly displaced  infront of
condyle
 Opening pattern
Deflection
• Deflecting to the side that is stuck in maximum opening
• Condyle in that side can only rotate but no translation
• Rigth tmj stuck  open towards that side

Deviation
• While opening there is deviation but at midline when closing
• No necessarily any problem with tmj
• Pain and tenderness
 Recurrent dislocation
• Mandibualr condyle translate/ dislocates anterior the articular
eminence
• And stuck there
• Secondary severe muscle of mastication spasm  make it hard to
reduce

Treatment
• Mechancial manipulation  for reduction
• Inj of la in muscles of mastication  for severe muscle spasm
• Botox inj of lateral pterygoid muscle or surgery  chronic
cases
Ankylosis
• Union b/w condyle and skull
• Can be  bony or fibrous
Cause
• Trauma
• Surgery
• Radiation
• Infection
Clinically
• Severly restricted range of motion
•
 Bruxism

• Clencing or gring teeth

• Diurnal (during day) or nocturnal (night)
Causes
• Stress
Treatment
• Night guards / occlusal guards (distribute forcec evenly &
relax muscles)
 Non surgical therapy for TMD
1. Counselling
• Parafunctional habits
• Stress amanagement

2. Medical therapy
• NSAIDs
• Steroids
• Muscle relaxants
• Anlagesics
• Anti depressants

3. Physical therapy
• Transcutaneous electrical nerve stimulation
• Massage
• Thermal treatment
4. Occlusion
• Occlusal guards
• Occlusar splints  reduce intra-articular pressure

5. Arthrocentesis
• Two needles to flush out superior joint space
• Puncture capsular ligament
• Flush in some saline & then flush out
 Surgical therapy
1. Arthoscopy
• 2 canullas
• Instrumentation with superior joint space
• Puncture capsular ligament

2. Arthoplasty
• Disc repositioning surgery  for painful perisistant clicking or closed jaw

3. Disectomy
• Disc remove or removal when it is damaged
• Removal material  temporalis muscle & fasica, oricular cartilage

4. Condylectomy
• Vertical ramus osteotomy which is not fixated  for soft muscle to grow
5. Total joint replacement
• Pathological joint
• In  arthritis
• Graft  osteochondro bone graft (rib joints), prosthetic joint
replacement

• Nerver damaged during tmj surgery  facial nerve

• Pre-auricular incision  best surgical approach to expose

tmj
 Myofascial pain syndrome

• Chronic muscular pain disorder

• Somatic pain

Common cause
• Masticatory pain
• Parafunctional habits

Clincally
• Trigger point  in muscles of mastication
• Diffuse pain in  preauricular region (ahead of ear)
• Crepitus & clicking
• Limited opening
• Pain at rest

Treatment
• Physcial therapy
• Stress management
• Occlusal splint
 Biopsy
Indicated
• After  2 weeks

Types
1. Cytology
2. Aspiration
3. Incisional
4. Excisional
Cytology / brush biopsy
• Called  oral exfoliative cytology
• Scrape with kit brush or tongue depressor
• Cells are smeared on a glass slide & immediately fixed
• For monitoring large areas  for dysplastic changes
• Many false positive

• Any thing that can be scraped off  candiasis

Fine needle aspiration
• Needle or syringe to suck up the lesion
• Done for  presence of fluid, ascertaing type of fluid or
exploration of intra-osseous lesion
• Fluid expelled on the slide & fixed

Eg:-
• Radiolucent lesion  odontogenic cyst, ameloblastoma
• Differentiate b/w  benign & malignant lesion of bone
 Incisional biopsy
• Lesion large then  1cm
• When malignant suspected
• Used in antomic area with high morbidity  floor of mouth
• Cut in a wedge fashion  Sample from the edge of the lesion &
margins should extend into the normal tissue
• Narrow & deep wedge  prefereable
• Avoid necrotic tissue
 Excisional biopsy
• Small lesion  less then 1 cm
• For benign
• For small vescular pigmented lesion
• Removal of lesion entirely & some healthy tissue (margin 2-3mm)
• Eliptical incision  easier to close
 Biopsy technique
• BLOCK anesthesia  should be performed ( not LA)
• Direct handling of biopsy specimen will  crush cells
(handle gently, forceps non-toothed)
• Store in  10% formalin
 Surgical management for cyst & tumor
Cyst
• Enucleation
• Marsupiliaztion
• Curretage

Tumor
• Enucleation
• Curretage
• Resection
Enucleation
• Removal of mass without cutting or rupturing it

Marsupialization
• Cut a slit into a abscess or cyst & suture the edges of slit to keep
it open for it to drain freely

Curretage
• Removal by scrapping or scooping

Resection
• Surgical removal of cyst or tumour with normal tissue
 Medical
emergencies
• Stop treatment
• Postion
• Oxygen
• Reassure
• Council

• SPORC
Syncope
Vasovagal
Syncope
• Reversible loss of consiousness due to inadequate blood flow in
brain
• Most common
• Fast onset
• Short duration
• Spontaneous recovery
• Mediated by  vagus nerve (10)

Causes
• Fear
• Pain
• Anxiety/ shock
• Dehydration
• Standing for long time
symptoms
1. Prodrome
• Pallor
• Sweating & feeling warm
• Nausea
• Hot & dizzy
• Blurry vision or tunel vision
• Feeling faint or light headed
• Ringing in ears
 Syncopal episode
• Terminate all the dental procedures
• Position patient in supine position with legs raised above the head (The
Trendelenburg position)
• Left lateral decubitus  pregnant

Check for breathing

If absent
• Start basic life support
• Have some one summon medical assistance
• Consider other causes of syncope  hypoglycemia, cerebral vascular accidents

If present
• Crush ammonia ampule under nose (respiratory stimulant)
• administer O2
• Monitor vital signs
• Have patient escorted home
 Post syncope
• The patient might feel fatigued and depressed shortly
afterwards
• Avoid standing immediately after regaining consciousness
to avoid fainting again
• Patient should not be subjected to additional dental care
and discharged with an escort
• Prior to dismissal , doctor should identify the fainting
triggers and discuss ways to might avoid them
 Orthostatic
hypotension
• 2nd most common cause of  syncope
• Dizzy spell or head rush
• BP falls suddenly due to standing
• Failure of  baro-receptor reflux to mediate peripeheral reistance

• Pt lying on chair & is dehydrated  make him stand = orthostatic

hypotension
Epinephrine
overdose
• Rare
• Due to rapid  i/v injection of LA with epinephrine
• Exact opposite of syncope

Signs
• High  BP
• High  HR
• Thumping heart

Treatment
Angina
• Strangling of chest = chest pain
• Mostly in 40+ men & postmenopausal women

Types
1. Stable
• 75% blocked by plaque (stenosis)  can cause schemia
• Enough blood supply to heart during rest but not during work
• Pain during work/excerise & stress
• S-T segment depression

Causes
• Srtherosclerosis of coronary artery

Symptoms
• Pain during work or stress (squeezing pain)
• Radiating to left arm, jaw & back
• Sweating
• Pain relieved by rest (pain last 20mins )
2. Unstable
• Due to clot + plaque
• Heart tissue is alive but ishcemic
• S-T segment depression

Symptoms
• Pain  not relieved by resting
• Emergency tratment  as it can progress to MI

3. Vasospastic / prinzemental
• May or may not have arthero-sclerosis
• But ishmeia is due to coronary artery vasospasm
• S-T segment elevation
• Also respnds to C-channel blockers other than nitroglycerin

Symptoms
• Episodes of pain can happen any time (no exertion needed)
Before appointment
• History
• Consult the physician about the patient cardiac status
• Take a detail and careful medical history
• Good night sleep & short morning appointment
• Anxiolytic before surgery
During procedure
• Follow anxiety reducing protocol
• Monitor vital sign closely
• No surprises
• No unnecessary noise
• La dose  epinephrine 0.04mg or 3 cartridges of la
After procedure
• Patient information on expected post surgical sequelae
• Reassurance
• Counselling
• Effective analgesics
Chest discomfort
• Terminate treatment
• Position patient in semi reclined position
• Loose tight cloths
• O2 administration
• Nitroglycerine spray / tab to be given (0.4mg) (NTG)
• Monitor vital

Still continues  after 5mins

• Another dose of nitroglycerine (vasodialator)
• Monitor vitals

Still not relieved  after 5mins

• Third dose of nitroglycerine
• Aspirin  to prevent blood clot
• Monitor vitals
Myocardial
imfarction
• Avoid surgery fro atleast 6 months (atleast takes 6 months
infarcted muscle scar to mature) can also cause arythhmias
 Management of patient with a history of MI
• Consult patient primary care physician
• Past medical history  drug history  anti-coagulants
• Short morning appointment
• Use an anxiety reduction protocol
• Nitroglycerin ( can use as prophylactic if physician advices)
• Supplemental O2 (optional)
• Give profound LA  epinephrine 0.04mg
• Consider nitrous oxide administration
• Monitor vital sign & maintain verbal contact
Discomfort still continues 3mins after third nose of NG
• Assumes MI in progress
• Administer 352mg of aspirin
• Iv crystalloids

If sever discomfort
• Morphine sulfate 2mg iv/sc
• Basic life support
• Call ambulance
 Diabetes
management
 Dental management of diabetic patient
Patient with controlled diabetes can be treated without any significant
precautions before starting the procedure.

1. Schedule an early morning appointment  avoid lengthy appointments.

2. Use an anxiety reduction protocol but avoid deep sedation techniques in outpatients.
3. Monitor pulse, respiration and blood pressure before, during and after the surgery.
4. Maintain verbal contact with the patient during surgery.
5. If the patient must not eat or drink before the oral surgery and will have difficulty eating
after surgery, instruct him or her to skip any oral hypoglycemic medications that day.
6. If allowed, have the patient eat a normal breakfast before surgery and the take the usual
dose of hypoglycemic agent.
7. Advise the patient not to resume normal insulin doses until they are able to return to
usual level of caloric intake and activity level.
8. Consult the physician if any questions regarding modifications of the insulin regimen
arise.
9. Watch for signs of hypoglycemia.
10. Treat infections aggressively
Before treatment:
• Take dental and medical history.
• Check glucose levels.
• Ask for the medication, dosage and duration.

During treatment:
• LA should be administered without vasoconstrictors like epinephrine
since they increase the blood glucose levels.
• A source of glucose should be available in the dental office to avoid
hypoglycemic shock
• Atraumatic extraction.

After treatment:
• Provide oral health related instructions.
• In case of extraction, continue with soft edible food items.
Hypoglycemic shock
 One of the most common dental emergency is hypoglycemia
(blood glucose below 60 mg/dl)

Symptoms
• Sweating
• Hunger
• Losss of consiouness
• Nummbing of lips or fingers
• Light head / dizziness
• Confusion
• Restlessness
• Tremors
• Tachycardia
Management:
• Place the patient in a supine position
• Immediately check the glucose levels through a glucometer
• Establish airway and breathing
• Turn on fans and air conditioners
• Loosen any tight scarves or clothing

If conscious
• Administer sweetened drink or any source of glucose
• Glucose tab, orange juice

If unconscious
• Administer 50 ml of dextrose in 50% of the concentration or 1mg
Hyperventilati
on
Symptoms
• Dizziness
• Tingling of toes
• Chest pain
• Increased and deep breaths
• Xerostomia
• Anxiety
 Management
• Terminate procedure and remove foreign objects from mouth
• Position patient in upright position
• Calm patient verbally
• Give patient a bag to breath in & out  CO2 rich air

If symptoms persist
• Administer diazepam i/m
• Monitor vital signs
• Perform any procedure using anxiety reduction protocol
Asthma management
• Episodic narrowing of inflammed small airways
• Constriction & inflammation of  bronchioles
• Harder to  inhale & exhale

Avoid  NSAIDs & narcotics

Triggers  stress, exercise, cold, allergy

Symptoms
• Wheezing
• Difficulty breathing
• Chest tightness
Dental management of asthmatic patients
• Take good thorough history  episodes, triggers
• Appointments should be scheduled in the afternoon
• Patient should be asked to bring their usual medication
• Counsel the patients regarding the treatment plan to reduce the
stress
• Anxiety reduction protocol to be followed, use nitric oxide, if
necessary, without respiratory depressants
• Consult patient's physician
• Postpone appointment if patient is unstable
• If patient is chronically taking the cortico-steroids the prophylaxis
for adrenal insufficiency to be provides
During attack
• Discontinue any treatment
• Sit the patient upright in a comfortable position with the arms thrown forward
over a chair back
• Administer bronchodilator by spray (metaproterenol, albuterol)
• Administer o2
• Monitor vitals

Signs continue
• Subcutaneous epinephrine  (0.3-0.5 ml) (1:1000 SC or IM) if patient does
not respond previous treatment (relax bronchial smooth muscles)
• Iv crystalloid solution
• Monitor vital signs

Still not relieved

• Theophylline 250mg IV & cortisone 100mg
Copd
• Chronic obstructive pulmonary disease (COPD) is the name for a
group of lung conditions that cause breathing difficulties 
emphysema + chronic bronchitis
• Long term exposure to pulmonary irritants
• 3rd leading cause of death in  USA
Causes
• Smoking

Symptoms
• Chronic cough with sputum
• Difficulty in breathing  during exertion
• Respiratory tract infection
• Barrel shaped chest
• Wheezing
 Clinical manifestation
1. Emphysema
• Damage to the air sacs in the lungs  alveoli (functional unit of lungs)
• Chronic smoke inhalation  damage lung epithelium  release elastase
• Elastase  destroy lung tissue = enlarged alveoli
• Loose elastic recoil

Sign & symptoms

• Known as  pink puffer (quite no cough or sputum)
• Breathing out  very difficult (expiration)
• Barrel shaped chest  over inflated lungs
• Smaller heart  squashes b/w over sized lungs
• Old thin pt
• Severe dyspnea
2. Chronic bronchitis
• Long-term inflammation of the airways, lose its elasticity
• Pollutants & smoke  irritates the bronchial wall & increase size of
mucous gland & goblet cells
• Causes  lots of mucous production + airway inflammation & narrowing

Sign & symptoms

• Known as  blue bloater
• Chronic productive cough  lots of sputum
• Rhonchi & wheezing
• Peripheral edema
• Elevated  Hb
• Cyanotic
• Over weight
• Radiograph  chest xray normal
Diagnosis of copd
1. Spirometer
• Measure amouth of air person can breath out
• FEV 1 / FVC  less then 70% = copd

2. Pulse oximetery
• Measure % of Hb saturated in oxygen
• 95-100 is normal
• Not diagnosis  but determine current health status
Anti-cholinergic (1st)
• Bronchodialators
• Decrease sputum production & relax smooth muscles (by blocking actylcholine)
• Ipratropium, tiotropium
• For stage 1

Inhaled beta adrenergic agonist (2nd)

• Bronchodialators
• Relax smooth muscles (by increasing cyclic-amps levels)
• Epinephrine (fast acting), isoprotrenol, albuterol, indacatrol (long acting)
• Add long acting fror stage 3

Cortico-steroids (3rd)
• Reduce inflammation & suppress immune response
• Fluticasone (inhaled), prednisone (oral)
• Add if stage 3

Phosphodiesterase inhibitors (4th)

• Theophylline
• Defer any treatment until the lung function has improved &
treatment is possible
• Afternoon appointments
• Use anxiety reduction protocol
• Avoid use of any respiratory depressant
• Consult patient's physician if o2 can be given or not
• If patient is chronically receiving the corticostriod therapy,
prophylaxis is given before the surgery
• Avoid placing patient in supine position, sitting position 
for them to handle their copious pulmonary secretion
• Keep broncho-dialtor inhalers near
• Closely monitor respiraotry & heart rate
Well controlled
• Encourage smoking cessation
• Avoid pulmonary irritants
• Semi-supine or upright (never in supine position)
• Bilateral blocks avoided
• Avoid rubber dams
• Avoid narcotics & barbiturate (respiratory depressants)
• Avoid macrolides (erithromycin) & ciprfloxacin with theophyllin
(cause theophylline toxicity)
• Use pulse oxymeter to monitor O2 saturation
• Avoid nitrous oxide sedation (accumulate in air spaces of
compromised lungs)
• Low flow o2 if saturation below 95
• Use general anesthesia cautiously
Uncontrolled
Someone who is
• Symptomatic  cough, dyspnea, upper respiratory
infection
• O2 saturation below 91%

• Defer treatment
• Refer to ER
• Things to avoid
 Airway
obstruction
Can be due to aspiration of things
• Files
• Instruments
• Tooth
• Vomit
• Food

Prevention
• Rubber dam
• Throat shield

• Hand-around neck  universal choking sign

Universal protocol

1. Clear pharynx
• Clear any  food, vomit, foreign body

2. Check for breathing

• Rise & fall of chest
• Sound of mouth & nose

3. Chin tilt
• Tilt chin up  to extend the neck
• Protrude tongue & mandibile to open airway
Foreign body
Aspiration
 Management of foregin body aspiration
• Terminate all procedures
• Position in sitting position
• Ask patient to try to cough it out

If patient becomes unconsious

• CPR
• Patient in supine position
• Ventilate  basic life support, o2
• Transport to emergency

If patient consious
• Heimlich maneuvers / Abdominal thrusts
• O2
• Medical assiatance & monitor signs
Seizure
• A seizure is a burst of uncontrolled electrical activity between brain
cells (also called neurons or nerve cells) that causes temporary
abnormalities in muscle tone or movements (stiffness, twitching or
limpness), behaviours, sensations or states of awareness

Types

1. Tonic-clonic / grand mal seizures

• Begin as focal seizures  start form 1 part of brain
• Then spread to whole body

Symptoms
• Tonic phase  unconsciousness, contraction of muscles cause
person to fall (last 10-20sec)
• Clonic phase  contract & relaxation of muscles (1-2mins)
2. Status epilepticus
• Continious seizure activity that last for more then 5 mins or two or more seizure
without complete recovery of consiousness

Sign & symptoms

Phase 1  first 30min

• Generalized convulsions
• Hypertension
• Tachycardia
• Muscle contraction & spasm
• Respiratory compromise

Phase 2 after 30-60mins

• Respiratory failure
• Pulmonary edema
• Cardiac failure
• Let the episode end
• No restraining
• Protect airway  celaring the mouth (using suction)
• I/V or I/M  benzodiazapines

During seizure

• Terminate dental treatment

• Place in supine position
• Protect from nearby objects
• Administer diazepam iv 5mg/min upto 10mg
• Medical assitance

• Grand mal seizure  dilantin / phenytoin

after seizure

1. If unconsious
• Medical assistance
• Place patient on side and suction airway
• Monitor vital signs
• Basic life support
• O2
• Transport to Emergency care

2. If consious
• Place patient on side and suction airway
• Monitor vital signs
• O2
• Observe for 1hr
Strokes
1. TIA
• Transient ischemic accident
• Mini stroke
• Last for  few minutes
• Blood supply to brain breifly blocked

2. CVA
• Cerebovascular accident
• Stroke
• Blood to brain stopped  by blockage or rupture
• If by blockage  ischemic stroke
• If by rupture  hemorrhagic stroke
CAUSES
• Hyponatremia  low sodium in blood

Signs
• Facial droop
• Arm drift
• Speech slur

Management
• Give pt  O2
• CALL  911
 Anaphylatic
shock (sever
allergic reaction)
• Anaphylaxis is caused by severe allergic reaction
• It happens when the immune system mistakes a food or
substance for something that's harmful
• In response, the immune system releases a flood of chemicals to
fight against it  causing shock

Sign & symptoms

• Skin reactions, including hives and itching and flushed or pale
skin.
• Low blood pressure (hypotension)
• Constriction of the airways and a swollen tongue or throat, which
can cause wheezing and trouble breathing.
• A weak and rapid pulse.
• Nausea, vomiting or diarrhea
Management  AEIOU
• Albuterol
• Epinephrine  0.3mg
• Im  antihistamine
• O2
• Call  911
Anti-coagulant
therapy
Blood reports
1. Cbc
• Anemia  low rbc
• Lukopenia  low wbc
• Thrombocytopenia  low platelets

2. Bleeding time
• Platelet function
• Aspirin  anti-platelt  will affect bleeding time

3. Pt  test for extrinsic clotting systme

• Anticoagulants
• Liver damage
• Vit k  deficiency
4. INR
• For pt on warfarin
• Normal value  1

5. PTT  intrinsic clotting factors

• Heparin
• Renal dialysis
• Hemophillia

Herbal anti-coagulants
• Ginger
• Garlic
• Ginkgo
 PT/INR APTT Bleeding time
• Prothrombin time/ • Activated partial • Assess platelet
International thromboplastin function and the
Normalized Ratio time body’s ability to
• An INR test • is a screening test form a clot.
measures the time that helps evaluate • To screen patients
for the blood to a person's ability to for bleeding
clot. It is also appropriately form tendencies before a
known as blood clots scheduled surgery
prothrombin time. • Measures intrinsic • Normal value: 6-9
• INR= (patient pathway min
PT/mean normal • Normal value: 25-
PT) IsI 35 sec
• Measures extrinsic
pathway
• Normal INR value:
1.0
• Normal PT value:
 Management
• History
• Consults patient's physician
• Prothrombin time & inr

If patient is on aspirin/platelet inhibiting drug  ptt

• Consult patient's physician about stopping the drug
• Defer surgery until the drug has been for 5 days
• Take extra measures during and after suregry to help promote
clot formation
• Restart drug day after surgery if no bleeding is present
Patient is on warfarin - inr
Local haemostatic measures b taken
• Compressive packing
• Extra sutures
• Topical thrombin
• 4.8% tranexamic acid mouthwash

INR
• 2 – 3  continue treatment
• 3– 3.5 simple surgery (yes)(single extraction), complex surgery (no) (refer)
• More than 3.5  defer to physician (stop medication 3-5 days)
Pain control
• Tylenol with or without codeine

Avoid
• NSAIDS  can increase bleeding
• Metronidazole
• Erythromycin
• Herbal supplements enhance bleding
On heparin
• Consult the physician to determine the safety of stopping heparin
• Surgery at least 6hrs after heparin is stopped (can
reverse heparin with protamine)
• Restart heparin one a good clot is formed
Oral medicine
 Antibiotic prophylaxsis
• Pro-active measure to prevent serious infection

To give prophylaxsis in
1. Previous endocarditis
2. Prosthetic heart valve
3. Cardiac transplant with valvular regurgitation
4. Congenital heart defects
• Unrepaired cyanotic heart disease (low blood oxygen level)
• Repaired cyanotic heart disease with  shunts , valvular regurgitation

Not to give in
1. Joint replacement (hip, shoulder or joint)(complicartions with it may be needed AB)
2. Mitral valve prolapse  with or without regurgitation
3. Rheumatic heart disease
4. Bicuspid valve disease
5. Calcific aortic stenossi
6. Congenital  all other then above
• Atrial septal defect
• Ventricular septal defect
 Other prophylaxsis
• Pt with yes coloum / who need prophylaxsis going through only these dental treatment will need
prophylaxsis as follows

Dental procedures  that require

• Manipulation of gingival tissue or apical regio or perforation of oral mucosa
• Extrsaction
• Cleaning
• SRP
• Fitting orthodontic bands
• Temporary anchorage devices (TADs)
• Biopsy
• Sutures
• Periapical micorsurgery

Dental procedures that does not require

• Rountine anesthesia inj through not infected tissue
• Radiographs
• Removable appliances  prostho or ortho
• Adjusting ortho appliance
• Placing ortho brackets
• Shedding of teeths
Immunocompromised
• HIV or AIDS
• Hematopoietic stem cell transplant
• Organn transplant
• Neutropenia
• Chemo or radiotherapy
• Rheumatoid arthritis  taking prednisone (more then 10mg/day)
• Severe combined immuno-deficinecy
• Autoimmune disease  SLE

Hyperglycemic state
• HbA1c  more then 10%
• Random glucose  200mg/dl
Penecillin
allergy (PCN)
Hypertension
Blood pressure
• Systolic  pressure when heart beats
• Diastolic  pressure when heart relaxes

Hypertension
1. acute
• Caused by stimulus
• Stress, physical exersion, anxiety
• Goes once the stimulus is gone

2. Chronic
• Consistant high BP with out without stimulus for long time

3. White coat
• Elevated bp in healthcare setting
• Treated  life style modification

• Treated  1 drug

• Treated  2 drugs

• Treated  medication change &

hospitalization (if signs of organ
damage )
Factors that contribute
• Obesity
• Smoking
• No physical activity
• High sodium diet
• Alcohol
• Age  old
• Geetic, family history
• Pain
• Medications  stimulants, decongestants, immunosuppresants, OC
• Disease  chronic kidney disease, hyperthyroid, acromegaly, sleep apnea

Essential or primary hypertenison

• Not asscoiated with systemic disease in the list
Secondary
 Hypertension oral manifestation
• There are no true oral manifestation
• Manifestation / side effectc occurs due to medication

1. Dry mouth
• Taste change
• Ulcers
Managements
• Frequent sips of water
• Biotene rinse

2. gingival hyperplasia
• Caused by Ca-channel blockers  NIFEDIPINE
• Treatment  surgical, discontinue drug

3. Angiedema
• Swelling under the skin  mostly lips  puffy lips
• Casued by  renin-angiotensin-aldosterone blockers

4. gingival bleeding
 Blood pressure reading
Methods
1. Ascultatory
• Manual method
• Sphygomomanometer & stethoscope

2. Oscillometric
• Automated
• Arm or wrist cuff + digital reading

• Arm cuff more accurate then wrist cuffs

Cuff size
• Cuff length  80% of arm circumference
• Cuff width  40% of arm circumference

• Most common error is due to smaller cuff

• At first visit it is recommended to redord BP  in both arms
• Then use the arm which goves  higher reading
Alpha adrenegic blockers
• Alpha 1 receptors  cause vessels constriction
• Moa  block alpha blocker = vessels relaxes = decrease in total peripheral resistance
• Zosin  prazosin, doxazosin, terazosin

Alpha adrenegic agonist (A2 in cns)

• Agonising alpha 2 receptors in cns give same affects as above
• clonidine, guanfacine, methyl-dopa

Direct vasodilators
• Act directly on smooth muscles cells of vessel walls to  potassium channels =
vasodilation = decrease in total peripheral resistance
• Hydralazine, minoxidil

Peripheral adrenergic inhibitors

• Block adrenergic receptors in indirect way by interacting with neurotransmitters
which activates them
• Guanadril, reserpine
Beta adrenergic blockers
• Beta 1 receptor responsible for activating  heart contraction
• Blocking receptor = relaxes heart = decrease bp by lowering cardiac output
• Olol  atenolol, bisprinolol, metoprolol, propranolol, timolol \

Beta & alpha adrenergic blockers

• Combine action of both
• Cravedilol, labetalol

Calcium channel blockers

• Block calcium influx into the smooth muscle cells of vessel walls  to cause vaso-
dilation
• Nifedipine, amlodipine, diltiazem, virapamil

Diuretics
• Block sodium re-absoprtion in kidney
• Keeps more sodium & water in urine & away from blood = decrease blood volume
Direct renin inhibitor
• Renin-angitension-aldosterone system  increase bp
• These medication blocks this system = drop in BP
 Pt consideration  BP
120/80
1. Short morning appointments
2. Stress management
• Kind & gentle
• Explain procedures
• Consider anxiolytic before appointment  benzodizapine
• Nitrous-oxide during appointent
3. Slow chair movement  may experience orthostatic hypotension
4. Limiting epinephrine
• Limit to  0.04mg & inject slowly (1 catridge 1:50000, 2 cat
1:100000, 4 cat 1:200000)
• Avoid epi retraction cord
160/100
• Do everything we did up there
• Repeat  measurement in 5mins
• Monitor bp during procedure

180 / 120 or above

• Hypertensive crises
If doing elective
• Defer treatment
If doing urgent treatment

a) Asymptomatic (hypertensive urgency)

• Call physician before proceeding
• Conservative dental treatment & refer to DR

b) Symtomatic (hypertensive emergency)

• Symptoms  altered mental status, blured vision, chest pain, difficulty breathing,
numbness, dizziness
Diabetes
 Diabetes mellitus
• Metabolic disease  resulting in high blood glucose

Insulin
• Hormone produced by  Beta-cells of pancreas
• Help cells to resorp glucose from blood (cause glucose uptake of
cell from blood)
Sign & symptoms
• Polydipsia (thirsty)
• Polyphagia (hungry)
• Polyuria (pee)
Oral manifestation
• Dry mouth
• Burning mouth
• Delayed healing
• Increased infections
• Caries
• High glucose in saliva
• Candidiasis
• Parotid gland enlargement
Type 1
• 5-10%
• Juvenile onset  affects children
• Insulin dependent  lack of insulin production
• Insulin deficiency

Sign & symptoms

• No insulin = no glucose for cells = cells burn lipid of energy – production of
ketone bodies
• Ketosis  if mild
• Ketoacidosis  severe
• Ketone breath (fruity breath)

Treatment
• Insulin
Type 2
• 85-90%
• Adult onset
• Non-insulin dependent
• Insulin – insensitivity
• Most cases can be prevented
• Late cases  insulin inj

Causes
• Diet
• Obesity
• Lack of physical activity
Gestational diabetes mellitus
• Occurs in pregnancy
• Due to  placental hormones
• Combination of both type 1 & 2  insulin deficieny + insulin
resistance
• Resolved after delivery
 Diabetes measurement
1. Blood glucose level
• Measure glucose concentration in blood  mg/dl
• Using glucometer
• Changes thoughout day  not reliable
• 99 or below  normal
• 100-125  pre ( impaired fasting glucose IFG)
• 125 above  diabetes

2. HbA1c
• Measures glycosylated Hb  Hb coded for sugar
• Stable for 3 months  tells sugar levels for pass 3 months
• Higher the % = worst blood surgar control is
• Below 5.7  normal
• 5.7 – 6.4  pre
 Impaired glucose tolerance
(IGT)

• Oral glucose tolerance test  Good standard

test  for diagnosis
• Under 7%  well controlled situation
• Above 7 %  poorly controlled
TYPE 1 MANAGEMENT
Prescription
• Rapid acting before meal & long acting / day  basal effect
• Keep glucose level low & controlled

Stogner & rapid

Strong & rapid affect

Weaker & longer

weaker & longest

Type 2 management
• Medication

1. Sulfonylurea
• Insulin-secretagogues  enhance insulin secretion
• Taken 30mins before meals
• Glipizide, glyburide, glimperide

2. Biguanide
• Reduce glucose production by  decrease gluconeogenesis,
decrease glucose uptake from intestine & decrease glucagon
production
• Taken with meal
• Metformin
Dipeptidyl – peptidase 4 inhibitors
• Inhibit breakdown of natural secretagogue  GLP-1 & GIP
• These are natural hormones  enhance insulin secretion
• Taken once / daily  regardless of meals
• Gliptin  sitagliptin, linagliptin, saxagliptin

Thiazolidinedione
• Improve insulin sensitivity  particularly for fat & muscle cells
(produce more glucose transporters  GLUT)
• Decrease blood glucose
• Taken with meals
• Glitazones  proglitazone, rosiglitazones
Alpha glucosidase inhibitors
• They delay carbs digestion in the gut  block the breakdown of
polysaccharides into glucose by alpha glucosidase enzyme
• Just before meals
• Losing glucose  excreting it
• Ci  abdomen pain, nausea, dirrhea (due to losts of glucose for
bacteria in gut)
• Acarbose, miglitol

SGLT2 inhibitor (sodium-glucose co transporter 2)

• Selectively inhibit this transporter  urinate glucose
• This transporter is expressed in proximal convoluted tubules in kidney
• Leaving sugar in urine can feed bacteria in urethra & bladder  UTI
• Decrease amount of glucose
• Glifozin  canaglifozin, dapaglifozin, empaglifozin
 Diabetes insipidus
• Condition where  kidneys are unable to retain water
• Body can not produce to react to  ADH
• Pituatary insuffiency
Sign
• Polydipsia (thirsty)
• Polyuria (pee)

Treatment
• Synthetic  ADH
• Low salt diet
• I/V solutions
 Management of diabetic pts
Well controlled sugar
• Short morning appointments
• Avoids NSAIDs in pts taking sulfonylurea  worsen hypoglycemia
• Avoid glucocorticoids  increase blood glucose & decrease
insulin sensitivity = hyperglycemia
• Avoid levofloxacin  can lower blood glucose = worsen
hypoglycemia

• Advice pt to take usual insulin dose & normal meals on day of

appointment
• Use glucometer  prior to treatment
• Have glucose source available
Poorly controlled
Elective treatment
• Defer treatment

Urgent
a) Symptomatic  for ketoacidosis
• Refer to ER

b) Asymptommatic
• Call physician before
• Manage infection aggresively  I & D, pulpectomy & AB
• Refer to dr
Brittle diabetes
• Very uncontrolled
• Higher than 200mg/dl fasting
• HbA1c  more then 9%
• Consider  AB prophylaxsis
 Hypoglycemia
• Blood sugar  less than 70mg/dl

Sign & symptoms

• Cold & sweaty  cardinal symptoms
• Tachycardia
• Irritation
• Restlessness
• Excessive hunger
• Dyphoresis (sweating)

Management
• If concious  glucose form (organe juice , sugar)
•
 Hyperglycemia
• Not as immediately dangerous as hypo
• Blood sugar  more then 126mg/dl for fasting or more then 200mg/dl

Sign & symptoms

• Hot & thirsty  cardinal symptoms
• Sweat breath
• Increased thirst
• Nausea & vomiting
• Poly urea
• Blurry vison

Can leas to life threatening complications

• Diabetec ketoacidosis
• Hyperosmolar hyperglycemic state
• Severe diabetes  should not go under anestheisa (if
possible)

Well controlled
• Can go under  I/v sedation & general anestheisa
Guideline
• Fasting  midnight to night before procedure
• Using only  half the usual insulin dose
• Supplementing with  i/v glucose during procedure as needed
 Asa classification
Asa 1
• Normal healthy  No disease
• No smoker
• No alcohol

Asa 2  all about well controlled diseases

• Most common
• Mild systemic disease  well controlled diabetes(Hba1C less
then 7%), hypertension, epilepsy, thyroid dysfunction
• Obesity  BMI 30 or less
• Current smoker
• Pregnancy
Asa 3  all about poorly controlled diseases
• Severe systemic disease  limit activity but not incapacitating
• Stable angina
• Past history of (more then 3 months)  MI, stroke, ischemia attack
• Exercise induced asthma
• End stage renal disease  dialysis
• Alcohol absuse
• Morbit obesity  BMI 40 or more
• COPD
• Poorly controlled  diabetes (HbA1c more then 7%),
hypertension (more then 140 /90), epilepsy, symptomatic
thyroid dysfunction
Asa 4
• Serious life-threatening diseases  severe systemic disease
• Unstable angina
• History of (less then 3months ) heart attack, MI, stroke, ischemia
• End stage renal disease  pt not on dialysis
• Uncontrolled seizures
• Hypertensive emergency
• Septic shock

Asa 5
• Pt survival  not expected next 24hrs
• End stage cancer
• End stage organ dysfunction
• Massive trauma

Asa 6  pt used for organ extraction

 CPR
Checklist
• Appraise scene safety (danger site, instruements)
• Assess  responsivenss
• Alert for help
• Assess  breathing & pulse (simultanously both in 10sec)
• Activate  EMS

Scenario
• Normal pulse & breathing  monitor till help arrivr
• Normal pulse but abnormal breathing  respiratory arrest
(maintain airway & rescue breathing)
• Absent pulse & abnormal breathing  CPR
 Basic life support

• First step when initiating CPR  establish unresponsiveness

• Time interval from cardiac arrest to 1st defibrillation is the most

important factor
• For every min delay in defibrillation from time of collapse 
survival declines by 7-10%

• Order of CPR  CAB (compression, airway, breathing) (new

guideline)
• Compression  lower half of sternum b/w nipples (using two
hands)(100-120 /min)
• Compression depth  2 inches
• 30 compression + 2 breaths
Cardio-pulmonary resuscitation (CPR)  (CAB)
a) Airway
• Head tilt
• Jaw thrust  if neck trauma suspected

b) Breathing
• Look, listen, feel
If respiration is absent / inadequate  rescue breathing
• Bag valve mask (BVM)
• Ventilation rate  1 breath / 5-6 sec ( 10-12 / min)

c) Circulation
• Check pulse  use carotid for adults / child & brachial for baby
• If pulse absent  initiate chest compression
• Compression to ventilation ratio  30:2 (100 compression / min)

d) Defibrillation
 CAB
1. Compression
• Compression  lower half of sternum b/w nipples (using two
hands)(100-120 /min)
• Compression depth  2 inches
• 30 compression + 2 breaths

2. Airway
• Head tilt – chin lift
• One hand on forehead & 2 fingers on chin to lift it up (lift tongue
away from back of throat)
• Jaw thrust  if neck trauma suspected
3. breathing
• 2 breaths / cycle
• Each breath = 1 sec
• Enough air to make chest visibily rise
 Automated external defibrillator (AED)
• Designed to stop an abnormally beating heart
• Need clean dry skin
• Attach pads  upper right & lower left
• Adults pads  over age 8
• Witness caridac arrest  use AED on arrival
• Did not witness cardiac arrest  uses AED after 5 cycles of cpr
(2mins)
 Child / infant CPR
• Pulse  brachial
• Unwitnessed collapse  CPR immediately
• 1 hand for child
• 2 fingers for infant
• Compression depth 1/3 depth of chest cavity
• 15 compression / 2 breaths for child & infant if u have 2 rescuers
Resuce breathing
• 1 breath / 3 sec  child
• 1 breath / 5 secs  adults
 Choking / foreign body obstruction
• Encourage  coughing (if ther r able to)

Conscious
1. Abdominal thrust / helminch manuver
• Position ur self behind pt
• Place 2 hands together to make a fist
• Push back of ur dominant hands thumb  b/w xiphoid process & naval
• For adults
Unconcious
• CPR

• For infants  5 back slaps + 5 chest thrusts

• Brain can survive  6min without O2
Asthma & copd
Copd
• Chronic obstructive pulmonary disease (COPD) is the name for a group of lung
conditions that cause breathing difficulties  emphysema + chronic bronchitis
• Long term exposure to pulmonary irritants
• 3rd leading cause of death in  USA
Causes
• Smoking

Symptoms
• Chronic cough with sputum
• Difficulty in breathing  during exertion
• Respiratory tract infection
• Barrel shaped chest
• Wheezing
Oral manifestation
• Halitosis, Stomatitis, stains, Peirodontal disease
• Aspiration pneumonia  poor oral hygiene
• Stevan johnson sydrome  theophylline
 Clinical manifestation
1. Emphysema
• Damage to the air sacs in the lungs  alveoli (functional unit of lungs)
• Chronic smoke inhalation  damage lung epithelium  release elastase
• Elastase  destroy lung tissue = enlarged alveoli
• Loose elastic recoil

Sign & symptoms

• Known as  pink puffer (quite no cough or sputum)
• Breathing out  very difficult (expiration)
• Barrel shaped chest  over inflated lungs
• Smaller heart  squashes b/w over sized lungs
• Old thin pt
• Severe dyspnea
2. Chronic bronchitis
• Long-term inflammation of the airways, lose its elasticity
• Pollutants & smoke  irritates the bronchial wall & increase size of
mucous gland & goblet cells
• Causes  lots of mucous production + airway inflammation & narrowing

Sign & symptoms

• Known as  blue bloater
• Chronic productive cough  lots of sputum
• Rhonchi & wheezing
• Peripheral edema
• Elevated  Hb
• Cyanotic
• Over weight
• Radiograph  chest xray normal
Diagnosis of copd
1. Spirometer
• Measure amouth of air person can breath out
• FEV 1 / FVC  less then 70% = copd

2. Pulse oximetery
• Measure % of Hb saturated in oxygen
• 95-100 is normal
• Not diagnosis  but determine current health status
Anti-cholinergic (1st)
• Bronchodialators
• Decrease sputum production & relax smooth muscles (by blocking actylcholine)
• Ipratropium, tiotropium
• For stage 1

Inhaled beta adrenergic agonist (2nd)

• Bronchodialators
• Relax smooth muscles (by increasing cyclic-amps levels)
• Epinephrine (fast acting), isoprotrenol, albuterol, indacatrol (long acting)
• Add long acting fror stage 3

Cortico-steroids (3rd)
• Reduce inflammation & suppress immune response
• Fluticasone (inhaled), prednisone (oral)
• Add if stage 3

Phosphodiesterase inhibitors (4th)

• Theophylline
• Defer any treatment until the lung function has improved &
treatment is possible
• Afternoon appointments
• Use anxiety reduction protocol
• Avoid use of any respiratory depressant
• Consult patient's physician if o2 can be given or not
• If patient is chronically receiving the corticostriod therapy,
prophylaxis is given before the surgery
• Avoid placing patient in supine position, sitting position 
for them to handle their copious pulmonary secretion
• Keep broncho-dialtor inhalers near
• Closely monitor respiraotry & heart rate
Well controlled
• Encourage smoking cessation
• Avoid pulmonary irritants
• Semi-supine or upright (never in supine position)
• Bilateral blocks avoided
• Avoid rubber dams
• Avoid narcotics & barbiturate (respiratory depressants)
• Avoid macrolides (erithromycin) & ciprfloxacin with theophyllin
(cause theophylline toxicity)
• Use pulse oxymeter to monitor O2 saturation
• Avoid nitrous oxide sedation (accumulate in air spaces of
compromised lungs)
• Low flow o2 if saturation below 95
• Use general anesthesia cautiously
Uncontrolled
Someone who is
• Symptomatic  cough, dyspnea, upper respiratory
infection
• O2 saturation below 91%

• Defer treatment
• Refer to ER
• Things to avoid
Asthma management
• Episodic narrowing of inflammed small airways
• Constriction & inflammation of  bronchioles
• Harder to  inhale & exhale

Avoid  NSAIDs & narcotics

Triggers  stress, exercise, cold, allergy

Pathophysiology
• Obtruction can be due to  smooth muscle spasm, inflammation, goblet cell hyperplasia

Symptoms
• Wheezing
• Difficulty breathing
• Chest tightness
Oral manifestation
• Increased caries  dry mouth
• Candidiasis  inhaled corticosteroids
• GERD
• Enamel defects  severe asthma in children
• Periodntal disease  severe asthma in adults
 Drugs
Corticosteroids
• Inhaled
• Most affective anti-inflammatory medication for asthma
• Reduce inflmaation
• Prednisone, budesonide, fluticasone

Inhaled beta adrenergic agonist

• Bronchodialators  activating beta 2 receptors
• Relax smooth muscles (by increasing cyclic-amps levels)
• Epinephrine (fast acting), isoprotrenol, albuterol, indacatrol (long
acting)
For acute asthma attack
• 1st line of therapy  short acting (alubuterol)
Anti-histamine
• Block histamine receptors
• Histamine  released by mast cells
• Histamine  redness, swelling, itching
• Diphenhydramine, fexofenidine  calm allergic response
• Given for allergy not asthma  if allergy causing asthma attack
then given to control

Decongestants
• Reduce nasal congestions
• Pseudoephidrine  alpha 1 selective agonist (vasoconstrictor)
• Consitric nasal blood vessels  reducing  nasal swelling &
inflammation
• Mostly used to treat  cold, flu, sinusitis,
Leukotriene receptor antagonist
• Leukotriene is a pro-inflammatory mediator
• This drug blocks leukotriene
• Montelukast, zafirlukast
Well controlled
• Stress management
• Confirm proper medication
• Have inhaler & epipen ready
• Excellent isolation
• Avoid NSAIDs  precipitate asthma
• Avoid narotics & barbiturates  respiratory depression
• Track O2 saturation  97-100%

Poorly contorlled
• Defer
• Refer
Dental management of asthmatic patients
• Take good thorough history  episodes, triggers
• Appointments should be scheduled in the afternoon
• Patient should be asked to bring their usual medication
• Counsel the patients regarding the treatment plan to reduce the
stress
• Anxiety reduction protocol to be followed, use nitric oxide, if
necessary, without respiratory depressants
• Consult patient's physician
• Postpone appointment if patient is unstable
• If patient is chronically taking the cortico-steroids the prophylaxis
for adrenal insufficiency to be provides
During attack
• Discontinue any treatment
• Sit the patient upright in a comfortable position with the arms thrown forward
over a chair back
• Administer bronchodilator by spray (metaproterenol, albuterol)
• Administer o2
• Monitor vitals

Signs continue
• Subcutaneous epinephrine  (0.3-0.5 ml) (1:1000 SC or IM) if patient does
not respond previous treatment (relax bronchial smooth muscles)
• Iv crystalloid solution
• Monitor vital signs

Still not relieved

• Theophylline 250mg IV & cortisone 100mg
 Nitrous-oxide sedation
Can be used
• Dental anxiety
• Gag
• Asthma  no attack at that time

Can not be used

• COPD (severe) due to reduced ability to moves gases in & out of lungs
• Nasal obstruction
• Muliple sclerosis  not chronic use
• Pregnancy ( never in first trimester )  enters fetal circulation & can b toxic to
cell going in mitosis
• Psychiatric disorder
• Communication barrier  hard to confirm the sedation with pts
• Otis media  ear infection = pressure buildup & gas diffusion
• Sickle cell disease  already have b12 deficiency & NO2 interferaes with b12
 Oxygen
Should be given
• COPD
• Asthma

Not to be used
• Bleomycin (chemo-therauptic drug)  this drug can damage lungs
• Paraquat poisioning ( toxic herbocide )
Steroids & adrenal insufficiency
Steroid
• Horomone which is a signalling molecule or messenger that travels to other
parts of body
• Derived  cholesterol
• Secereted by  steroid gland (adrenal cortex, testes, ovaries, placenta)

Corticosteroids
• Glucocorticoids  cortisol (immune suppresant)
• Mineralocorticoids  aldosterone (helps regulate bp through na-water balance)

Sex steroids
• Progestorgens  progesterone (regulate cyclic chnages in endometrium &
maintains pregnancy
• Androgens  testosterone (development & maintainence of secondary sex
features of males)
• Estrogens  estrodials (development & maintainence of secondary sex features
of females)
 Cushing’s syndrome
• Excessive  cortisol

Etiology
1. Endogenous  tumour
a) Primary  excessive cortisol at adrenal cortex
b) Secondary  excess ACTH at pituatary (true cushings disease)
c) Tertiary  excess CRH in hypothalamus
• CRH ACTH  cortisol
2. Exogenous  due to taking to much gluco-corticoids
(cushinggoids)
• Eg:- prednisone for asthma, Ra, SLE, (any auto-immune disease )
• Long term drug use  cause cortex to stop relasing cortisol naturally
• Then when u stop the durg  adrenal crisis

Rule of 2
• If pt has taken 20mg of drug for 2 weeks with-in last 2 years 
suspect adrenal function supression or adrnel crises
• Prednisone 4x more potent then exogenous cortisol (hydrocortisone
20mg)
• Dexomethsone 6x more potent then prednisone
• 20mg hydrocortisone = 5mg of prednisone = 0.75 mg of
dexamethasone
Signs & symptoms
• Moon face
• Buffalo hump
• central obesity  protruted abdomen & slim extremeties
• Hypercalcemia & hyper tension
• Mood changes & chronic tiredness
Addisons disease / adrenal insufficiency
• Too little  cortisol
Etiology
1. Endogenous  immune response agaisnt body tissue
a) Primary  less cortisol production by cortex
b) Secondary  less ACDH production from ant pituatary
c) Tertiary  less CRH from hypothalamus
Sign & symptoms
• hyper-pigmentation  bronzing, brown macuules on lips &
mucosa
• Immuno-compromised
• Fatigue
• Muscle weakness
• Weight loss
Addisonian crisis / adrneal crisis
• Corticosteroids levels  extremely low
Causes
a) Primary
• Uncontrolled addisons
• Destruction of gland (cortex)
b) Secondary
• Atrophy of cortex  due to long use of steroids
• Withdrawal of steroids

Sign & symptoms

• Stress  Hypotensions, vomiting, hypovolemic shock

Management
• EMS
• Monitors vital signs
• Cold / wet or ice pack
• i/v saline  for hypovolemia
 Pt consideration  adrenal crisis

Well contorlled
• Stress reduction / management
• General anestheisa  contra-inidcation (use with caution if using)
• Monitor vitals  BP (if drops below 100/60  i/v fluids)
• Supine postion  if hypotension
• Adequate supplemental cortico-steroids (pre & post for stress-full surgery)

Drugs to avoid
• Phenobarbitol
• Medalozam
• Phenytoin
• Rifampicin
• Ketokanzole & flucanozole
• Imipramine
Poorly controlled
• Defer
• Refer
 Bisphosphanates
• Stops bone resoprtion  by osteoclast apoptosis (decrease
number & function)
It causes
• Increased bone density
• Slow tooth movement
• Impairs healing
• Osteonecrosis
Uses
• Osteopenia
• Osteoporosis
• Fibrous dysplasia
• Hyper-parathyroidism
• Pagets
• Multiple myeloma
• Metastatic bone lesion
• Malignancy associated hyper-calcemia
• Osteogenesis imperfecta
• Gauchers disease
• Retts syndrome
• Dronates
• Most potent  zoledronate (zometa)
• Least potent  etidronate (didronel)

Nitrogen side group

Pharmaco-kinetics

• Oral form  les bio-availability (2%)

• I/V form  highest bio-availability (100%)
• Have high binding affinity  calcium, magnesium & iron (in
intestinal tract)
• That why absorption decreased when taken with  milk, organge
juice, antacids
• Excreted  kidney (rapidly in hours)
• Attracted to  hydroxyapetite binding sites on the bone
• Concentrate higher in  trubacelour bone than cortical
• Half life  10hrs (ibandronate), 10yrs (alendronate)
Pharmaco-dynamic / MOA
MRONJ (medication related osteonecrosis of jaw)
• Medication  bisphosphonates, denosubam / bevacizubam
• Osteonecrosis  dead bone due to lack of blood

• If u take these drugs following any procedure causing bone to

expose  extraction, flap raise = necrosis due to no blood
• Higher dose, more frequent administration, longer
duration & I/V  more chances of MRONJ

Risk factors
• Use of  estrogen / glucocorticoids
• Over 65 yrs. ages
• More potent nitrogen containing bisphosphonate cause  BRONJ
Signs & symptoms
• Starts  asymptomatic
• Progress  bony dehiscence & paranesthesia / pain
• Site  posterior mandible mostly (near mylehoid ridge, tori)

• Eg:- painfull abscessed tooth  extracted  bone exposed with is

necrosed Site

Diagnosis
• Current or previous use of these drugs
• Exposed bone  more than 8 weeks
• No history of radio-therapy
Prevalence
• IV  1% spontaneously  10% extraction
Risk of MRONJ
• Treat all infections
• Non-surgical treatment
• Conservative treatment
• Antibiotic coverage
• Consider alveolectomy  no sharp edges
• Drug holiday

Active MRONJ
• Chlorhexadine mouthwash 0.12%
• Local debridement
• Hyperbarrci oxygen
• Aggressive use of systmeic AB, irrigation & local AB (penecillin)
(combination AB can b considered)
 INR &
Bleeding
 Hemostasis
4 phases
1. Vascular
• Vaso-constriction

2. Platelet plug
• Prmary hemostasis

3. Coagualtion
• Fibrin clot
• Secondary hemostasis

4. Fibrinolytic
 Vascular wall defects
• Rare bleeding episode after extraction
1. Marfan syndorme affects the C.T = effect
vascular wall
2. Ethlers – danlos syndorme

3. Osler – weber – rendu syndrome / hereditary hemorrhagic

telangietasia
• Affects blood vessels directly

Management
• Consult with hematologist
• Minimally invasive
• Local hemostasis measure
 Platelet pathway
1. Adhesion
• Endothelial damage releases  von willibrand factor
• Platelets & VWF join via glycoprotein 1b = adhesion

2. Activation
• Platelets gets activated & release  Thromboxan A2 & ADP
• These causes more platelets to come to join (+ve feed back
effect)

3. Aggregation
• Platelets now begin to express - glycoproteins (GP 2b & 3a
complex ) & fibrinogen
Von willibrand disease
• vWB  helps in adhesion & carries factor 8
• Deficiency of  vWB
• Step of adhesion not happens & coagulation also effected

Thrombocytopenia
• Low platelts
• 150000 – 450000 /ul normal level
• Below 50000  clinical bleeding
• Below 20000  spontanous bleeding
 Anti-palatels medication
• Designed to intefere with  adhesion / activation / aggregation

1. Aspirin
• Inhibits COX-1
• Prevents synthesis of  thromboxane A2
• Irreversible (other NSAIDs are reversible)

2. Clopidogrel
• Competes with  ADP at its receptor to block activation

3. Abciximab
 Platelet testing
Quantitative
• Platelet count  (low platelets in thrombocytopenia, hiv)
• Bleeding time  how long does it take to stop bleeding
(unreliable)

Qualitative
• Bleeding time
• Peipheral blood smear  morphology of cells
• Platelet aggregation test check how well platelet clump together
to form plug
• Platelet function analyzer (PFA-100) instrument measure platelet
dependent coagulation under flow condition (not sensitive
enough for mild disease)
Coagulation factors
1. Extrinsic pathway
• Outside the vessel
• Quicker then intrinsic pathway
• Triggered by  external trauma (which causing blood to escape
vessel)
• Damaged endothelial release  thromboplastin / tissue factor
(factor 3)
• 3  7  10 (see diagram)

2. Common pathway

• Watch video for coagulaltion pathway

 Clotting factor defects

1. Von-willibrand disease

2. Hemophillia a
• Deficiency of  facto 8
• Autosomal ressisive x-linked  affects males mostly
• Most common
• 80% chance after  IAN block (withou prior factor 8 infusion)
• Stick with infiltrations

3. Hemophilla b
• Deficiency of  factor 9

4. Hemophilla c
• Deficiency of  factor 11
5. Vit k deficiency
• Most common acquired disease
• Requires vit k for synthesis  2, 7, 9, 10 (synthesized in liver)
 Medication for coagulation cascade
1. Warfarin (coumadin)
• Block redution recylation of VIT – K
• Blocking factors  2,7,9,10
• Indirect

2. Heparin
• Pulls anit-thrombin & thrombin together  blocks  factor 2
• Indirect

3. Apixaban (eliquis)
• Inhibits factor 10a
• Indirect

4. Dabigatrin
• Directly binds to thrombin (factor 2 a)
 Test

APTT (activated partial thromboplastin time)

• No of secs it takes to make a clot in a sample of blood after some agents are added to
it
• Used to check  intrinsic system & common pathway
• Best single screening test for coagulation disorders
• Normal time  25-35
• Below that  more clotting
• Longer time  bleeding

Prothrombin time (PT /INR )

• How long it takes to make a clot in a sample of blood after some agents are added to it
• Used specific for  warfarin
• Used to derive  INR (international normalized ratio)
• Normal  11-15 secs
• Smaller the inr  clotter
• Larger the inr  bleeder
Patient is on warfarin  inr
Local haemostatic measures b taken
• Compressive packing
• Extra sutures
• Topical thrombin
• 4.8% tranexamic acid mouthwash

INR
• 2 – 3  continue treatment
• 3– 3.5 simple surgery (yes)(single extraction), complex surgery (no) (refer)
• More than 3.5  defer to physician (stop medication 3-5 days)
Pain control
• Tylenol with or without codeine

Avoid
• NSAIDS  can increase bleeding
• Metronidazole
• Erythromycin
• Herbal supplements enhance bleding
Oral manifestation of bleeding disorders
• Spontanous  gingival bleeding
• Petechiae or echymosis
• Hemarthrosis of tmj  bleeding in jaw joint (hemophila)
Substance
abuse
Substance absue
• Recurrent use of substance over the past12 months with subsequent
adverse sideeffect
• Interfering with work, job or relationship

Dependence
• Uncontrollable need for use of substance despite the side effects
• Addiction

a) Tolerance
• Need for increased amount of substance to achiece desired affect
• With diminesh affect with same amout of substance (body gets used to it)

b) Withdrawal
• Groups of symptoms which emereg due to absence of habitual substance
Substance abuse
• 8.7 %  12 or above use it
• More in men
• 18-25yrs
• More common in dental personnel
• Disrupts domapine circuits
 Marijuana
• Most used drug (common)
• From  cannabis plant
• THC  psyoactive ingredient
• Smoked or orally
• Peak affects  20-30min (inhale), 2-3 hrs (oral)
Affects
• Pain reduction
• Seizure alleveation
• Altered perception

Abuse
• Chronic broncitis
Oral manifestation
• Xerostomia
• Leukoplakia
• Leukoedema
• Caries  high sugar diet (due to THC)
• Periodontal disease
• Candidiasis  immuno-suppresion effect
• Oral cancer
 Opiods
• From  poppy plant
• Natural forms  morphine, codiene
• Narcotics
• Naloxone  reversal agent
• Prescription drug monitering programme recommended (PDMP) &
DEA number required
• use  NSAIDs (for pain in opioid abuser pt) (1st line)

Effects
• Pain reduction
• Sedation
• Euphoria
Abuse
• Pupil constriction
• Repiratory deprsssion  even lead to hypoxia
• Make person drowsy

Oral manifestation
• Dental phobia
• Caries
• Candidiasis
• Periodontal disease
• Bruxism
 Cocaine
• From  coca leafs
• Stimulant  stimulates CNS  makes alert
• It is  LA & vasoconstrictor
• Administered  all ways
• Moa  blocks the reuptake of dopamine, serotonin & norepinephrine
• After alcohol  it is leading drug of abuse (frequency, domestic viollence)

Abuse  hard on heart

• Tachycardia
• Arrythmia
• Hypertension
• Pupil dilation
• Heart attack or stroke

Oral manifestation
• Gingival recession  max teeth
 Amphetamine
• Psyo-stimulants  cns
• Made syntehtically in lab
• Oral, I/V, inhale
• Moa  release dopamine stores into synapse
• Half-life longer then cocaine

Uses for
• ADHD
• Weigh loss
• Narcolepsy
• Depression
Abuse
• Tachycardia
• Hyperactivity , alterness
• Dysphonia  diffuclty speaky
• Headsache & confusion
• Mimic  schizoprenia

Oral manifestation  meth mouth

• Xerostomia
• Caries
• High sugar
• GERD  acid in mouth  erosion
• Bruxism
• All above lead to  rampant caries, periodontal disease, tooth
 Sedative hypnotics

• Benzodiazepine & barbiturates

• Benzo  most frequently abused
• Barbiturates  2nd most common
• Longer use or higher doses  cause  dependence

Withdrawal symptoms
• Nausea & vomitng
• Weakness
• Tachycardia
• Sweating
• Anxiety
• Tremors
• Loss of appetite
• Tinnitus
Alcohol
• Depressants  cns
• Temporary stimulant  raise heart rrate

Chronic use
• Congnitive impairment
• Distress
• Personality change
• Liver cirrhosis
• Hepatic encephalopathy
• GI bleeding
• Cardiac arrythmias
• Ascitis
Withdrawal
• Loss of appetite
• Tachycardia
• Anxiety
• Insomnia
• Delirium trenums  shaking + hallucination
• Impaired attention & memory

Management
• Nutrition & rest
• Benzodiazipines / beta-blockers in gradually decreasing doses

Oral manifestation
• SCC  lateral tongue, floor
• Glossitis & loss of tongue papillae  due to nutritional deficiency
• Gingival bleeding, petechiae, echymosis  due to vti k deficinecy
 Pt consideration  substance abuse
For all pts
• Defer & refer if  intoxicated

Marijuana
• Slow chiar movements  risk of hypotension
• Oral cancer screening  have higher risk of squamous metaplasia

Opiods
• If anxious  short acting benzo or nitrous oxide (intra-operatively)
• Have naloxane available  reversal for overdose

Cocaine or meth
• Wating period 6-8 hrs  after last dose / use of substance
• Avoid LA with epinephrine for 24hrs  after last dose (could result in hypertenisve crisis)
• Avoid retraction cord with epinephrine
• Monitor BP & pulse
Alcohol
• Brief advice or discussion  counselling
• Beware of excessive bleeding  due to liver problems (do a lab
test)
• Oral cancer screen  risk factor for SCC
• Avoid acetoaminophen  can synergise live damage
Oral manifestation
• Oral neglect  poor OH
• Missing dentil visit
• Increased risk of blood-borne diseases (HEP C & B, HIV)
Dental stuff if he is abuser
• Approach person quietly & candidly

If abuse affecting their work

• Recommed support line or counseller
• Follow-up

If he is threat to the public safety

• Suspend them & report

Dentist intoxicated
• They will be charged with  public drunkiness & reckless
endangerment
• Suspend licsence & jail time
Thyroid
1. Follicular cells
• T3(tri-iodo-thyronine) & T4 thyroxiene
• T3 + T4 = thyroid hormone

Regulate
• Temp
• Metabolism
• Heart rate
• Groth & maturation

2. Parafollicular cells / c-tells

• calcitonin
• Opposite action to parathyroid hormone

Regulate
• Serium calcium (decreases it)
• Phosphorus level
Epidemiology
• 12% usa population  develop thyroid disease in
lifetime
• Common in female
• Age late teen – 40
 Hyperthyroidism
• Thyrotoxicosis
• Excess thyroid hormone in blood

Oral manifestation
• Pre-mature loss of primary teeth
• Early eruption of permanent teeth
• Lingual thyroid  thyroid tissue posterior to foramen cecum of tongue
• Osteoporosis

Types
1. Endogenous  tumour, immune-mediated stimulus
• Primary  high T3 & T4 at thyroid gland
• Secondary  high TSH in ant pituatary
• Tertiary  high TRH in hypothalamus
Drugs

1. Thyroid peroxidase inhibitors

• It is a enzyme responsible for neutralizing iodine
• It is attached to thyroglobulin to create  T3 & T4
• Without this enzyme  no creation of these hormones
• Propylthyrouracil, methimazole (active form), carbimazole (pro
drug)
• Propylthyrouracil  can cause  ulcer, silaolith & necrotizing
gingivostomatits

2. Radioactive iodine (rai)

• I135
• Kill thryoid cells via radiation
 Pt consideration
• For all pt  palapte thyroid
Avoid
• Epinephrine  limit to 2 carpules max (avoid retraction cord)
• NSAIDs  limit them (can increase circulating T4)
 Graves disease
• Auto-immune disease
• Auto-antibodies against TSH receptors (more release of thyroid
hormone)
• Epinephrine can trigger  thyrotoxicosis

Symptoms
• Fatigue
• Nervous
• Intolerance to hot
• Weight loss
• Tacycardia
• Exophtholmus
• Goitre
 Thryotoxic crisis / thyroid storm
• Untreated hyperthyroidism
• T3 & T4  critically high

Triggers
• Stress

Symptoms
• Tachycardia
• Atrial fibrillation
• Sudden fever (differntiating from hyperthyroidism)
• Excessive sweating
• Nausea & vomit
Management
• Activate EMS
• Monitor vitals
• Cold ice packs / wet cloths  help with fever
• i/v hydrocortisone / oral dexamethasone  inhibit thyroid
hormone release
• i/v glucose
• Propylthiouracil  anti-thyroid medication
• CPR  if needed
 Hypothyroidism
• Exaggerated response to CNS depressants (sedatives &
narcotics)
Common cause
• Iodine deficiency  under-developed country (primary)
• Autoimmune  hashimotos (developed countries) (primary)

Hashimotos thyroiditis
• Anti-thyroglobulin antibodies attack  thyroid gland
Symptoms
• Wieght gain
• Cold intolerance
• Bradycardia
• Wormian bones  small extra bones found in the suturs of
cranium
• Goiter

Oral mainfestation
• Delayed eruption
• Macroglossia
• Xerostomia
• Radiating pain  if hashimotots
Drugs
1. Hormone replacement drugs
• Lyothyroxine  expensive, T3 hormone replacement
• Levothyroixine  cheap, longer half live, T4 hormone replacement

Pt consideration

Avoid
• CNS depressants narcotics, barbiturates & sedative  produce
exaggerated response
 Cretinism
• Hypothyroidism in  children
• Decreased  T3 & T4

Symptoms
• Stunted physical growth
• Stunded mental growth
 Myxedematous coma
• Opposite to thyroid crises / thyrotoxicosis
• Critically low  T3 & T4

Stressfull situations infection, surgery etc

• Bradycardia
• Low body temp
• Hyptenison
• Coma
Management
• Activate  EMS
• Monitor vital
• Cover pts with blanket  to conserve the heat
• I/V levothyroxine  thyroid replacement
• I/V hydrocortisone
• I/V glucose
 Thyroid cancer
Multiple endocirne neoplasia type 2 (MEN 2)
• Multiple neuromas + medullary thrylid cancer +
pheochromocytoma of adrenal gland
• Kidney (MOST COMMON) site of orgin for Metastasis to the
thyroid gland

Oral mainfestion
• Multiple neuromas  MEN 2
Drugs
1. Radioactive iodine (rai)
• I135
• Kill thryoid cells via radiation
Side effects
• Xerostomia
• Sialadenitits
• Caries
• Loss of tasdte
Parathyroid
• 4 glands  located posterior surface of thyroid gland

Made up of 2 types of cells

1. Chief cells
• Release parathyroid hormone (PTH)  regulates amount of calcium in body
Bone
• Hormones binds to osteoblast  increase RANKL & decrease OPG (it activates
osteoclast)
Kidney
• Increases calcium reabsorption at  distal tubules & collecting duct
• Inhibit phosphate phosphate reabsorption
Intestine
• PTH  activates VIT – D  promotes absorption of calcium in intestine

2. Oxyphill cells
 Hyperparathyroidism
• Excess  PTH = more bone resorption  calcium from bone to
blood

Sign & symptoms

• Kidney stones
• Painful bones 
• Abdominal groans  constipation, nausea, vomiting
• Psychiatric moans  fatigue, depression, psycosis
• Brown tumours Giant cell lesion
• Radiolucency’s  salt & pepper
• Loss of lamina dura
• Elevated alkaline phosphatase
Primary
• Parathyroid gland tumour (most common)
• Hypercalcemia
• Treatment  tumour removal

Secondary
• Insufficent VIT-D or chronic renal failure
• Hypocalcemia
• Gland relasing more  PTH
• Treatment  correct underlying cause, vit supplemnts or renal transplant

Tertiary
• Due to chronic secondary hyperparathyroidism
• Causing  hyperplasic gland
• Even after secondary hypoparathyroidism is treated  baseline PTH is high 
hypercalcemia
 Hypoparathyroism
• Most commonly due to  damage or removal of gland
(thyroidectomy)
• No  PTH or less production
• Over accumulation of Calcium in bone

Sign & symptoms

• Paraesthesia & tetny (muscle spasm )
• Radioopacity in skull by the basal ganglia
• Hypoplasia of enamel
• Later eruption
• Dilacerations
• Increased radio-opacity of jaw
Pregnancy
1st trimester
• 0-13 weeks
• Organ formation

2nd trimester
• 14-26 weeks

3rd trimester
• 27-40 weeks

Premature
• Born before 37 weeks

Viable pregnancy
Effects of pregnancy
• Low iron
• Low plateltes
• Increase coagulation factors  1, 7, 8, 9, 10
• Increase wbc
• Decrease lunng capacity (by 5%)

Complications
• Acid reflux  increased intra-abdominal pressure
• Increased urination  more pressure on bladder
• Gestational diabetes
• Preclampsia  Hgh BP, porteinurea, edema & blurred vision
• Miscarriage
 Oral manifestation
• Pregnancy gingivitis  cause risk of pre-term labour
• Increased  caries
• Pyogenic granuloma / pregnancy tumour  (labial of ID papilla)
• Sinus congestion  excess estrogen
• Dental erosion
• Hypersensitive Gag
Folic acid
• For neural tube formation
• Prevent  anencephaly & spina bifidia

Acetaminophen
• Safest in pregnancy

NSAIDs
• Safe in  1st & 2nd trimestes
• Avoid in  3rd trimester  cause early closure of ductus
arterioris = fetal pulmonary hypertension

Lidocaine & prilocaine

• Safest LA to use
 Supine hypotensive syndrome
• Compression on  aorta & inferior vena cava

Caues
• Hypotension
• Pallor
• Sweating
• Nausea
• Weakness
• Air hunger
• Dizziness

Prevent & management

 Pt consideration
• Postion  recline
• Monitor vital  if BP goes over 140/90  call OBYN = risk of preclampsia
• Radiographs  not to use if needed  limited (use lead apron & thyroid
collar)
Avoid
• Elective care  1st trimester & 3rd trimester
• Nitrous oxide  1st trimester
• Tetracycline & excessive fluoride  2nd & 3rd trimester (2nd trimester
to 8 yrs of age)
• NSAIDs  3rd trimester
• Benzodiazepines

• If nitrous-oxide being used in other trimesters  limit use to

Pain & infection
management
Pain levels (acute)
 Analgesic use
Mild pain
• ibuprofen 400mg / 6 hrs for 1 day
• Or  ibuprofen 400mg / 6 hrs as needed

Moderate pain
• ibuprofen 400mg + acetaminophen 500mg / 6 hrs for 1 day
• Then ibuprofen 400mg + acetaminophen 500mg / 6 hrs as
needed

Severe pain
• ibuprofen 600mg + acetaminophen 650mg + hydrocodone
10mg / 6hrs for 1-2 days
Safe
• Pregnancy  acetaminophen
• Liver disease  low does acetaminophen (not exceed 2g/day)
• Kidney disease  acetaminophen
• Heart  acetaminophen
• Stomach disease / ulcers  acetaminophen
• Asthma  acetaminophen (NSAIDs induce broncho spasm,
optiods are respiratory depressants )
 Antibiotics use
Swelling
• Immuno-compromised
• Urgent dentasl care not feasible
• Severe swelling

Systemic involvement
• Fever, malaise, lymphadenopathy
• Amoxcillin 500mg / 8 hrs for 1 week
If allergic to penicillin / amoxicillin
• Azithromycin 500mg on day 1 & 250mg from day 2 – 5

• Clindamycin was used earlier but due to risk of  clostridium

 High
cholesterol /
hyperlipidemia
• High levels of lipids circulating in blood

Lipids are one marco-molecules that make-up all living things

1. Cholesterol
• To make sex hormones, steroid hormones, integrity of cell memb

2. Triglycerides
• Convert to  phospho-lipids (important for cell membrane)
Lipo-proteins
• They carry  lipids through blood stream
• Lipids + protein

1. HDL (high density lipo-proteins)

• Less lipids & more protein
• Transprot cholesterol from peripheral tissues to liver
• It is processed in liver & expelled from the body
• Hdl  helps get rid from excess cholesterol
• Ideal  above 50mg/dl

2. LDL (low density liupo-proteins)

• High lipids & less protein
• Transport lipid to the walls of arteries  lead to fatty build-up in the
arteries
Oral manifestaion
• Pulp calcification  pulp stones
• Muscle of pain & weakness  side affects of statin
• Increased  periodontal disease
 Atherosclerosis
• Build of fat in the arteries

Causing
• Constriction of diameter of artery
• Separate endothelial cells from smooth muscle cells  block nitric
oxide (no vasodilation)

Increase risk
• Stroke
• Heart attack
 Drugs
• Statins
• HMG-CoA reductase  responsible for cholesterol
synthesis in liver
• These drugs affects only cholesterol made in liver & no affects on
cholesterol taken from diet
• These drugs decrease  Serum LDL
 PT CONSIDERATION
If pt taking statin drugs avoid
• Marcolide  antibiotic (erythromycin & clorithromycin) &
antifungal (ketoconazole, flucanazole, itraconazole)

See hypertension or diabetes guidelines if applicable

Cancer, chemo &
radiaiton
 Epidemiology
• 2nd most common cause of death in the us

Male
• Prostate > lung > colorectal > bladder > melanoma of skin
Female
• Breast > lung > colorectal > uterine > thyroid
 Head & neck cancer
• Visual inspection then palapation
• Fixed or matted lymph nodes
• SCC  most common
• Oral cavity > oropharynx > larynx > nasopharynx >
hypopharynx
 Oral cancer
Risk factors
• Tobacco > alcohol > HPV > immuno-compromised
Site
• Tongue > lower lip > floor of mouth
 Complications of cancer treatment
• Xerstomia (C & R)  damage glands (2nd week of treatment)
• Mucositis (C & R)  2nd week (common on non-keratinized
tissue)
• Taste alteration (C & R)  2nd week (due to damage of micro-villi
of taste cells)
• Secondary infection (C & R)  weakend immune system (candida)
• Bleeding (C )  supress bone marrow = low platelet /
thrombcytopenia
• Radiation caries (R)  labial surface of teeth near gum & progress
fast
• Hypersensitive teeth -
• Trismus ( R)  damage vasculature of jaw muscle
• Carotid atheroma (R) 
Mucositis
• Saltwater rinses
• Supplemental zinc
• Chlorhexidine rinse
• Oral cryotherapy
• Soft fluid diet
• Topical anesthesia & analgesic

Osteoradionecrosis
• Mostly post mandible
• Risk always present  never extract tooth without consultation
 Pt consideration
1. Before chemo / radio
• Comprehensive exam  OPG
• Maintain excellent OH  fluoride use, diet modifcation,
• Eliminate all sources of infection or irritation  abscess, gum
disease, active careis, sharp bony speckules, gingival operculum,
orthodontic bands
• Extract all non-restorable teeth

2. During chemo / radio

• Remove removable prostho appliances  to avoid irritation
• Manage salivary flow  pilocarpine,
• Manage complication
3. Aftere chemo / radio
• Call physician for outcome
• Oral recall programme  once / 1-3 months every 2 yrs, then
once / 6months for 3 year
• Avoid extraction if possible
• Manage complication

Extract teeth
• Week / 7 days before chemotherapy
• Two weeks / 14 days before radiation
HIV & AIDS
 EPIDEMIOLOGY
• 70 million affected
• 35 millinon dies of aids
• More commin in males
• Age  25 -29
• Black > Hispanic > Asian > white

• Pt should but are not legally bound to disclose their HIV

status (except Arkansas)
• dentist are required to
 HIV
• Enveloped RNA retrovirus (lento-virus family)
• Found in  bodily fluids (tears, semen, blood, vaginal secretions, cvs,
breast milk, amniotic fluid, urine ) (except for saliva & sweat )

Infects cells with CD4 receptors

• T-helpers cells (t lymphocytes)
• Marcophages

Transmission
• STD
• NEEDLES SHARING
• VERTICAL TRANSMISSION  mom to infant
• OCCUPATIONAL TRANSMISSION  pt to dr or dr to pt
 Stages
Stage 1
• Begin immediatily after infection
• Last  several years
• T – help cells  more then 500 cell/ ul
• HIV antibody positive
• Asymmptomatic

Stage 2
• Symptomatic
• T – help cells  200 -499 cell/ ul
• Immunocompromised  fever, malaise, thrush, weigh loss,
lymphadenopathy
Stage 3
• AIDS
• After 10-11 yrs after HIV begins
• T – help cells  below 200 cell/ ul
• Symptomatic  malignanacy, wasting, demtia, oppuotonistic
 Diagnosis
1. ELISA  enzyme linked imunoosorbant assay
• Imp test
• Detect  anti-bodies to HIV
• Test once  +ve
• Test again  +ve

2. Western blot
• After ELISA +ve twice
• Detect specific protein molecules

3. PCR
• To detect viral load of HIV in blood
 Oral manifestation
• Xerostomia (40%)
• Increased caries
• Increased peridontal disease  NUP/NUG
• Linear gingival erythema
• Candiasis
• HSV 1 & 2
• HPV
• Oral hairy leukoplakia  EBV
• Kaposi sarcoma  HSV 8
• Cytomegalo-virus
• non-hodgkin lymphoma
 Medications
• Anti-retro virals (ART)
 Pt consideration
HIV
• Treat as u treat all pt  no discremination (violation of justice if
not treated due to hiv)
• Standar precautions  gloves, mask, eyewear, gowns
• Post exposure prophylaxsis (PEP)
Avoid
• Acetaminophen with zidovuine
• Mepreidine with ritonavir
AIDS
• Non invasive  same as above

Invasive
• Consult with physician
• Antibiotic prophylaxsis  cd-4 less then 200 or neurophil less then
500
• Platelet replacement  thrmobocytopenia
• Avoid  NSADs (aspirin & others )
GERD & peptic
ulcers
 GERD

• Gastric ph  1.5 – 3.5

• Esophagus  connects mouth & stomach
• Reflux  acid going in opposite  into esophagus to
mouth
Pt consideration
• Ask about diet  acidic foods can increase this
• Test salivary function  ph & buffing capacity
 Peptic ulcers
• Break in the lining of  stomach, esophagus or deodenum

Cause
• H.pylori  gram –ve (most common)
• NSAIDs chronic use
• Old age
• Smoking
• Stress
• Alcohol
• Nitrogen bisphosphonatesd

• Nsaids block  cox 1  inhibits PG (pg helps protect stomach

 Pt consideration.
• Encourage OH  (h.pylori I bacteria and can harbour in plaque)
• Reconsider antibiotic (if pt already using ab and need one for
dental use ab of different class then)

Avoid
• NSAIDs (cox2 selective inhibitor if need to be used)
• PPI with  ampicillin, ketoconazole, itraconazole, bezodiazepine,
warfarain, phenytoin,
• Antacids with  tetracycline & erythromycin
Oral manifestation
• Candidiasis  due to AB USE
• Taste alteration  PPI
• Erythema multiform  H2 blockers & PPI
• Erosions teeth GERD
• Xerostomia  PPI
 Tooth erosion
Teenages
• Sugar diet & eating disorders
• Bulimia common in girls
• Sodas

Middle age
• GERD, OSA (obstructive sleep apnia)

Elders
• Poly pharmacy  mulitple drugs = xerstomia
 Signs of erosion
Perimolysis
• Acid erosion due to acid reflux

Cupping
• Smooth bowl shaped dot on the cusp tips

Standing proud
• Restoration standing proud  sticking up relation to tooth
• Restoration there and tooth disolving / eroding faster

Whipped clay
• Loss of anatomical detail  ridges & grooves
Sleep acid traid
Sleep apnea
 Sleep disorders
• 70 million american have sleep disorders
• Mostly female

• 17 million have obstructive sleep apnea (OSA)

• mostly male
Sleep
• Active process which follows its own programme & sequence
• Contribute to  1/3 of persons life
• Avg human has  5 sleep cycles / night (90min each)

2 phases
1. Non-rapid eye movement (NERM)
• Dreamless sleep
• Quite brain & resting body
• 80% of total sleep time
Stage 1  dossing off

Stage 2  drop in temp, muscle relaxes, slow breathing, decreased heart rate &
brain activity slow

Stage 3 & 4  slow wave / deep sleep , decreased muscle tone, delta wave brain
2. Rapid eye movement (REM)
• Dreaming sleep
• Active brain in paralyzed body  skeletal muscle hypotonia
• 20% of sleep
• In children obstructive events occur during this cycle
 Sleep disorders
Insomnia
• Difficulty sleeping

Parasomia
• Sleep walking, night terrors

Sleep related breathing disorders

• Snoring, central sleep apnea, obstructive sleep apnea

Sleep related mvement disorders

• Restless leg syndrome, nocturnal bruxism

Narcolepsy
• Sudden day time drowsiness
• Sleepin during day

Circadian rhythm sleep-wake disorders

 Snoring
• 40% adutls do it  males more
• Result from  vibration of loose soft tissue as air pass over them
(soft palate, uvulea, post tonsilers pillars)

Snoring in children
• Due. To  enlarged tonsils or adenoids
 Sleep apnea
Central sleep apnea
• Airflow stops as a result of temporary lack of inspiration
• Cns issue
Due to
• Poliomyelitis
• Spinal cord injury
• Encephalitis

Obstructive sleep apnea

• Airflow stops as a result of physical blockage
Due to blockage of
• Nasopharyngeal
• Oropharyngeal
 Episodes
• Apnea  cessation of airflow for 10secs
• Hypopnea  reduced airflow for 10 secs
• Respiratory effort related arousal  increased respiratory effort
for 10 secs leading to an arousal
 Apnea – hypopnea index (AHI)
• No of episodes of complete blockage / 10secs + no episodes of
partial/ 10sec blockage & divide by total sleep hours

ADULTS
• Mild  5-15 ep / hr
• Moderate  15-30 ep / hr
• Severe  30 or more ep / hr

Children
• Mild  1-5 ep / hr
• Moderate  5-10 ep / hr
• Severe  10 or more ep / hr
 Arousal
• Partial or complete air blocakge will lead to  hypoxia &
hypercarbia
• Frequentt arousals = poor fragmented qauily
• Obstructive events in children  REM sleep
 Signs & symptoms
• Snoring
• Somnolence  excessive daytime sleep
• Framented sleep
• Nocturanl sweating  night sweats
• Nocturia  urination
• Poor memory
• Morning headache
• GERD increased intrathoraic from apena
• Nocturanl bruxism
• Cardiovascualr symptoms  hypertension, arrthmia,
stroke
Risk factors
• Obesity
• Age
• Male
• Family history
• Alcohol
• Supine sleeping
• High narrow palate  increase nasal resistance & decreased
space for tongue to rest
• Increased  ant facial height & overjet
• Large tongue
• Retronathia
• Sickle cell anemia
• Mucopolysaccharidosis  accumulation glucoseaminoglycans
• Down syndrome
 Screening
1. Mallampati score
• Tongue size when not protruted & in relaxed position (original
mallampati score )
• Modified score  protrude tongue as much as u can and see if
posterior pharyngeal space blocked or visible
• Class 1 & 2  can see uvuela & tonsiler pillar
• Class 3  base of uvuela not visisble
• Class 4  completely not visible
2. Scalloped tongue
• When tongue presses agains teeth  scalloping of tongue
• This is 70% diagnosis for OSA
3. Brodsky score
• Size of tonsils
• Coreleates with OSA & severity
4. Stop bang questionnaire
• Snoring
• Tired
• Observed apnea
• Pressure of blood
• Bmi elevated
• Age above 50
• Neck has increased circum ference
• Gende  male
 Diagnosis
Polysomnogram (psg)
• Gold standard
• EEG  brain waves
• EMG  leg & jaw muscle movement
• EOG  eye movement
• Thermistor  oronasal airflow
• Strain gauges  chest & abdomen movement
• Pulse oximeter  o2 saturation
• ECG  heart rate & rhythm
 Treatment
1. Behavioural modification
• Weigh loss  if it is one of the factor
• Encourage  lateral decibus position for sleeping
• Avoid  alcohol, benzo, barbiturates, muscle relaxants
• Encourage  good sleep
• Nasal steroids  mild apnea

2. Positive airway pressure

• CPAP  continious +ve airway pressure (gold standard )

3. Oral appliacnes
• Reposition & maintian  mandible & tongue anteriorly
4. Orthodontic treatment
• Narrow maxilla  RPE (for children before puberty only)

5. Surgery
• Septoplasty
• Tonsilectomy
• Adenoidectomy
• Uvelo-palato frangeoplasty (UP3)

6. Hypoglossal nerve stiumulation

Hepatitis
• Inflammation of liver
Causes
• Most commonly due to  viral hepatitis
• Alcohol  alcoholic hepatitits
• Chemical (phosphorus, carbon tetrachloride, actaminophen,
chloroform)  toxic hepatitits
• Immune  auto-immune hepatitis
 Immunology
B lymphocytes
• Humoral immunity
• First cell to recognize antigen
• Becomes a plasma cell &  produce ab

T-lympthocytes
• Cellular immunity
• T-helpers cells
• Cytotoxic – t cell

• IgA  saliva
• IgE  bind to mast cells & basophills  involved in allergic resposne
• IgG  principle antibody (most common)
• IgM  first responder to most foreign bodies , neonatal B cell predominatly
 Transmission of viral
• HEP – A  fecal-oral  contaiminated food / water, diapers, poor
hygiene
• HEP – E  fecal-oral

• HEP – B  blood, bodily fluids (semen also)

• HEP – C  blood, bodily fluids (semen also)

• HEP – D  direct contact (blood & fluids ) but usually acquired

after HEP B (previous infection co infection or super
infection )
 HEP A
• Fecal-oral
• Incubation period  2-6 weeks
• Acute rapid onset
• Does not lead to  chronic disease or carrier state

Sign & symptoms

• Jaundice
• Fever
• Malaise
• Loss of appetite
• Nausea

Treatment
 HEP – B
• High transmission risk (30%)  blood, per-cutaneous
• 1- 6 months incubation
• Dna virus (only this is dna virus) dane particle
• intra-orally great concentration of this virus is at  gingival
sulcus

Sign & symptoms

• Jaundice
• Fever
• Malaise
• Loss of appetite
• Nausea
Treatment
• Vaccine available  and very effective (administered in 2-3
inj over 6 months)
• Post exposure prophylaxis is available  vaccine & immunogloblin
therapy
• OSHA requires employers  vaccine available freely for all
employee occupitionally exposed

Diagnosis
• Surface antigen (HBsAG)  ACTIVE INFECTION (can spread to
others)
• Surface antibody (ANTI-HBs)  recovery & immunity
(vaccinated)
• Core antibody (ANTI-HBc)  natural immunity persistant for
life, had infection
 HEP C
• Most common bloodborne pathogen in us  blood
• 1.8%  transmission risk
• RNA virus
• 2 week – 6 month incubation period
• Usually asymptomatic
• Acute hep c  goes on its own
• Chronic  cause cirhosis (need medicines)

Treatmetn
• No vaccine
• But treatment is available  weekly interferon alpha & daily
riboviron
 Pt consideration
Active hepattits
1. Elective
• Defer & refer
2. Urgent
• Isolated  operatory
• Standard precautions
• Minimal aerosols
• Avoid drugs metabolized in liver

Carriers / recovered
• No treatment modifications
Drugs metabolized in liver
• Amides  Lidocaine
• Anaglesic  NSAIDs, acetaminophen
• Sedative  diazapam, barbiturates
• Antibioticcs  ampicillin & metronidazole

• If dental personal have acute hepatitis (hep a)  stay home away

from work atleast week after onset of jaundice
 Oral manifestation of liver dysfunction
• Jaundice  yellow oral mucosa
• Petechiae  pinpoint bleeds
• Tendency to bleed  vit k (no coagulation cascade)
• Fetor hepaticus  bad breath due to liver disease
• Atrophic glossitis  smooth tongue no pappila
• Xerostomia
• Lichen planus  hep b & c
• Hepatocelluar carcinoma
Smoking
 Tobacco use
• Leading cause of  preventable death & disease in usa
• Smoker die  10yrs earlier then non-smokers
Associated with
• Cataracts
• Pnemonia
• Cancer
• copd
• Asthma
 Nicotine
• Primary addicitve componend of ciggarrete
• Come from  nicotiana tabacum plant
• 1-2mg / cig
• Peaks with in 10 secs of inhalation
• Dopamine circuits
• Epinephrine rush increase HR, BP, respiration
 Nicotine withdrawal
• Try to quit own there own  relapse 1 week

• Begins  hours
• Peaks  days
• Subscides  weeks

Symptoms
• Irritated
• Craving
• Depression
• Anxiety
• Cognitive & attention deificts
• Sleep disturb
 Cigarettes
• Chopped tobacco leaves wrapped in paper
Contains
• Menthol, tar, carbon monoxide, formaledehyde

• Second hand smoke  same adverse effects

Cigar
• Larger & wrapped in tobacco

Cigarillo
• Small & wrapped in tobacco
Pipes
Conventional
• Loose tobacco leaves

Hookah
• Shredded tobacco leaves + flavours
• Water pipe
 Smokeless tobacco
Snuff
• Finely grounded tobacco
• Pinch of tobacco  place at b/w buccal mucosa & gingiva for
30mins

Chaw
• Chewing tobacco
• Coarse tobacco

Snus
• Tea bag like poch of tobacco
• Hold it in the lip
 Electronic nicotine delivery system
• A liquid heated into aersol or vapour
• Does not contain tobacco

Contains
• Nicotine
• Propylene glycol
• Gllycerin
• Diacetyl  cause popcorn lungs

• Not recommended as method to prevent relapse from cig

smoking
 Tobacco cessation
1. Behavioural
• Counselling
• Telephone quit line 
• Hypnotherapy
• Acupuncture

2. Pharmalogical
• Medication  not for pregnant, ligh smokers (less then 10cig / day
/ half pack /day ), epilepsy
• NRT  Nicotine replacement therapy (nictine receptor agonist)
• Buproprione  antideppressant  block re-uptake of nore-
epinephrine & dopamine (NDRI)
 Pt considerations
Smokers
• Ask, advice, assess, assit, arrange
 Oral manifestation
• Leukoplakia
• SCC
• Nicotine stomatits
• Smokers melanosis
• Hairy tongue
• Halitosis
• Smokless tobacco keratosis
• Periodontal disease
Tuberculosis
(TB)
2. Tuberculosis
• Cause  inhalation  mycobacterium tuberculosis (ACID FAST
BACILLIS)
• Oral non healing ulcer (stellate / star shaped )+ lung
infection
• Africa  higher incidence
• Transmission  Air borne  droplet nuclei
• Hiv pt  high risk of progressive disease

Vaccine
• Available  BUT NOT NEEDED
• Bacillus calmet guerin (BCG)
Types
a) Primary
• Ghon complex  bateria surronded in granuloma that undergoes
cesation necrosis + infected hilar lymph node draining the first
lesion)

b) Secondary
• Widespread lung infection  with cavitation

c) Miliary
• Systemic spread

Treatment
• Multidrug  isoniazid, + rifampin + ethambutol
Oral mainfestaiton
• Painfull deep  ulcer on tongue
• Tuberculous osteomyleitis
• Scrofula  tb infection outside lungs (irritated lumph
nodes )
• Oral non healing ulcer (stellate / star shaped )+
lung infection
 Latent TB Active TB

• Tb lives but not grows • Tb acitve & growing

• Does not have symptoms • Can spread to others
• Not active Have symptoms
• Can not spread to other people • Cough
• Can advance to active • Night sweats
• Blood sputum
Treatment • Chest pain
• Isoniazid • Fever
Treatment
• Isoniazid + rifampin +
pyrazinamide +ethambutol
 Infection control
1. Administrative
• Written tb infection control plan
• Give instruction to pt  cover mouth when cough
• Educating stuff about tb
• Screen for tb  when hiring staff

2. Environmental
• Reduce spread
• isolated rooms  for suspected or confirmed cases
• Air filters  heppa filters
• Ultraviolet germocidal irradiation

3. Protective
• Respiratory protective measures  n95 mask with tb
 Diagnosis
1. TB skin test / mantoux tuberculin skin test
• First day  inj 0.1ml ppd  into skin
• Second day  after 2-3 days, delayed hypersensitivity reaction
• Bcg vaccine  might lead to false positive

• Test at beginning of empolyment, but routine testing no

longer recommended

2. Tb blood test / inteferron gama released assay (IGRA)

• Single visit test
• No false positve on BCG vaccine
• Test at beginning of empolyment, but routine testing no
 Pt consideration
1. Latent
• No treatment modification

2. active

Elective
• Refer & defer

Urgent
• Isolated operatory
• Standar precaustion + n95mask
Multiple
myeloma
• Also called  plasma cell myeloma
• Cancer of plasma cells
• Mulitple tumours scattered through out skeletal system
• IgG > IgA > IgD
• Amyloidosis due to accumulation of complex amyloid protien

Symptoms
• AGE  70
• Bone resoprtion & bone marrow replacement
• Bone pain
• Anemia, leukopenia, thrombocytopenia
• Death by infectio or renal failure
• Amyloidosis of tongue
Radiograph
• punched out radiolucency in skull

Treatment
• Chemo
• Poor prognosis

Diagnosis
• Bence – jones protein  urine
Medications
Pt consideration
Betel nut
• Seed of areca palm fruit
• Quid  betel leaf package for chewing
• Stimulant
Oral manifestation
• Oral submucous fibrosi (OSF)  premalignant
• SCC
• Attrition
• Gingival recession
• Extrinsion stain  reddish brown

• No xerostomia
Oral radiology
 Power-supply & tube head

Filaments & electrons

Xrays
• High frequency & high energy waves
• b/w uv rays & gamma rays
• Similar to  visible ligh rays
Photons
• Rays packed into energy package  photons
• Produced by xray tube, scattered & absorbed by human tissue
Attenuation
• How the xrays beam weakens as it moves through matter
• Thicker & dense tissue  less xray photon make it through to
other side where receptor is

Receptor
• Sheet of film processed with chemicals  traditionally
• Films / sensors
 Inonizing radiation
• Form of energy that act by removing electrons from atoms &
molecules to create ions
• Material that inculde  air, water, living tissue
• Invisible, odorless
Two forms
1. Electromagnetic
• Movement of energy through space as of combination of electric &
magnetic field
• Wavelength  distance b/w crest of waves
• Shorter the wavelength = higher energy
• Gamma > xray > UV > violet to red > infra red > microwave >
radio
2. Particulate
• Atomic nuclei or subatomic particle moving at high velocity
• Descrete particle
• ALPHA & BETA particle  decya from radioactive

• Alpha particles  helium nuclei

• Beta particle  electron, posotrons
• Gamma (Y) particles  electromagentic rays
 Types of xray production
Bremsstrahlung xray production
• Principle source of xrays photons
• High energy electrons attracted to positve nuclei of tungstan &
strike target as a result  this results in deacceleration / braking
of that electron = loss of kinetic energy
• Loss of kinetic energy is converted to  xray
• This creates  continous spectrum of energy
Characteristic
• Secondary source of xray production
• High energy electron strikes another electron & knock it out with
in the atom = vacancy
• Electron in high energy state drops into lower energy state (k
shell)  emits the energy difference b/w two shells as  xrays
• Emits photons of specific energy
Intensity
• Quantity of electron
• Number of photons
• Density  darkness of image

Energy
• Quality of energy
• Energy of photons
• Contrast  diffence among grey values
Exposure time
• Length of time measured in  secs
• High voltage current applied & time during which tube current
flows & xrays are produced
• Affects intensity  number of electrons & photons
• This is setting most frequently changed
• Too long  too dark, over-exposed
• Too short  noisy, underexposed
• For audlts  increase time
• For children  decreased
Tube current
• Measured in  mA
• Flow of electron through the xray tube from the filament to the
anode & then back to filament
• This setting can not be adjusted
• Current increased  no of xray photons generated at anode
(linear increase)
• Affects intensity
• Too much too dark, over-exposed
• Too little  noisy, underexposed
Tube potential
• Measured in  kVp
• Accerlation of electrons from cathode to anode
• Affects  INTENSITY & ENERGY (increased number & energy
of photons)
• Too high  too grey, not enough contrast, mostly compton
scattring
• Too low  too white, very high contrast, photoelectric absorption
Filtration
• Involves  aluminum
• Removes lower energy photon from beam to reduce pt exposure
• Conceptually  same as  beam hardening
Collimation
• Collamator  metallic barrier, reduces scatter radiation by
limiting size of xray beam
• To reduce exposure
• Commonly used  lead
• Rectangular collimation  best method (greatest method
to reduce radiation dose)
• Improves image quality also

• Scatter radiation also known as  noise (redues image

contrast)
Distance
• Inverse squar law  FAR FROM SOURCE = LESS PHOTON / UNIT
AREA
• Operator distance from source  6 feet
• Xray anode  where xrays produced
• Film / sensor  image collected here

Source to object distance (SOD)

• From xray source to the tooth
• SOD increase = decrease in INTENSITY
• Larger SOD = SHARPER IMAGE

Object to image (OID)

• From tooth to sensor
• Lower OID = SHARPER IMAGE

• Source to image distance (SID)  source to film (ALSO CALLED FOCAL

FILM DISTANCE (FFD) )
 Geometry

Umbra
• Shadow behind a image
• No light gets here

Penumbra
• Side shadow
• Occurs around the umbra
• Where some light is present
• We don’t need it
• Penumbra = FSS / SOD X OID
Size depends of three thing
• Focal spot size (fss) (SMALLER THE SOURCE = SMALLER PENUMBRA =
SHARPER PICTURE)
• SOD
 Radiation dose
1. Coherent scattering
• Incident photon interacts with outer shell electron & becomes
scattered photon
• Incident photon  outer shell electron = scattered photon
• Bascillay is change in direction of photon
• No ionization here  no formation of ionized pair
• No energy loss
• Results in  lower image contrast
• 8%  photon interaction in xray beam
2. Photoelectric absorption
• Incident photon conntacts an inner electron & form a ion pair
• Incident photon  inner electron = ion pair
• Ionizing radition
• Increases  contrast
• Decrease in  density
• 30% of interaction in dental xray
3. Compton scattering
• Incident photon conntacts ancouter electron & form a ion pair
• Incident photon outer electron = ion pair
• Decrease  contrast
• kVp high  more comptom scattering = darker image
• 62% of interaction in dental xray
Gray = severt

= 1 (for
xray)
 Effects of radiation
1. Deteministic effect
• Hair loss
• Cataract
• Mucositis
• skin damage
• Dental radiographs  way too low dose, no defects / effects

Threshold  below this nothing happens

• 0.1 gray  in-utero birth defects
• 0.5 gray  cataract
• 3.0 gray  skin burn
2. Stochastic effects
• Cancer  leukemia
• Heriditary effects

Linear no threshold model

• No minimum threshold
• Any amount can increase risk of above
• Higer dose = higher risk

• 0.1 gray  anything below this assume that risks depends on

dose
• 0.0017% risk increase by 1 gy
 Radiation chemistry
1. Direct
• Direct alteration  DNA, proteins
• Accounts for about 1/3 of biological affects
• Dominant process for  alpha particle & neutrons

2. Indirect
• Inonizing radiation converts water to free radical with in the
tissue  which alters biological moleculs (protein, DNA )
• Accounts for about 2/3 of biological affects
• Dominant process for  XRAYS & GAMMA RAYS
• Cells that are mitotic active  more radio senitive (sperm
cells, GI cells, skin cells, BM)
• Least radio-sensitive  nerve cells, muscle fibers
• Cell 1st to damaged  hematopiotic & epithelial cells
 Sources of radiation exposures
Background radiation
• Natural
• 3.1mSv / year
• From  food, cosmic, radon

Man made
• 3.1mSv / year
• From  builing material, smoker detectors, medical imaging,
nuclear medicine, CBCT

Avg annual exposure

• 3.1 + 3.1 = 6.2
 Dose reduction
• Occupational exposure limit  50mSv / yr
• ALARA  as low as reasonably achieveable
• ALADA  as low as diagnostically actepable

• e/f speed flims / digital imaging

• Use >18cm sourc to image distance
• Use  rectangualr collumination
 Film Digital
• Require chmical to process • No chemical
• Time to develop • Instant
• Superior quality of image • Image enhancement with
• More radiaiton computer software
• Less radiation
• PSP & CCD/CMOS
 Xray film
Base
• Flexible plastic

Film emulsion
• Silver halide crystals in a gelatin material (silver bromide)
• Sensitive to  both xrays in visible light
• This is wht captures the image

Intensifying screen
• Coated with  fluroscent phosphor
• To reduce amount ot exposure needed
• Also decrease image resolution
 Film speed
• Faster the film = less exposure it need
• A  B  C  D  E  F (slow to fast)

Determined by
• Larger crystal size = faster film
• Double emulsion = faster film
• Radiosensitive dyes = faster film
 Film imaging
• Xray photons chemically change  silver halide crystals into
neutral silver atoms  in emulsion layer to create  latent image
• Radiolucenct  darkness of image (photons able to pass
through tissue & reach the film)
• Radioopaque  lightness in image (photons are not able to
pass through tissue & reach the film)
 Chemical processing
• Conducted in the dark rooms

1. Developing
• Make metallic silver atoms turn black
• Turn invisible latent image into the visible image
Developer solution
• Phenidone  1st electron donor that reduces silver ion to metallic silver
• Hydroquinone  provides an electron to reduced oxidzed phenidone to orignalc active
state

2. Fixing
• Wash away any unexposed & undeveloped silver grains
Fixer solution
• Ammonium thiosulfate  cleaning agent
• Aluminum salt  tannig agent, hardens the emulsion
• Acetic acid  maintain fixer acidity & neutralize developer
• Sodium sulfite  preservative , increase shelf life
3. Washing
• Washing away residual chemicals

4. Drying
 Digital
1. Photo-stimuable phosphor (PSP)
• Barium fluorohalide plates  store xray
• Then read by scanner

2. Charged couple device (CCD / CMOS )

• Silicone sensor chip captures the xray & instanly display on the
monitor
 Detector characterisitcs
Contrast resolution
• Ability to distinguish b/w different greys
• Film > digital

Spatial resolution
• Ability to istinguish two close points
• Film > ccd > psp

Detector latitude
• Exposure range providing usefull image intensities
• Psp > ccd > film

Detector sensitivity
• Dose required to achieve a standard grey level
 Radiographic quality assurance
• Programme implemented to ensure optimal & consistant
operation of each in imaging chain
• Daily task  record all errors
• Weekly task  review the error log
• Monthly task  examine psp plates for scratches, aprons for tears
• Yearly  claibration of of machine & verify digital sensor with a
phantom
1. Underexposed

2. Overexposed

3. Creases

4. Static electricity  black tree branch lines

5. Film placed backward  herring bone effect (tire track pattern)

1. 

2. 

3. 

4. 
 Interpretation radio-lucent
• Unilocular  one compartment
• Corticated  radioopaque border

• Non corticated  diffuse borders

• Multilocular  multiple compartments, separated by the

radiopaque septa
• multi-focal  multilpe point of origin
• Confluent  beginning to converge to eachother

• Mouth-eaten  irregular ragged edges (can b generalized /

localized )
 Radio-opaque
• Focal opacity  single site
• Homogenous  same density
• Hetrogenous  different density

• Target lesion  radio-opaque center + radio lucent band +

corticated border
• Eg : complex odontoma
• Multifocal  multiple origin
• Confluent  converge to eachother

• Irregular  ill defined edged

• Eg :- osteo-sarcoma

• Ground glass  fine granular or orange peel appearance

• Mixed densitiy  both radio-opaque & radiolucent

• Soft tissue opacity  opacity embeded inside the soft tissue

Soft tissue opacity in pano
 Caries detection
• Carious lesion are always smaller radiographically then clinically
• Tooth needs about 30-40 mineral loss to show on xray

1. Interproximal
• Lesion at contact point
• Smal traingle

2. Occlusal
• Subtle radiolucecny beneath a fissue

3. Buccal / lingual
• Pit caries
• at level of buccal / lingual pit
4. Recurrent
• Under or gimgival to restoration
• Bitewing  hide them if small
• Periapical  reveal it

5. Root caries
• Hemispherical at or below  CEJ (hard to trace outline of root)
• Hard to Distinguish from cervical burnout (can trace root outline)
 Pharmacology

See tufts pharma

 Local
anaesthesia
1. Amides
• Amides have  I + Caine in their names
• Metabolized by  liver

Lidocaine (xylocaine)  2% sol

• Safest in children

Mepivicaine (carbocaine, polocaine)  2% & 3% sol

• Least  vasodilation

Bupivacaine (marcaine)  0.5% sol

• Not safe in children
• Longest duration
Articaine (septocaine)  4% sol
• One ester chain
• Metabolized in both  liver & plasma
• Shortest duration

Prilocaine (citanest)
• Associated with  methamglobinemia (abnormal amount of
meth -hb in blood = too little O2 reaching tissues)
2. Esters
• More toxic & allergic
• Metabolized  by pseudocholinesterase in blood plasma
• Novocaine

Procaine

Cocaine
• Vasoconstrictor

Benzocaine
• Topical jel prior to inj
• Methimoglobinemia  in infants

Tetracaine
Pharmacodynamic
• Pain signals to transdute requires depolarization from influx of sodium
through these channels
• Sodium channels are in a membrane of neuron
• Sodium channel blocker  this is wht LA do

Pharmaco-kinetics
• Increase blood flow = shorter during of action of LA
• Increase lipidsolubility / hydrophobacity – more poten, longer DA
• Increase protien binding = longer DA

Lower the pKa = stronger the acid = faster onset

• Mepivicaine  7.6
• Lidocaine, articaine, prilocaine  7.8
 Calculating LA

• 1 L = 1g
• I carpule / catrige has  1.8 ml liquid = 1.8g or 1800mg

• 100% have  1800 mg or 1.8 g

• 1% la have  18mg (remember this number & multiply it by the
5 of lidocaine u get )
• Eg:- 2% la = 2 x 18 = 36mg lidocaine per carpule

To calculate epi
 Vasocontrictor in la
1. Prolong numbness
• Due to decrease in blood flow

2. Reduce toxicity
• Due to less blood flow = less oportunity to go systemically &
cause toxicity

3. Promote hemostasis
• Less blood
• Max epinephrine for ASA 1 pt  0.2mg
• Max epinephrine for cardiac pt  0.04mg
• Max lidocaine without vasocontrictor  4.4mg/kg
• Max lidocaine with vasocontrictor  7mg/kg
• Max carpules with 1:200000 epi for cardiac pt  4 carpules
• Max carpules with 1:100000 epi for cardiac pt  2 carpules

• 1:100000 = 0.001% epi

• 1:200000 = 0.0005% epi
• Multiply with  1.8
Eg
• 1.8 ml of 0.0005 = 0.009 mg / carpule (for 1:200000)
• Toxicity of epi & lidocaine
• Phentolamine  LA reversal
LA delivery
• 1carpule / min  slow

Needle dimensions
1. Length
• Short  20mm
• Long  32mm
2. Diameter
• 20 gauge  0.3 mm
• 27 gauge  0.4 mm
• 25 gauge  0.5 mm
 Type of anestheisa
1. Inferior alveolar nerve block
• Higest failure rate
Techniques
• Halstead  classic
• gowgates  open mouth (block IAN & branches, auriculotemporal, lingual & buccal) (block
most nerves)
• Akinosi  closed mouth (block IAN & branches, lingual & buccal)

2. Buccal block
• Done alon IAN

3. Mental nerve block

• Mental formane  apices of premolars
• Numbs the soft tissue facial to premolar & ant
• It wont numb the actual teeth

4. Incisvie nerve block

• Same as mental  hold pressure on foramen after block for nerve to numb (for 2min)
1. Posterior superior alveolar nerve / high tuberosity approach
• Numbs  maxillary molars
• Palpate zygomatic process & aim posterior to that
• Retract check inj into mucosa ar5ound 2nd molar  45-degree
angle to occlusal & vertical plane
• High hematoma risk
• 16mm depth (half length of the long needle )
• 75 % chance  does not numb mesio-buccal cusp of the 1st max
molar
2. infra-orbital nerve block
• Numbs  premolars = anterior
• True  ASA block
• Infra-oribital foramen

3. Greater palatine nerve block \

• Blocks  posterior har palate
• Landmark  greater palatine foramen

4. Nasopalatine nerve block

• Canaine to canine
• Most painful
 Local infiltration

• Most commonly used in maxilla

• Aim fo root apex
• Works well in anterior  thin facial cortical plate
Complications
Antibiotics
 Sulfonamindes
• Bacteriostatic
MOA
• Folate synthesis inhibitors  compete with PABA
• Cause folic acid / folate deficicnecy  impact DNA of bacteria

Examples
• Sulfadiazine, sulfamethoxazole
 Fluoroquinolones

• Bacteriocidal

MOA
• DNA synthesis inhibitors

Examples
• Ciprofloxacin, levofloxacin
 Penicillin
• Bacteriocidal
• Beta-lactem drugs  b-lactem ring in their molecular structure
• Borad spectrum  gram +ve to - ve
• Cross-allergenic to cephalosporin (allergic to one might be allergic to other
also because they are chemically related)

MOA
• Inhibit cell wall synthesis

Examples
• Penicillin G  I/V & deep I/M inj (more sensitive to acid degradation)
• Penicillin V  oral
• Amoxicillin  broad spectrum
• Augmentin  amoxcillin + clavulanic acid ( beta – lactamase resistant)
• Methicillin  beta – lactamase resistant
• Ampicillin  broadest sepctrum against  gram –ve bacteria
Drug-induced immune haemolytic anaemia
• The anaemia is caused by the drug triggering the immune system
to attack its own red blood cells, which can present with cyanosis

Sign & symptoms

• Blue tint of lips
• cyanosis

Causes
• Amoxicillin
• Cephalosporin

Treatment
• Discontinuing the drug usually resolves the anemia
 Cephalosporin
• Bacteriocidal
• B-lactum antibiotics

MOA
• Cell wall synthesis inhbitors

Examples
• Cephalexin  1st gen
• Cefuroxime  2nd gen
• Ceftriaxone  3rd gen
• Cefepime  4th gen
• Ceftaroline  5th gen
 Monobactams
• Bacteriocidal
• B-lactum antibiotics

MOA
• Cell wall synthesis inhbitors

Examples
• Aztreonam
 Carbapenams
• Bacteriocidal
• B-lactum antibiotics

MOA
• Cell wall synthesis inhbitors

Examples
• emipenam
 tetracycline
• Bacteriostatic
• Chelation  bind ca & other ions (do not take this drug with dairy products)
• Concentrate very well in  gcf
• Broadest antimicorbial spectrum

MOA
• Protein synthesis inhbitor  attack  30s ribosomal sub-unit

Examples
• Tetracycline
• Doxycycline
• Minocycline

Side effects
• Tetracycline  liver damage, teeth stain (avoid 2nd trimester to 8 yrs of age)
 Macrolides
• Bacteriostatic

MOA
• Protein synthesis inhbitor  attack  50s ribosomal sub-
unit

Examples
• Erythromycin
• Clarithromycin
• Azithryomycin
 Lincosamides
• Bacteriostatic

MOA
• Protein synthesis inhbitor  attack  50s ribosomal sub-
unit

Examples
• Clindamycin  concentrate very well in bone
• Lincomycin

Side effects
• Clindamycin  gi upset & pseudomonas colitis
 Antibiotic prophylaxsis
• Pro-active measure to prevent serious infection

To give prophylaxsis in
1. Previous endocarditis
2. Prosthetic heart valve
3. Cardiac transplant with valvular regurgitation
4. Congenital heart defects
• Unrepaired cyanotic heart disease (low blood oxygen level)
• Repaired cyanotic heart disease with  shunts , valvular regurgitation

Not to give in
1. Joint replacement (hip, shoulder or joint)(complicartions with it may be needed AB)
2. Mitral valve prolapse  with or without regurgitation
3. Rheumatic heart disease
4. Bicuspid valve disease
5. Calcific aortic stenossi
6. Congenital  all other then above
• Atrial septal defect
• Ventricular septal defect
 Other prophylaxsis
• Pt with yes coloum / who need prophylaxsis going through only these dental treatment will need
prophylaxsis as follows

Dental procedures  that require

• Manipulation of gingival tissue or apical regio or perforation of oral mucosa
• Extrsaction
• Cleaning
• SRP
• Fitting orthodontic bands
• Temporary anchorage devices (TADs)
• Biopsy
• Sutures
• Periapical micorsurgery

Dental procedures that does not require

• Rountine anesthesia inj through not infected tissue
• Radiographs
• Removable appliances  prostho or ortho
• Adjusting ortho appliance
• Placing ortho brackets
• Shedding of teeths
Immunocompromised
• HIV or AIDS
• Hematopoietic stem cell transplant
• Organn transplant
• Neutropenia
• Chemo or radiotherapy
• Rheumatoid arthritis  taking prednisone (more then 10mg/day)
• Severe combined immuno-deficinecy
• Autoimmune disease  SLE

Hyperglycemic state
• HbA1c  more then 10%
• Random glucose  200mg/dl
Penecillin
allergy (PCN)
Side effects
• Gi upset & pseduomona colitis  clindamycin
• Superinfection  borad spectrum antibiotics
• Aplastic anemia  chloramphenicol
• Liver damage  tetracycline
• Allergic cholestatic hepatitis  erythomycin
 Drug interactions
• Penicillin with probenecids  alters renal clearance of penicillin
• Tetracycline with antacids / dairy products  products reduces its
absorption
• Borad sepctrum with anti-coagulatants  enchance
anticoagulanats response
• Antibiotics & oral contraceptive  reduce effect of oral
contraceptives
• Macrolides & seldane, digoxin  inhibits metabolism of seldane &
digoxin
Facts
Drugs used for
• Acyclovir, valcyclovir  HERPES
• Fluconazole, ketoconazole  candidiasis
• Clotrimazole (mycelex)  is in troche form
Analgesics
Aspirin (ASA)
• Non selective
• Cox 1 & 2 blocker
• Irreversibily block
• Can cause reyes syndrome in  children

Therapeutic affects
• Analgesic & anti-inflammatory  inhibit cox 1 & cox 2= inhibit PG
• Antipyretic  inhibit PG synthesis in the hypothalamus (temp regulation center)
• Bleeding time  inhibits TXA2  inhibit platelet aggregation

Toxicity
• Gi bleed
• Tinitus
• Nausea vomiting
• Mtabolic acidosis
• Decreased tubular resoprtion of uric acid
• Salicylism
• Delirium
Ibuprofen (motren, advil)
• Cox 1 & 2 blocker
• Reversibily block
• NSAIDs  first choice of drug in peadtric (if not allergic to it)
Causes
• Kidney  hard on kidney
•

Indomethacin
• Cox 1 & 2 blocker
• Reversibily block
Causes
• Blood dyscrasias
Phenylbutazone (bute)
• Cox 1 & 2 blocker
• Reversibily block
• For animals

Diflunisial
• Cox 1 & 2 blocker
• Reversibily block
• Longer half-life
Celecoxib (celebrex)
• Cox 2 inhibitor
• Selective

Meloxicam (mobic)
• Cox 2 inhibitor
• Selective
Causes
• Arthritis
 Acetaminophen (tylenol)

• Not an  NSAID
• Inhibits pain  in cns
• Metabolized by  liver
• Drug of choice in children  with fever
• Drug of choice in  asthma

Side-effects
• Hepato-toxic  more damage if taken with alcohol
 Max dose
Ibuprofen
• 3.2g / day

Acetaminophen
• 4 g / day
• 1-3 (Mild Pain)  Use ibuprofen or acetaminophen alone.
• 4-6 (Moderate Pain)  Use a combination of ibuprofen and
acetaminophen.
• 7-10 (Severe Pain)  Stronger medications, such as those
containing opioids (e.g., acetaminophen-hydrocodone or
acetaminophen-oxycodone), may be necessary
 Cortico-steroids
• Prednisone
• Hydrocortisone
• Triamcinolone
• Dexamethasone

If a pt takes 20mg of hydrocortisone for 2 weeks in last 2 yr. = chances of adrenal

insufficiency (this pt will need supplemental dose prior to the surgery / procedure)

Theraputic effects
• Analgesics & anti-inflammatory effects  inhibit phospholipase A2  inhibit arachdonic
acid

Side effects
• Immuno-suppresion
• Gastric ulcers
• Acute adrenal insufficiency
• Osteoporosis
• Hyperglycemia
 Narcotics / opiods
• Mu-opioid receptor agonist  in cns

• Morphine
• Hydrocodone
• Oxycontin  controlled release
• Codeine  suppresses cough syrup (found in cough syrup)
• Tramadol (ultram)  similar to codeine
• Heroine
• Fentanyl
• Sufentanil
• Carfentanil
• Mepredine (demerol)  lethal if combined with MAOI (monoamine
Naturally occuring opiods
• Morphine
• Codeine

Semi synthetic
• Oxycodone

Synthetic
• Methadone

Prodrug
• Codeine is prodrug of morphine  metabolized in liver into
codeine
 Combination narcotics
• Vicodin  hydrocododne + acetaminophen (APAP)
• Percocet  oxycodone + APAP
• Tylenol 1  300mg APAP + 8mg codeine
• Tylenol 2  300mg APAP + 15 mg codeine
• Tylenol 3  300mg APAP + 30 mg codeine
• Tylenol 4  300mg APAP + 60 mg codeine
Morphine
• Theraputic & side effects
1. Miosis  pupil constriction (toxic effect)
2. Out of it  sedation
3. Respiratory depression  (toxic effect)
4. Pneumonina (apsiration type)
5. Hypotension
6. Infrequency  urinary retention, constipation
7. Nausea & vomiting  trigger CTZ of medulla
8. Euphoria & disphoria  happy & sad
 Overdose & addiction
• Naloxone  for overdose emergency
• Naltrexone  antagonist  for addiction
• Methadone  addiction
 Nitrousoxide
• Provide mild angesic affect as  inhalation agent
• Also called  laughing gas
• No tank  blue
• O2 tank  green
• Hoarse well  first to use it for extraction of his assistant

• MAC (minimal alveolar concentration)  105%

• 30%  for children (No)
• 30-50%  for adults (No)

• Minimum O2 concentration with No is  30% (for both

adults & kids)
Signs of NO sedation
• Sensation before sedation  tingling
• Side effect  nausea
• Longe term effect  peripheral neuropathy

• Always give pt 100% O2 for 3-5min to flush out nitrous

oxide out of lungs to prevent  diffusion hypoxia
Contrainidcations
• Nasopharyngeal obstruction
• Closed air-containing tissue spaces (such as pneumothorax,
pulmonary blebs, and bowel obstructions)
• Bleomycin chemotherapy (due to increased risk of pulmonary
toxicity)
• Claustrophobia (or inability to tolerate a nasal mask)
• Chronic obstructive pulmonary disease (COPD), especially
in severe cases
• Recent retinal detachment surgery (within the last 3
months)
• Recent eardrum repair

Not contraindication
Stage 1 Sedation
• This stage is typically achieved with 30-40% nitrous oxide. At
this level, patients remain conscious, experience analgesia,
amnesia, and are often euphoric.

Stage 2 Sedation
• It generally requires a higher concentration of nitrous oxide,
typically around 50-70%. During this stage, patients might show
signs of excitement, delirium, and involuntary movements.

Stage 3 Sedation (Surgical Anesthesia)

• This is usually achieved at even higher levels, often over 70%,
and may require the combination of other anesthetic agents. In
this stage, patients are unconscious, and there's a significant
reduction in eye movements and respiratory function
 Pharmaco-
kinetics
What body does to the drug
 Administration (0)
• How thr drug is delivered

• Oral  through mouth (enteral route)

• Sublingual  under tongue (NG)
• Subcutanous  injected under skin (insulin)
• Intra-muscular  into the muscles (epi pen)
Sub-enteral
• intra-venous  into the vein
• Inhalation  breathed int (albuterol)
• Topical  applied to skin or mucous membrane
 Absorption (1)
• How does drug get into the body
• Drugs must cross epithelial / enodthelial layer  to the blood

Local drugs
• Administerd & active at the site of administration
• Eg : - topical LA , LA

Systemic drugs
• Goes to blood to all the body
• Lumen  apical membrane  basolateral membrane  basment
membrane  interstial fluid  endothelial cells  blood
• Drugs cross membranes through different diffusions

1. Passive diffusion
• Most drugs cross epithelium through passive diffusion
• Drug must be neutrally charged, hydrophobic, non ionized to
cross plasma membrane by diffusion

2. Facilitated diffusion
3. Active transport
Bio-availability
• A fraction of drug dose that reaches the blood circulation
• It is never the 100%  some what lost during process
• 100% available when administered  I/V
PH consideration
• Important for the absorption
• Acid & base properties of the drug often described by  pKa
• PH of different body fluids important for the absoprtion

• Most drugs as weak acids or weak bases

• Weak acids  concentrate in high PH compartment
• Weak bases  concentrate in low PH compartment
 Distribution (2)
• How does the drug get to the target site
• Most drug reach blood to be distributed
• Topical drugs  exception
• Systemic drug reach vessel rich organs first  heart, brain, lungs
etc

• Blood  endothelium  interestial fluid  basolateral membrane

First pass effect
• Oral drug goes through first pass effect
• Drug absorped by the gi system (hepatic portal system)  porta
vein  liver

• Liver metabolizes drug  just the small amount of active drug left
to go into the circulation
• This first pass effect by liver is called  first pass effect
• This reduce bioavailability of the oral drug
Volume of distribution
• Distribution of drug across the three body water compartments
• Plasma  4%
• Interstial  16%
• Intracellular  40%

• Obese have less water content then normal

• Adipose has lowest water content
• Brain & muscle have highest water content
 Metabolism (3)
• How a drug molecule is chemically altered by the body
• Done primarily in the liver

phase 1 phase 2

• Drug  metabolite  inactive

Phase 1
• Functionalization  involves changing functional characteristics of the drug
• By  oxidation, reduction, hydrolysis
• Cytochorme P450
• Makes molecules more polar = elimination through kidneys

Phase 2
• Conjucation  covently attaching large polar sides to the drug
• By  glucouronide, glutathione, glycine
• UDP – glucouronosyltranferase
 Acetaminophen
• It goes under
Phase 1  reduction
Phase 2  glutathionation

Acetaminophen  reduction  glutathionation  inactive

 Clearnace / elimination (4)
• How the drug is eliminated out of body
• Mostly done through kidneys but not always
 Elimination kinetics
First order kinetics
• Constant fraction of drug is eliminated per unit time = %/hr
• Rate is porpotional to the concentration of the drug administered
• More common

Zero order kinetics

• Constant amount of drug is eliminated per unit time = mg/hr
• Less common
• Higher risk of drug accumulation
 Drug – drug interaction
• One drug affects pharamco-kinetics of other durg
• Most comonly  metabolism

a) Induction
• Drug 1 induction liver cytochrome enzyme resulting in increased
metabolism & reduced effect of drug 2

b) Inhibition
• Drug 1 competes for metabolism or directly inhibits liver
cytochrome enzyme resulting in decreased metabolism &
increased toxicity of drug 2
 Pharmaco-
dynamics
Wht drug does to the body
• Almost all drug targets are proteins
1. Receptors
2. Ion channels
3. Enzymes
4. Carriers

• How drug interacts with it target

1. Agonist
2. Antagonist
3. Inverse agonist
 Agonist
• Mimics the effects of endogenous agonist molecules

a) Full agonists
• Produce 100% of desired effect

b) Partial agonist
• Do not produce 100 %
 Antagonist
• Inhibits the function of endogenous agonist
a) Competitive antagonist
• Competes against agonist for the same binding site on the
receptor

b) Non- competetive antagonist

• Binds to different binding site but still prevents agonist to bine on
the site
 Inverse agonist
• Inhibits the basal acctivity of the recepotor in the absence of
normal agonist
•
Type 1 dose-response curve
Intrinsic activity
• Maximum effect (EMAX) of the drug
• Peak of the drug

Full agonist
• Emax of 1
• In chart represented as 100%

Partial agonist
• b/w  0-1

Antagonist
• Has intrinsic activity  0

Inverse agonist
Competitive antagonist
• Shifts the agonist curve towards right
• Compettive antagonist  increase the amount of endogenous
agonist needed to produce same response (need more drug for
same response)
• A  competitive agonist
• B & C  competitive antagonist

Non – competitive antagonist

• Shifts the agonist curve down
• It decreases the maximum affect of the agonist
• B  non competitive antagonist
Efficacy
• Effect of drug as function of binding

Affinity
• Attractivetiveness of drug to its receptor
• Represented by dissociation constant (KD)
• Higher the kd = lower the affinity (inverse proportional)
• Kd  conc of drug needed to occupy 50% of the receptor

Potency
• Power of a drug at a specific concentration
• Usally measured by effective concentration of drug (EC50)
• EC50  how much drug is needed to achieve its 50% of maximum response
• Higher potency = lower the EC50
• Eg:- drug 1 has some effect at 500mg & drug 2 has same effect at
5mg = drug 2 is more potent
Type 2 dose-response curve
ED50
• Effective dose
• Where 50% of the population responded effictively (treated)

TD50
• Toxic dosse
• Where 50% population experienced toxic effects

LD50
• Lethal dose
• Where 50% of the population responded lethally (died)
Therapeutic index (TI)
• Larger the theraputic index = safer the drug

a) In animals
• TI = LD50 / ED50

b) In humans
• TI = TD50 / ED50

Therapeutic window
• Top of the blue curve
• Minimally at the bottom of green curve
 Summary
• Type 1  dose vs efficiacy of drug
• Type 2  dose vs response of the patient
 Additives / drug combination
• Combining drugs  combines individual effects of the drug
• Additive effect
 Antagonistic affect
• Combination of the drug cause lesser effect the either one alone
• Chemical antagonism  drug binds directly to the other drug to
put it directly out of commision
• Receptor antagonism  competion b/w drugs for the single
receptor for binding
• Phamrmacokinetic antagonism  one drugs affects pK of other via
PH
• Physiologic antagonism  two drugs production opposing effects
on the same tissue via distinct receptors
 Syngergistic affect
• Combining drugs produce affects more then the sum of two
 Autonomic
nervous system
(ANS)
ANS divided into two
• para-sympathetic nervous system (PSNS)
• Sympathetic nervous system (SNS)

• In general PSNS & SNS control same organs but have opposite effects
• PSNS  rest & digest / feed & breed
• SNS  fight & flight

• All nerve pathways originate from CNS (brain + spinal cord)

• PSNS  12 cranial & 5 sacral (CRANIOSACRAL)
• SNS  12 thoracic & 5 lumbar (THORACOLUMBAR)
• O cervical

Exceptions
• Vasculature controlled by  SNS
 Receptors in ANS
Ionotropic
• Ions channels
• Eg  NA channels, ca, k

Metabotropic receptors
• G-protein coupled (GPCR)
• Eg  7-pass trassmemebrane domain receptor
1. Cholinergic receptors
• Binds acetylcholine
• In PSNS
2 forms

a) Nicotinic (nAChR)
• Ionotropic
• Also binds nictoine

b) Muscarinic (mAChR)
• Also binds muscarine
• Metabotropic
2. Adregernic
• In SNS
• Binds epinephrine & nor-epinephrine (produced in adrenal
glands)
• Metabotropic
PNSN
• Long preganglionic nerve and release  acetylcholine
• Short post ganglionic gland  acetylcholine

SNS
• Short preganglionic nerve and relase  acetylcholine
• Long Post ganglionic nerver  nor-epinephrine
• Or to adrenal medulla and release  nor-epinephrine & epinephrine

• All ganglionic receptor & medulla receptors are ionotropic nicotinic

receptors in both PSNS & SNS

All target organs are metabotropic  g-protein coupled

• PSNS  MUSCARINIC METABOTROPIC
• SNS  ADRENERGIC METABOTROPIC
N
A

N
A

N
M
 Synthesis of acetylcholine
• Catalyzed by  choline acetyl transferase
• Reversed by  acytylcholinesterase
Molecule can activate
• Nicotininc & muscaranic receptors

Muscarinic receptors (post ganglionic)

• M1  CNS
• M2  HEART
• M3  SMOOTH MUSCLE
• M4  CNS
• M5  CNS
M2 receptor
• Acts on heart
• Inhibits  SA & AV node = decrease HR & electrical conduction
• Chronotropy (dec HR)
• Domotropy (dec CONDUCTION)

M3
• Relaxes smooth muscle
• SLUDS  salivation, lacrimation, urination, defecation, sweating
• BAM  bronchoconstriciton, airway constriction, abdominal
cramps, miosis (pupil constriction)
 M agonists
• Non selective for M-receptors
• Should not be given systemically  Activates all (1-5)

Not to be used with these conditions

1. Gastric ulcers
• Will cause more relase of gastric juices = excurbate the condition

2. Asthma / copd
• Bronchoconstriction = more hard to breath

3. Congedtive heart failure (CHF)

Direct acting
1. Pilocarpine
• Stimulates  saliva
• Eyedrops  miosis

Indirect acting
1. Neostigmine
• Reversibly inhibits  acetylcholinesterase

2. Organophosphate / insecticides
• Irreveribsle inhibits  cholinesterase
• Poisoning can be treated by  pralidoxime
Atropine
• Reduce saliva
• Emergency drug to treat  bradycardia to increase HR (can cause
tachycardia)
Potent effect to supress
• PSNS
• Also  SNS

Non depolarizing drugs

• Used for treating  hypertenison
• But can cause  orhtostatic hypotension

Depolarizing
• Nicotine  addictive
• Block nictotinic receptor at the neuro-muscular junction in the
somatic nervous system
• Outside  ANS
• These drugs used as  skeletal muscle relaxants
 Synthesis of epinephrine & nor-
epinephrine
• Tyrosine  L-dopa  Dopamine  NE  EPI
• Catecholamine  dopamine, EPI, NE
• Monoamine  dopamine, EPI, NE, serotonin (5-ht), histamine

Adrenergic receptor
• Activated by both  EPI & NE
 Adrenergic receptors
Alpha 1
• Smooth muscle  vasculature
• Vasocontrictions
• Urinary retention
• Mydriasis (pupil dilation )

Alpha 2
• Smooth muscle  vasculate
• Vasocontrictions
Beta 1
• Heart
• Sa & av node or heart
• Tachycarida  increase HR, Conduction & strength of contraction
• Increase renin release from the kidney

Beta 2
• Smooth muscle relaxs
• Bronchioles relaxes  open
• Bronchodilation
• Vasodilation
• Stop peristalsis
Sympathomimetics
• Don’t bind to  alpha or beta receptors
• They mimic the effects of sympathetic agonist

By different ways
1. Release of stored NE
• Amephetamine
• Tyramine  wine, cheese, choclate
• Ephrdrine

2. Inhbit reuptake of NE & dopamine

• Cocaine

3. Inhbit reuptake of NE & serotonin

 Sympatholytics
• They mimic the affect of sympathetic antagonist
• Inhibits NE release  guanethidine
• Depletes NE stores  reserpine
• Alpha 2 agonist which blocks SNS signal  clondine, methyldopa
 Epinephrine reversal
• Vasoconstrictore or epi converted to the vasodilator effect in the
presence of Alpha blocker, whereby the b2 vaso-dilator effects
becomes the major vascular response
• Basically a-blocker cancels out EPI Alpha activation
effects & only activates B-2 effects = vasodilation
 Vaso-vagul reflex
Baro-receptors
• Monitor BP
• Alter rate & strength of the heart contraction
• Alter diameter of blood vessels accordingly

• NE released by SNS  activates baro-receptors 

stimulates vagul reflux  decreases the HR
• Leading to the opposite response of the NE

• Atropine blocks this system

Cardio-vascular
system
• Human circulation system is a closed system

Pressure within the system depends on

1. Pump / heart
• Cardiac output (CO)
• Strength & rate of heart beat

2. Tubing / vessels
• Peripheral resistance (PR)
• Depends on how dialted or constricted vessels are

3. Fluid / blood
• Blood volume / stroke volume (SV)
BP (arterial pressure)
• BP = CO x PR

Cardiac output
• CO = SV x HR

Mean BP
• BP = SV x HR x PR

Systole
• Pressure in arteries when heart contracts
Diastole
• Pressure in arteries when heart relaxes

Preload
• Pressure in ventricles before heart contracts
Afterload
 Antihypertensive drugs
Diuretics
• Decrease renal reabsorption of sodium = water loss = decrease
in bp
• Low pottasium / hypokalemia  thiazide
• High pottasium / k sparing  spirionolactone

Acts in loop of henle

Acts in distal
Acts in collecting duct
tubbule
Vasodilators
• Cause inside of cell to be hyperpolarzied (more –ve) =
vasodilation
Ace inhibitors
• End with pril

Angiotensin receptor blockers (ARBs inhibitors)

• End in sartan
 B-blockers inhibit
renin

ACE inhibitors inhibits ACE

ARBs inhibitors
competitivly antagonise
angiotensin 2 receptor
 Anti-anginals
• For insufficient O2 to cardiac muscle

B- blocker
 Anti-CHF (congestive heart failure)
• For failure of heart to pump enough blood
Cardiac glycosides
• Increase the strength of contraction of the heart (+ve inotropy )
• Work by blocking  na/k atpase enzyme = increased Ca influx
 Anti-arrythymics
• For irregular heart beat
Types

1. Type 1
• Na channel blocker  for cardiac muscle only
• 1 A  incresse refractory period to slow heart beat
• 1 B  shorten refractory peripd to hasten heartbeat

2. Type 2
• Beta blockers

3. Type 3
• Potassium channel blocker

4. Type 4
For afibrillation
• Quinidine
• Verapmil
• Digitalis

Digittalis induced arrythmia

• Phenytoin used to reverse
Central nervous
system
Dopamine & seratonin receptors
• When activated cause  cns excitability

GABA receptors
• When activated cause  depress CNS
 Anti-psychotics
• For schizophrenia
• Brain is too active in this and we need to calm brain down
• Receptors we r concerned with are dopamin & serotonin (we
need to block them )
1st generation
a) D2 BLOCKERS
• Have anti-cholinergic side effects  fight or flight symptoms
• Long term use can cause  tardive dyskinesia (stiff and jerky
movement of face & body )
• Phenothiazine
• Haloperidol

2nd generation
a) D2 & 5-HT BLOCKERS
• Not much side effects
 Anti-depressants
• For depression
• Cns needs to be  stimulated = excitation
• Do this by increasing presence of mono-amines (NE, DOPAMINE,
EPI, SEROTONIN, HISTAMINE)
• LITHIUM  drug of choice for maniac depression ( bipolar
disorder )
 Anxiolytics / sedative
• For anxiety or sedation
• Not analgesic  provide no pain relieve

1. Bezodiazepine
• Bind to site on  GABA a receptors
• This increases binding of GABA binding & chloride ion influx = slow
CNS
• Ideal drug for oral sedation  in dental setting (less chance
for respiratory depression )
• Propyl glycol (present in i/v benzodiazepine)  can cause 
thrombophlebitis in large veins

• Diazepam (valium)  commonly presicribed prior to dental surgery

2. barbiturates
• Same MOA as  BZD
Contrainidcation
• Pt with  intermittent porphyria (they will aggrevate disease )
• Over dose  respiratory depression
 General anesthesia
• Used to induce medically induced come  for surgery
• Onset of general Anesthsia is inversely porpotional to the solubility of the anesthetic in the
blood
• More soluble in blood = more u need to reach critical tension in brain

• Stages
1. Stage 1
• Analgesic / pain relieve

2. Stage 2 Toxic to liver

• Delirium  altered state of conciousness

3. Stage 3
• Surgical anesthesia
• Desirable stage

4. Stage 4
 Parkinsons disease
• Result of  dopamine deficiency in brain
• Treatment is to  give dopamine (but its not as simple)

Dopamine
• Can not cross  blood brain barrier

L-dopa / levodopa
• Precurrsor of the dopamine
• It can cross  blood brain barrier
• But is quickly converted to dopamine by  dopa decarboxylase

Carbidopa
• Blocks  dopa decarboxylase
• Allows L-dopa to cross BBB & then convert to dopamine in the brain

Treatment
Hypersenitivity
reaction
• Innappropriate immune to benign antigen
• Response to  External antigen (drug, food, pollen etc)
• These are antigen specific reactions
 Type 1
• anti-body mediated
• Immediate / allergic reaction
• Soluble  antigen
• IgE  on mast cells

Reactions
a) Early phase
• Antigen  cross links with IgE on mast cell  degranulation of mast cell
release  histamine  vasodilation & increased vascular permeability  cause
neutrophil to extravasate
b) Late phase
• degranulation of mast cell release  leukotriene, PG, ECF a
• Leukotriene  increase vascular permeability & bronchoconstriction
• PG  bronchoconstriction
Time
• Immediate phase  minutes
• Late phase  8-12 hrs

Symptoms

a) Local
• Urticaria
• Ezema
• Angioedema
• Hay fever
• Asthma

b) Systemic
• Anaphylaxsis  administer adrenaline fast
• Hypotension
• Edema of lips & neck
• Broncoconstriction
 Type 2
• Cytotoxic reaction
• Cell-bound antigen  Antibodies produced & bound on antigen on the surface of
plasma memebrane  activate compliment proteins
• Antibody  IgG / IgM
• Time  hrs – days

CAUSES
• Acute transfusion reaction  after blood transfusion
• Haemolytic disease of newborn / erythroblastosis fetalis  mother and child have
different blood group (mother 1st child is normal as u need 1st exposure to make
antibodie b ut 2nd child is affected)
• Bullous phemphigoid
• Graves disease
• Mysthia garves
• Phemigus vulgaris
 Type 3
• Immune-complex  antigen-antibody complex
• Antigen-antibody complexes deposited into the tissue around
body  inflamatory response by activating complement protein

Causes
• Arthurs reactions  hypersensitivity pneumanitis
• Rheumatoid Arthritis
• Post streptococcal glomerulonephritis

b) Systemic
• Serum sickness  serum from the animal 
• Lupus erythematous
 Type 4
• Cell mediated  T - cells (T-helper cells)
• Delayed reaction
• Time  days

Causes
• Contact dermitis  metal allergy, latex
• Tb skin test
• Graft rejection
• Graft vs host disease
• Type 1 diabetes mellitus
Ethics
 ADA code
• A written expression of the obligations arising from the implied contract
b/w the dental profession & society
• An evolving document with goes under continious review
Three componenets

1. Principle of ethics (pe)

• These are aspirational goals of the prefession
• These provide guidance and justification for following componenets,
theye may overlap and compete with eachother

5 principles
a) Autonomy  self – governance
b) Non maleficence  do no harm
c) Beneficience  do good
d) Justice  fairness
2. Code of professional conduct (cpc)
• Expression of specific kind of conducts  which are either
required or prohibited
• Product of ada legislation system means  they are legally
binding & must be obeyed (violation of this may lead to
disciplinary action)

3. Advisory opions (ao)

• Interpretations that apply the code of professional conduct to
specific situations
Ethics
• To do the right thing because u r obligated to do wht is morally
right
• Ethics generally function at a higher level than laws do
• Ethics remian constant through-out moslty

Law
• To do the right thing or else u will be punished
• Laws simply enforce us to do what ethics already tell us
• Laws are subject to change with time & from society to society

• Ethics are superior than law

 Patient
Autonomy
• Also referred as  self governance
• Must respect pt right to  self-determination (wht they want) &
confidentiality
• Do what pt wants within the reason
• Involving pt in treatment decisions
• Safe-guard  pt privacy
• Safeguard the confidentiality of patients records (HIPPA
privacy rules)

Pt involvement
• Inform pt of proposed treatment  benefits, risk & alternatives
• Informed conscent
Consent
1. General consent
• Discussion
• Pt have given permission to simple things  exams, radiograph, la,
cleanings, minor restoration
• This relases DR from charge of  batery & allows to bill pts insurance

2. Informed consent
• Discussion & document
• Educate pt about treamtent plan
Dental problems u have observed
Proposed treatment
Benefit & risk of that treatment
Alternative treatment / no treatment options
Benefit & risk of alternative treatment, including about no treatment
Minors
• 1-7  infants (not responsible for actions)
• 8-14  competent
• 15-17  responsible

• Minor below age 18 can give  implied consent or ascent but not
actual consent

Exception
• Emancipated minor  who are free from control & care of parents
• Married
• Pregnant
• Parent themselves
• Military
 Patient records
1. Provide records to pt if requested
• For free or nominal cost
• Xrays
• Even if account / bill has not be settled by the pt

2. Provide records to other dentist if needed for future treatment of pt

3. Protect confidentiality of pt records

• Never let anyone see
• Or records lying here and there
• Seek pt permission to tranfer data
• If pt does not agree then u can terminate pt-doctor relationship only if the
data is necesaary to be transferred for pt care

• Keep all documents for as long as possible  (for exam)

Risk management
• Constantly weigh  risk & benefits of ur practice

Documentation is most essential

• Be specific
• Be objective
• Be complete  full info
• Be timely  avoid gaps
• Never make or sign entry for someone else
• Naver change or delete  instead provide addendum
• All writings are discoverable  don’t write anything u don’t want
to be read aloud in court
• Avoid abbrevations
Non-maleficence
• Do not harm  by ur own hands
• Doc have duty to protect pt & do not harm him

1. Education
• Keep ur knowledge & skills updated

2. Consultation & referral

• Refer  when needed (eg:- general dentist referring pt to omfs for
impacted molar)
• Provide 2nd opinion  without vested interest (no personal gain ki niyat)
• Eg:- just doing veneers for financial gain  do informed consent first & tell
pt wht is best and provide alternates & let pt decide then)

3. Use of Auxillary personnel

• Assign to staff only wht they can legally perform
4. Personal impairement
• Do not practice under influence  alcohol or substance
• Urge impaired colleague to seek treatment
• Report colleague / person  under influence

• Be sure before reporting a person

5. Post exposure for blood borne pathogen

• Immediately inform pt if they have be exposed to  potentially
infecious material / blood
• Refe pt to post-exposure evaluation & follow up (eg:- doc nicked
by instrument, some blood contamination & even if he/she is not
infected he need to inform pt & refer for post evaluation)
• Submit yourself to testing if you are the source  get tested to
6. Patient abandonment
• Once course of treatment started  do not stop treatment without giving
adequate notice & opportunity to obtain dental services elsewhere

Written letter  with reasons

• Did not follow instructions
• Did not show up to appointments
• Did not pay for treatment

30 days atleast

7. Perosnal realtionship with patients

• Avoid inter-personal relationships with pt that might cause impaired
judgement
• Ada does not prevent dentist from treating their family but  should be
avoided
Beneficence
• Do good  going out of ur way to help pt
• The dentist has a duty promote the well-being of the pt
• Everyone deserves good dental care  no matter how they pay
• Promote pts welfare  preventive dentistry

1. Community service
• Use ur skill to improve the dental health of public (eg:- free clinic, school
seminars, going to other countires for help)
• In times of public health emergency  postpone elective treatment (eg:- during
pandemic like covid)

2. Government of a profession
• To join a professional dental society & follow / observe its ethical code/rules (eg:-
ADA, specialization organisations)

3. Research & development

• If u doing any research which may promote health of the public  make that info
4. Patents & copyright
• Intellectual property (patents & copyright) cannot be used to
restrict the research & practice
• Eg:- u make a mouth rinse that is beneficial, so u can not restrict it
from being researched and used

5. Abuse & neglect

• Be familiar with signs of  abuse & neglect
• Report suspected cases to the authority

6. Professional demeanor in the workplace

• Provide  respectfull & collaborative work environement
• Don not engage in disruptive behaviour
• Eg:- coming late everyday, vulgar language infront of pts, talking
 Abuse & neglect
Abuse
• Willfull infliction of  pain, injury or mental trauma

Neglect
• Not recieving essential services from  caretaker,
parent/guardian
• Intentional / un-intentional

1. Recognize
2. Report
3. Record
4. Render treatment
1. Recognize
• Bruises
• Burns
• Bite marks
• Fractured teeth
• Facial fractures
• Red swollen eyes
• Multiple un-treated injuries
For child
• Poorly dressed child
• Dis-shevled appearance
• Hungry
• Thirsty
• Frightened
• Social withdrawal
• Parents telling different story
2. Report
• Mandated / required  suspected cases of child abuse

Child
• Report immediately  social services

Adult
• Ideally ask them first (autonomy)
• Then report to DHSS (beneficence)

Elderly
• Report immediately

Disabled
3. Record
• Date & time of disclosure
• Description of injuries
• Use their own words
• Descriptions of behaviours (also record if response of
spontaneous or ans to the question u asked)
• Details of witness

4. Rendeer treatment
• Do treatment or refer
Justice
• Fairness
• It is dentists' duty to Treat every pt fairly (without prejudice / bias)
• Improve access to care for all people

1. Patient selection
• Do not refuse pt on basis of  cast, color, race, creed, gender,
sexual orientation, national identitiy
• Don not refuse pt just because they have  disability or blood
borne disease

• U can reasonably refer pt  if u don’t have knowledge &

means to treat that pt

• Eg:- If someone abusive to staff or disrespectfull  dismiss

them or no treamtnet (beneficence)
2. Emergency service
• Be available if pt calls after hours
• Make reasonable arrangement for the emergency care of the pt
weather or not they r ur pts
• After treatment is completed  refer them back to their old
dentist

• Eg:-doc is on vacation on weekend & is not available by call or

mail & practice is closed with no staff  violation of justice

3. Justifiable criticism
• Report faulty treatment by other doctors to the  concerned
board
• Do not slander other dentist
4. Expert testimony
• Provide expert testinomy  when requested
• Do not agree to contigent fess

5. Rebate & split fees

• Do not offer or accept  rebate or split fess
• Rebate  return part of orignal payement to the pt
• Split fees  if u setup a deal with referring pt (giving 20% on pt u
referred)
• Applies to  other dentist & advertising companies

• Eg:- paying magazine % to help advertise on front cover

Veracity
• Truth-fullness
• Dentist have a duty to communicate truthfully (honest)
• No deception

1. Represntation of care
• Don not lie or mislead about the dental treatment
• Do not remove amalgam or any restoration material because it is toxic (not toxic
according to the data)
• Do not make unsubstantiated claims (eg:- do not make any claim not backed by scientific
evidence)

2. Representation of fee
• Don not lie or mislead about treatment fees
• Do not waive co - payments & lie to the insurance company (eg:- bill is 500 and insured for
400, do not waive the remaining 100 & lie to insurance company)
• Do not overbill just because pt has a insurance
• Submit a correct fee to the insurance company
• Submit a correct treatment date to the insurance company
• Submit corrrect dental procedure to the insurance company
3. Disclosure of conflict of interest
• Reveal any monetary or special interests during presentation & clinic
• Eg:- doc is presenting info in article or seminars, if they are endorsed
by that company they need to disclose it

4. Devices & therapeutic methods

• Use drugs & devices that are availabe to the dental profession
(approved & safe to use)
• Report adverse affects to  FDA (of drugs, devices)
• Do no coerce pt to purchase certain productive (if u have a financial
incentive

5. Professional anouncement
• Do not represent training or competence in a false or misleading way
• Do not misrepresnt  facts
6. Advertising
• Do not advertise / promote in false or misleading way
• Do not trick people to use ur services in a dental health article
• Do not advertise that u r superior to other dentist
• Do not use unearned or non-health degrees (non-credited)
• Do not pay a referral service based on pt seen (okay to use, yearly or
monthly charges type )(don’t use service asking doc to pay based on
how many pts see them because of service)
• Do not misrepresent infectious diseases test result
• Do not use false of mislead (search engine optimization) SEO
techniques on ur website

7. Name of practice
• No misleading names
• Do not use the doctors name who is retired or not work there anymore
8. Specialization & limitation of the practice
• Do not call yourself a specialist  until u have one
• Same is true for dual degreed dentist practicing medicine
• Do not call yourself specialist in a speciality not recognized by
NCRDSCB

9. General practioner annoucement of service

• General dentist do not announce service that need specialization
• Do no call ur self diplomate without having credentials
• Do no abbreviate fellowships at the end of ur name to imply
additional degress
Professional
liability
 Statue of limitation
• Laws that set a limit on the amount of time u can go to the court
after the even has occurred

Occurance rule
• Statue of limitaiton start to run after the injury or malpractice
have occurred

Discovery rule
• Statue of limitaiton start to run after the injury or malpractice
have being discovered
 Witness
Expert testimony
• Some expert giving / telling his opinion / testifying to the existing
standard of care & how it has been breached
• Standard of care  minimum acceptable care (eg :- rubber dam)
• Do not agree to contigent fess

Fact witness
• Someone who was present there
 Good samaritan act
• Offers legal protection to health professional & anyone who
provided reasonable assistance to individuals who are

a) Injured
b) Ill
c) In peril  In danger
d) In capacitated
HIPPA
• Health insurance portability & accountability act 1996
• It is a fedral law that required the creation on national standards
to protect sensitive patient health information (PHI) from being
disclosed without pts consent or knowledge

Three rules for guarding the security & privacy of pts medical
information
1. Privacy rule
Osha
 Patient
management
Communication
& interpersonal
skills
 (1) Active listening
• Prepare to listen  set aside time free form distraction
• Repeat back wht u hear  paraphrase
• Lean forward
• Good eye contact
• Face patients
• Ask questions
• NOD
• Smile
• Maitain close proximity
 (2) Rapport
• Mutual sense of  trust & open-ness
• Ask about pts interest  school, work, family
• Disclose about urself  as appropriate
 (3) Empathy
• Ability to understand & share the feeling of another
• Reflection & showing understanding
• Acknowledge their concerns
• Open-mindness
• Not sharing personal experience

• Usko smjo  pt k rr usko (apne nhi batao)

• Usko dard ho rha hai tou smjo uski baat yeh nah bolo k
yeh tou kuch nhi mera dard zyada hai
 (4) Non verbal communication
• Body language - reading pts body language
• Continious, autommatic, informative
• Monitor pt
• Look at their  eye & eybrows movement (discomfort)

First sign of discomfort

• Eye
• eyebrow
 (5) Verbal communication
• Be simple, specific & direct
• Do no just advice bbut also information & education  allow pt to
make informed decision
• Do not falsly reassure & say  everything will be fine or
don’t worry
• Make expectations clear
a) Clinical interviewing
• Open ended questions  allow to pt to explain wht is important to
them
• Closed question  specific
• Leading question  never use
• Probing  gather aditional information
• Laundry list  ask pt to respond from a list of choices
b) Treatment planning
• Present treatment alternative in  desending order of
desirability (1st should be ur choice don’t tell them just
list them)
• Only present options that are consistent with ur standard of care
• Ask pt wht their understanding is of the treatment option to verify
their understanding  teach back method
Health behaviour
change
 Behvioural change (ABC)
• Involves complex interplay of persons thoughts, emotions & behaviour

Antecedent
• Factor that facilitates behvaiour  factors affecting behaviour
• Eg : - food caught in the teeth

Behaviour
• Itself  to eliminate the factor
• Eg :- using floss

Consequences
• Consequences of that behaviour  end result
 Stages of change
1. Precontemplation
• Not considering any behvaiour change
Eg :-
• Pt do not want to stop smoking
• Doctor  educates him & tells about pros & cons

2. Contemplation
• Beginning to consider behaviour change
Eg :-
• Pt thinking to stop smoking
• Doctor  reinforce the reasons for change & explore new pros &
cons
3. preparation
• Preparing to take steps to change, often expresses desire to change
• Also called  determination
Eg :-
• Pt getting ready to stop smoking, mostly on board
• Doctor pick a stop date, taking about barrier to quitting smoking

4. Action
• Taking some sort of practical step to change
• Requires support
Eg :-
• Pt has stopped smoking & actively apply cessation skill
• Doctor help them stay away from tobacco products, to prevent relapse

5. Maintenance
• Once behaviour has changed, u take steps to maintain it
Eg :-
• Pt has smoke free living
• Educate pt  ask about
pros & cons of smoking
• Bring awareness

• Reinforce reasons for

change
• Explore new pros & cons

• Pick a stop date

• Identifying barriers

• Help them stay away from

tobacco products and
relapse
• Manageing withdrawal
• Encourage and praise the
successful behavioural
change
 Social cognitive theory
• Model to study behavioural change
• Motivation to change behaviour is influenced by 3 factors

1. Self-efficacy
• Cognitive perception that u can execute behaviours necessary fro a given
situation
• Telling urself that u can do it
• Long term impossible goals  go for short term easy goal = more motivation

2. Behavioural modeling
• Learn behaviour from  role models

3. Social reinforcement
• Positive social consequences  change bring positive social results
 Health belief model
• Motivation to change behaviour is influenced by several factors

1. Percieved susceptibility
• To given disease or problem
• Perception or ur belive to ur health  u believe u can get a disease u try
to change the behaviour
• Eg:- u can get caries

2. Percieved costs & benefits

• Severity of consequences

3. Cues to action
• Prompts to engage or not engage into certain behaviours
Behavioural
learning
1. Classical conditioning

• A neutral stimulus associated with a natural response

a) Food (US)is the stimulus causing  triggers unconditioneed reaction (salivation)

• US = UR
b) We add a neutral stimulus (NS) = No unconditioned reaction
c) Now add NS + US = UR
d) Conditioned stimulus produce conditioned response  CS = CR

Eg:-
• Whistle dog = come for food / food time / food ready
In dentistry
• US = injection
• UR = pain & anxiety
• NS = presence of dentist to give injection (white coat)
• With multiple times doing this pt will be anxious and stressfull with just presence of
1 2

3 4
2. Operant conditioning
• A response is increased or decreased due to reinforcement ot punishment

Positie reinforcement  do good thing = reward

Negative reinforcement  do a good thing = remove bad stimulus

(appointment faster) (brushing well = no tooth ache / cavity)

Positive punishment  do bad thing = punishment (everytime no

brushing = cleaning room)

Negative punishment  do a bad thing = remove good stimulus

(behaving bad on appointment we take ur phone)

Eg:-
• Rat pull lever the food come out
3. Observation learning
• Learning by observing others
• Based on  modeling

Eg:-
• Asking anxious or uncooperative child to observe his cooperative
sibling getting a procedure done
Behavioural
strategies
Altering antecedents
• Eg:  placing floss on nightstand  so u can remember to do it

Altering consequences
• Eg :- reward urself after flossing with playing video games

Shaping
• Setting small Attaining goals & reward urself after each step

Premack principle
• Making a behaviour that has higher probability of being performed
contingent on a behaviour that has lesser probability of being perfomed

Ability to change locus of control

• Internal motivation  khudse (more succesfull)
 Motivational
interviewing
• Counselling

OARS
• O  OPEN QUESTIONS
• A  AFFIRMATION
• R  REFLECTIVE LISTENING
• S  SUMMARIZING

4 steps here
1. Engaging  form a relationship
2. Focusing  exploring motivation, goals & values
3. Evoking  eliciting their own motivation
4. Planning  exploring how one might move to change
a) Sustain talk  not ready to change

b) Change talk  movement toward change

c) Commitment talk  express readiness & willingness to change

(ready to change)
Anxiety & pain
management
 Dental anxiety
Stress
• Percieved threat to ones well being

Anxiety
• Subjective experience involving cognitive + emotional +
behavioural + psychological factor
• Cognitive  affecting thoughts & believe
• Emotional  anger or fear
• Behavioural  affect sleep & apetite
• Psychological  fight or flight response

• Anxious pt  more likely to sit still and say much

 Stress management
1. Trust
• Provide pt with sense of control
• Provide info  what is going to come before hand (no surprises)
• Hand signals  pt can raise hand to break (can stop treatment with
signal)
• Time structuring  using egg timer or clock

2. Comfrot
• Acknowledging the patients experience
Be empathetic & tactful in ur initial resposne
• I can see that
• Seems like
•
3. Coping
• Using cognitive – behavioural interventions

a) Diaphragmic breathing
• Deep breathings
• It helps with activating physiologic relaxing resposne

b) Progressive muscle relaxation

• Tensioning & relaxing certain muscle groups, focusing on difference b/w tension
& relaxation

c) Guided imagary
• Making them imagine  a nice scene (beach, mountains)

d) Hypnosis
• Attentional focus

e) Rehearsals
• Allow pt to practice the coping strategy in a simulated procedure  eg :- deep breathing
Systemic desensatization
• Also called  graded exposure
• Exposing pt to items slowly
• From low fear stimuli to hight (relaxed period in b/w)
• Less fear to high fear

Eg:- needle phobia

• 1st  show then needle
• 2nd  place needle in mouth with cap
• 3rd  simulate procedure
• 4th  actual injection
Distraction
• Tv, games etc
• Less effective for  hyper vigilant anxious pts

Tell-show-do
• Instructional method

Habituation
• Decreased in resposne occurs due to repeated exposure to
a conditioned stimulus

Rational response / reframing / cognitive coping

• Developing more adaptive tought or statement as means of coping
• Eg: - from I cant do this – I can do this
 Cognitive apparisal of threat
Controllability
• How controlable the situation seems to be

Familarity
• How familar the situation is

Predictablity
• How predictable the situation is

Imminence
• If the situation seems to be approaching near

Less control + less familar + less predictable + more imminent =

Child behaviour
management
• Create a child oriented environment
a) Toys
b) Books
c) Posters
d) Ask about interest
e) Parent with them

• Ask them to be a helper  praise them when they r good

• Tell – show – do
• Ask about their fears
• Counting  good technique to help
 Dental Pain
management
 Dental pain
• Pain is complex phenomenon involving cognition & emotion
• Anxious pt  more likely to report pain & discomfort

• Wong baker faces pain rating scale  for kids

 Behavioural pain management
• Start with simplest & least invasive procedure first
• Given pt the choice when ever possible & appropriate
• Use hand signals & respond immediately to the discomfort
 Pharmacological pain management
• 1-3 (Mild Pain)  Use ibuprofen or acetaminophen alone.
• 4-6 (Moderate Pain)  Use a combination of ibuprofen and
acetaminophen.
• 7-10 (Severe Pain)  Stronger medications, such as those
containing opioids (e.g., acetaminophen-hydrocodone or
acetaminophen-oxycodone), may be necessary

Nitrous oxide
• Before onset  tingling
• Side effect  nausea

Iv sedation
Epidemiology
 Public health
• Science & art of preventing disease, promoting life & promoting
physical health & efficiency through organized community efforts

Epidemiology  branch of public health

• Study of distribution & determinants of disease
 Epidemiologic measures
• DFMT index Irreversible

• Gingival index
• Periodontal index reversible
• Simplied oral hygiene index
 Dmft
• Conventional method of defined dental caries in a
population
DMFT
• Decayed + missing + filled + permanent teeth

DMFS
• Decayed + missing + filled surfaces due to caries ( permanent
teeth )

DEFT
• Decayed + extracted + filled teeth due to caries ( permanent
teeth )
 Gingival index
• Use four surfaces on 6 indicator teeth (sixtans)
• four surfaces  facial, mesial, distal, lingual

• 0 = normal ginigva
• 1 = mild inflammation
• 2 = moderate inflammation
• 3 = sever inflammation, ulcerated tissue with tendency towards
spontaneous bleeding
 Periodontal index
CPITN  Community periodontal index of treatment needs
• 0 = healthy
• 1 = bleeding
• 2 = calculus
• 3 = shallow pockets
• 4 = deep pockets

• AAP does not like this because it does not account for 
recession (no account of CAL)
 Simplified oral hygiene index (OHI-S)

• Quantifies for the amount of debris (DI-S) & calculus (CI-S)

Oral hygiene
• Good
• Fair
• Poor
 Disease processes
• Caries  decay
• Periodontal disease  gum disease
• Oral cancer
 Early childhood caries
• Also called  baby bottle
• Defined as  1 or more dmfs  b/w birth & 71 months of age
• Ages  3 – 5
• Site max incisors & molars
• 5% of us infant & toddler population
 Oral cancer
• Tongue most common site
• Should be screened at every dental visit
Prevention
1. Primordial
• Prevention of risk factors of the disease  which have not appeared yet
• Eg:-

2. Primary
• Prevent before disease occurs
• Eg:- water fluoridation, fissure sealants

3. Secondary
• Eliminate or reduce disease after it occurs
• Eg :- restoration  composite & amalgam

4. Tertiary
• Rehabilitates the pt after the disease process has taken place
 Fluoride

Topical
• Strengthen teeth which are already present in mouth  resistant
to teeth
• Enters saliva  bath teeth

Systemic
• Ingested & incoporated in tooth during development
• Also provides topical effect
 Community water fluoridation
• Most cost efficient & effective way  most effective &
practical
• Optimal value  1ppm
• Odorless, tasteless & colourless when from range  0.7 –
1.2
• 74% amercians live in fluroidated setting (210 million)
School water fluoridation

• 4x the normal community water fluoride levels

 Salt fluoridation
• For developing countries with no clean water to drink
• Value  200-350 fluoride per kg of salt
• Combination of both water & salt fluroidation together is
not recommended
 Fluoride supplements
• Prescriptions only
• For kids living in non fluoridated areas
• Less then 3 age  fluoride drops
• More then 3 yrs  tablets & lozenges
• More then 6 yrs  mouth washes

Mouthwash
• 0.2% Naf  weekly
• 0.05% NaF  daily
 Topical fluoride
• Best for  smooth surfaces (facial, lingual)

• Help with  root caries & ECC

• Varnish is adhesive & maximizes fluoride- tooth contact with 5%

fluoride

Acidulated phosphate fluoride (APF)

• Ph 3
• 1.23% fluoride
• Initial  demineralize to remineralize enamel
 Stannous fluoride
• Antimicrobial
• Bad taste
• Causes  yellow brown tooth stains
 Fluoride toxicity
Acute toxicity symptoms
• Nausea
• Vomiting
• Loss of consiousness
• Cramping
• Stomach lining damage

Chronic
• Fluorosis

Rules of 5s
• Toxic dose  5mg / kg
• Trearrment / management
 Sealants
• Best for  occlusal surfaces
• Recommended  1st & 2nd molars of children at risk of caries

• Fluoride  least effective on occlusal surface

 Mouth guards
• Made for athletes  prevent tooth trauma
• Protruding upper incisors  common / susceptible to
trauma
 Health education
Health literacy
• Capacity at which individuals obtain, process & understand basic
health information & services
• Education alone can not function as the preventive measure
 Toothbrushing
• Pt should know the  dental plaque is main cause for caries
& periodntal disease
• Pt below age 6 should be supervised with brushing using
fluroide tooth-paste

Flossing
• Good for gum health
• Does not prevent tooth decay
 Diet
• Frequency of sugar more important ten quantitiy

Other factors
• During day or immediately before bed
• Length of time sticky food remains in the mouth
Research
Coponents of a
scientific paper
• Title  summarizes the topic of the research in few words

• Abstract  brief summary (100-150 words)

• Introduction  background of topic & purpose, hypothesis

• Methods  population, variables, sampling, how it was conducted

• Results  present the findings

• Discussion  interprets the findings / result

• Conclusion  answer the research question

Hypothesis
• Statement aout expected outcome of the study

Forms
1. Null
• There is not association b/w two groups
• No affects, relationship or difference b/w two or more groups
being studied

2. Alternative form
• There is an association b/w two groups
Example
• Does the application of fluoride varnish every 3 months reduce
the incidence of dental caries b/w 6-12 yrs old more affectively
then fluroide toothpaste used daily

Null hypotheisis
• The application of fluroide varnish every 3 months does not
reduce the incidence of dental caries b/w 6-12 yrs old more
affectively then fluroide toothpaste used daily

Alternative hypothesis
• The application of fluoride varnish every 3 months will reduce the
incidence of dental caries b/w 6-12 yrs old more affectively then
fluroide toothpaste used daily
 Descriptive /
Epidemiological
study
• Study of distribution & determinants of the disease
• Large scale community study
• To quantify the disease status in a community
• How many people in population have this  caries gum disease

Prevelance
• How many people are affected in a population in given time
• Porportion of a given popoulation affected by the condition at a
given time

Incidence
• No of New cases of disease in the population
 Analytical /
observational
studies
• To determine the etiology of disease  cause of disease

All designs follow  tell association not the cause of disease

1. Cross – sectional study

• Smaller scale them community based
• Survey or measurement
• To represent a snapshot in time  done at one point of time
• Prevelance
• No need for follow
• Try to determine the possible exposure factors after a
known disease incidence
• Eg:- group of people drinking alcholo  we determine how many
have cancer and how many does not have
Longitudional

2. Case – control
• Involves people with condition  case
• People without condition  control
• Down in past  retrospective
• We have data and we do research  no new data
• Odd ratio  how likely (eg:- how likely alcohol is associated with cancer)

3. Prospective cohort
• Followed through the time to see if they develop a condition
• Incidence
• Relative risk  probability of drinker & non drinkers getting cancer
• We track the pts  in future not past
• Eg:- track people over 5 yrs  calculate incidence ofcancer in drinker & non
drinkers
4. Retrospective cohort study
• Look back after following the cohort & decide wht disease
u want to look for
• Incidence eg:- incidence of caries b/w drinker & non
drinkers
• Relative risk
• Risk of developing a disease with already know factors
Experimental
studies
• Determine the affectivness of the given therapy

Randomized Clinical trial

• Aim to isolate on factor (eg:- new drug) & examine its contribution to
pts health by holding all factors as constant as possible
• Randomization  best tool (it minimizes selection bias)

a) Random sampling  randomly select people

b) Ramdon allocation  randomly allocate them into different treatment
groups (drug group & placebo group)

Blinding  concealing allocation information (minimizes biased

assement of outcome)
c) Single  participants don’t know wht group they r in (placebo or drug)
d) Double  participants & clinician both blinded
Biostatistics
Statistics
• Science of collection, presentation, analysis & presentation of
data from logical analysis

4 main components of statistics

• Collection on data
• Presentation of data
• Analysis of data
• Interpretation of data
Biostatistics
• Branch of applied statistics that applies statistical methods to
medical & biological problems

Uses of biostatistics
• To define  wht is normal or healthy in a population
• Find relative potency of new drug realtive to standard drug
• Compare efficacy of particular drug
• Find association b/w two  smoking & cancer
• To identify sign or symptoms of disease / syndrome
 Data collection
Primary
• Direct from source  eg:– from tb pts (individuals)

Secondary
• Through other sources  eg:- tb data from hospitals (records)

Types of data
1. Quantitative
2. Qualitative
1. Quantitative
• We can count it
• Like  numericals  Hb level, blood glucose level

Discrete
• When data present in  whole numbers (no units)
• Eg:- no of pts, no of doctors

Continious
• When data has units
• Meter, watt, mg etc
• Eg:- height, weight, size, bp
2. Qualitative data
• Quality of something  categorical data
• Eg:- eye color, OH,

Nominal
• Names
• Eg:- gender,

Ordinal
• Sequence  in order (order can not b changed)
• Eg:- high to low, ranks,
Grouped data
• Putting in groups
• Eg:- 20 people we group them in young & old  15young 5 old
people

Ungrouped
• All the data we have is different  which we can not put in the
groups

Interval data
• Data in interval
• Eg:- 50 - 60, 60 – 70 (in interval of 10)
 Methods to collect data

1. Observation
2. Survey
3. Experiment interview
4. Census
5. Recorded data
6. Internet source
 Data presentation
For quantitative data
• DOT plot diagram
• Histograms
• Line charts
• Frequency curve

For qualitative data

• Bar diagram
• Pie charts
• Map diagram
• Pictogram
1. Line charts
• Relationship b/w only two variables
• X axsis  horizontal
• Y axsi  vertical

2. Histogram
• Frequency distribution is there
• Variable characters  x-axsis
• No space in b/w

3. Frequency polygen
• Make point in rectangle in histogram sin b/w & make line

4. Dot plot
• Tell natures b/w two variable
1. Bar diagram
• Spaces in b/w values  separated
• Bars can be placed  vertically & horizontally
• Only 1 variable is present

2. Pie chart
• Angles to tha data
• Sector diagram

3. Map diagrams
• Showing on the map
• Like:- crops, population density

4. Pictograms
 Frequency
distribution
Normal distribution / gausian curve
• Bell – shaped curve
• Mean = median = mode

Skewed distribution
Tail / curve goes to right
• +ve positive
• Mean is greater than median & median greater then mode
• Mean > median > mode

Tail / curve goes to left

• - ve negative
• Mean < median < mode
Mean +- 1SD = represent = 68.2 %
Mean +- 2SD = = represent = 95.4 %
Mean +- 3SD = = represent = 99.7 %
Bimodal distribution
• Two peaks in graph
 Measure of
central tendency
• Measure the values which come in centre

1. Mean
• Average value
• Add all the values (number) & divide total numbers of value
• Least reliable
• Effected most by  outliers

Eg:-
• Data 1,1,2,3,4,4,4,5,6
• 30 / 9 = 3.3
2. Median
• Middle value
• most appropriate measure of central tendency  most
reliable
• No affected by  outliers & skewed data

Eg
• Data 1,1,2,3,4,4,4,5,6
• Median  4 (middle value)
• If u have even numbers at middle  tak their average (add middle
values & divide by two)
Eg
• Data 1,1,2,3,4,5,4,5,6,7
• 4+5 = 9 / 2 = 4.5
3. Mode
• Most frequent value in the set
• If more then 1 frequent value
• Then  3 x median – 2 x mean
• Least affected by  outliers

Eg
• Data 1,1,2,3,4,4,4,5,6
• Mode = 4
Outliers
• Extreme value
• Effects mean  most
Eg
• Data  1,2,3,4,5,6,1000
• Outlier = 1000 (extreme value)
Measure of
dispertion
• How spread-out values are from each other

Range
• Maximum – minimum (max minus min)
Eg:-
• Data 1,1,2,3,4,4,4,5,6
•6–1=5
Mean deviation (md)
• How much the value is deviated from the mean (eg:- mean is 5 & value is 2  how much mean is
deviated from the value)
• ∑ x- x̄ / n
• n = total number
• X = each value (every value in data )
• x̄ = mean
Eg:-
• Data 10, 20, 30, 40, 50

• Mean (x̄) = 30
• X = each value

x- x̄  don not consider minus sign & add all

• 10 – 30 = 20
• 20 – 30 = 10
• 30 – 30 = 0
• 40 – 30 = 10
• 50 – 30 = 20
• x- x̄ = 20 + 10 + 0 + 10 + 20 = 60
Standard deviation (SD)
• Square root of mean deviation / variance
• Larger this number is the more spread-out the values are from each other

Eg:-
• Data 10, 20, 30, 40, 50
• N  if value is 30 = n, if value is less then 30 then = n – 1
• (∑ x- x̄ / n – 1 ) square  in this formula is n – 1 because the n value will be less then 30

• Mean (x̄) = 30
• X = each value
• N-1 = 5 – 1 = 4

x- x̄  don not consider minus sign & add all

• 10 – 30 = 20 square = 400
• 20 – 30 = 10 square = 100
• 30 – 30 = 0 square =
• 40 – 30 = 10 square = 100
• 50 – 30 = 20 square = 400
• x- x̄ = 1000
Coefficient variance
• Used to compare variability
• Cv = SD / MEAN x 100

Eg:-
• Data 10, 20, 30, 40, 50
• MEAN = 30
• SD = 250

• Cv = 250 / 30 x 100 = 833

Variance
• How spread-out the individual values are from the mean
• Find mean & substract them from exh number of set & then
square them
• Then calculate the average of squared numbers
 Quality of diagnositic test

1. Reliability
• Precision
• Are u getting consistant results
• Multiple operators using it & how mmuch do they agree
with each other

2. Validity
• Accuracy
• How close to the truth are thoso results
• Eg:-
3. Sensitivity
• Disease
• Test is correctly identifying who has disease
• High sensitivity  when we have higher TRUE POSITVE & low
FALSE NEGATIVE
• IDEAL  1.0
• IF  0.5

4. Specificity
• Health
• Correctly identifying the healthy pts
• High specificity  when we have higher TRUE NEGATIVE & low
FALSE POSITIVE
• IDEAL  1.0
True positive
• Have it & diagnosed it
• Eg : - have caries & diagnostic test confirms it

True negative
• Do not Have it & diagnosed it
• Eg : - don not have caries & diagnostic test confirms it

False positive
• Do not Have it but diagnosed it as have it
• Eg : - don not have caries but diagnostic test says otherwise

False negative
• Have it but diagnosed it as. not have it
 Inferential statistics
1. Statistical significance (P-value)
• Probability that two variables are unrealted
• 0.05

2. P less then  0.05

• Reject null hypothesis
• Statistically significant
• If null hypothesis  alcohol has no relation to cancer (we reject this
hypothesis)

3. P more then  0.05

• Accept null hypothesis
• Not significant
• If null hypothesis  alcohol has no relation to cancer (we accept this
Null hypothesis (H0)
• Hypothesis the researcher tries to  reject, nullify, disapprove
• Eg:- there is no difference in caries prevelance b/w fluoridated & non
fluoridated population
• We conduct research to disapprove the hypotheiss

Type 1 error / alpha error

• When we reject the null hypothesis which should have been accepted
• 0.05  if less than this = statistical significance
• 0.05  if more than this = no statistical significance

Type 2 error / beta error

• When we accept the null hypothesis which should have been rejected
4. chi-squared test (x2)
• Measures the association b/w two categorical values
• Eg :- ask group of people (men & women) wht they like cats or dogs
• This test will tell u  gender & preference are related to one and another

5. T - test
• Measure statistical difference b/w two means
• Small sample size
• Null hypothesis  there is no difference b/w groups
• Eg:- placebo group & drug group

7. Z test
• Measure statistical difference b/w two means
• Larger sample size
• Variance is known
8. Analysis of variance (ANOVA)
• Measure statistical difference b/w two or more means
Correlation analysis
Correlation coefficient (r)
• Statistical measure that represrent the strength of
relationship b/w two quantatative variables
• Always b/w  -1 TO 1
• 0 means  no linear relationship
 Operational variables
Qualitative  description
• see in chi square test

a) Nominal  names or labels

• Genotype
• Blood type
• Eye color
b) Ordinal  ranking
• high school, bachelors
• High , moderate , low
• Dds, dmd
• Mild, moderate, severe
Quantitative  numbers
• T test
• Z test
• Anova

a) Ordinal  ranking
• Scale  1-10
• Representated by numbers

b) Interval  range of values

• Tempreture
• Ph scale
• Sat scores

c) Ratio  range of values with clear definition of zero

• Reactionary pulse
• Weight
• Length
Independentnt variable (X)
• Explanatory predictable
• Factors controlled / manipulated by investigator

Dependant variable (y)

• Though to change by presence, absence or manipulation of
independent variable
• Outcome
• Predictable
• Mortality
• Disease outcome
• Health status
• Cost
Confounding variable
• Co-variate
• Adversly affect relationship between these 2
• Gender
• Age
• Ethnicity
•
Evidence based
dentistry
 Acuracy of
screening &
diagnosis
Screening
• Detection targeted at large asymptomatic population

Diagnosis
• Classification provided to symptomatic pts seeking seeking care
(showing signs & symptoms )
1. Reliability
• Also known as  reproducibility / consistency
• Doing same tests overe & over & getting consistent results
Two methods to check
a) Intra-examiner
• Done by one doctor
• Screens a pt waits for time being & again does the test to see if
they get same test
b) inter-examiner
• Different people and different docters  to see if u get similar
results

• Second test must be blinded to result of first

• A  examiner a
• B  examiner b
• Theyr arescreening / diagnosing pts for the present & abscenece
of caries
Measure reliabilty of test
• % agreement = no of agree / total no of pts (not very accurate
way)
Kappa value = complicated
• > 0.75 = excellent reliability of test
• 0.40-0.75 = acceptable
• <0.40 = poor
2. Validity
• Distinguishing b/w health & disease
• U need to have a reliable test in order to have a valid test
• Gold standard : Ideal method (not feasible in clinic)
• A  new treatment modality
• B  gold standard, old proven method

Sensitivity (measures the accuracy of test in detecting disease)

• Se= TP/ TP + FN (total no of diseased pt)
• High senstivity = low Fn )

Specificity (measures the accuracy of test to detect health)

• Sp = TN/ TN +FP
• High sp = low FP

To judge Validity
• Se + sp = 2.0 perfect
• Se + sp = >1.6 good
 Summary
Reliability
• % agreement
• Kappa value

Validity
• Se
• Sp
• Roc value
 Disease
frequency
Three study methods
1. Cross –sectional surveys
• Prevelance of disease
• Severity
• Sampling variability

2. Prospective cohort
• Incidence of disease
• Sampling variability

3. Case studies
• Rare conditions
 Cross-sectional
• Random sample  from sampling frame (target population)
• Snapshot of time  done at one point of time
• Quentionaiire / interviewsSmaller scale them community based  Survey or
measurement
• Prevalance
• No need for follow  can be done in same day
• Try to determine the possible exposure factors after a known disease incidence
• Eg:- group of people drinking alcohol  we determine how many have cancer and how
many does not have

Target population
• Eg: - entire us population (not possible to interact with all then we same a sample)

Case defination
• Cases  with disease
• Non-cases  not with disease
Prevelance
• prevalence is the proportion of a particular population found to be affected
by a medical condition at a specific time
• Frequency of diseae for population (in present )

• Prevelance = diseased people / total no of people

• In % or decimal
• Eg:-  10% or 0.10 of study pouplation have caries
Severity
• Improved prevelance
• Avg value of disease index at that time
Instead of yes & no we look at
• Mean
• Threshold
• Eg:-  dmft

• Severity = complicatio
• Eg:- 1.8 teeth caries / child = 18 teeth caries / 10 child
Sampling variability / error
• Everytime we take a random sample from target population &
make a estimate about that targert population we have 
sampling variability
• We see for each of the study
• 95 % confidence intervals (CI)

P value
• Type 1 error (alpha)
• % of probability that different in the result is due to chance
• We need a low P value
Bias
1. Convinience sampling
• Non random sampling
• According to ur convinience

2. Incomplete data
• Non response
• Different rate of response
 Prospective cohort studies
• Take a random sample of healthy at risk population
• 1 group  1 random sample
• We take baseline or initial assesement of healty pt or their teeth
& follow (wait to see if any new disease event happens)

Incidience
• Rate of developing new diseas in a population over time
• Incidence rate = new disease at a given time / total at risk
population

Sampling variability
• Same as above
Case studies
• Rare or unknown case
• No statistical data
Etiology
• Talking about causes or risk factors associated with the disease

1. Prospective cohort
• Incidence of disease
• Relative risk
• Sampling variability

2. Case control studies

• Odds ratio
• Sampling variability
 Prospective cohort studies
• Take a random sample of healthy at risk population
• Equal random population of this population into  2 groups
(cohort)
Based on
• Exposed to risk predictor
• Non exposed predictor
Risk predictors
1. Risk factors
• Factors associated with disease
• Eg:- smoking, periodontal disease

2. Risk indicator
• Marker of exposure to this risk factor
• Eg:- halitosis side effect of smoking
Incidience
• Rate of developing new diseas in a population over time
• Incidence rate = new disease at a given time / total at risk
population

Relative risk
• RR = incidence rate in exposed to risk predicator / incidence rate
in unexposed to risk predictor
• RR = 1  null (not associated with disease)
• RR = >1  associated with increasing disease
• RR = <1  associated with decreasing disease
Sampling variability
• CI = 95%
• If CI curve too wide = poor results
• Check if it overlaps with null value of 1.0
 Case control
• Take random sample from the population  selected based on  absence or prescence of
the disease (instead of just at risk)
• People with condition compared with people with no conditon
• Look back in time  ask them question (eg:- did u smok)  Down in past  retrospective
• We have data and we do research  no new data

Two groups
• Have disease  case
• No disease  control

Odds
• Odds = exposed / unexposed

Odds ratio  how likely (eg:- how likely alcohol is associated with cancer)
• OR = odds in cases / odds in control
• OR = 1  null (not associated with disease)
• OR = >1  associated with increasing disease
ODDS
For cases
• exposed / unexposed = 40/5 = 8
For control
• exposed / unexposed = 30/15 = 2

ODDS RATIO
• Odds in cases / odds in control
•8/2=4
• Exposed one is 4times more likely to get disease

CONVERT TO THIS TO
MAKE LIFE EASIER
Limitation
• Looking back in time
• Pts make have gotten disease then might have been exposed

Sampling variability
• CI = 95%
• Check if it overlaps with null value of 1.0
Upgrade from risk predicator to being a risk factor
• Strength of association  relative risk more then 1

• Consistency of association  reliable results (b/w diff population &

time )

• Specificity of association  only associated with disease

• Temporality  exposure must provide disease onset(exposure

before disease)

• Plausibility . Biological evidence (link characterisitcs to the

disease)
Treatment
efficacy
• How effective the treatment is

1. Randomized control clinical trials

• Best available

2. non-randomized clinical trials

3. Systemic reviews
 Randomized control clinical trials (rcts)
• Random sample of  diseased & diagnosed population
2 groups
• Treatment group
• Control group (exposed or unexposed)

• Or we can take random samples of healthy at risk population to test a preventive treatment

Randomization
• Randomly selected people who are all equal and distributed randomly to groups

Blinding
• Single, double, triple

Surrogate end point (SEP)

• Subsitute
• Subsitute measurement of a specific treatment that may or may not relate with real clinical
end point
Treatment effect
• TA = mean from control – mean from treatment

Statistical significance
• 95 ci
• P value

• Power  probability that study detects a effects where there is an effect to be detected
(>0.80 good)
• Type 2 error (beta)  probability of getting a no result on a good treatment (<0.20
good)

Clinical significance
• Clinical value to pt & community
• Only considered if p = <0.05
Nnt
• Number need to treat in order that one pt be cured from disease or have disease
prevented
• p-value = <0.05  statistically significant result

P-value = <0.05
Treatment have good
effect

P-value  > 0.05

Treatment have no effect
 Rct  Randomized cross-over design
• Random sample of diseased population
• Control & test group
• Washout period  we do orignal assessment and wait some time
• Cross-over or swap the the group  then we swap control & test
groups

• Subjects experiences both control & test treatments

Limited
• Requires recuring disease  gingivitis
 Rct  split mouth design
• Random sample of diseased population
• Control & test group
• Randomly assign the contorl or test to right of left side of mouth

Limited application
• If u have periodontal disease involving whole mouth
 Rct bias / problems
• Subjects who enroll don’t typically represent entire population
• Limited application
• Ethical dilemma
 Single group historical control
• Non-randomized clinical trials
• Non random pts with disease
• 1 groups gets all the treatment and compared to the historical
control (old research / study)

Problems / bias
• Spontaneous remission  unexpected improvement in disease
which differ from historical control
• Hawthorne effect  people in study behave differently then
people who dont
• Regression to mean 
• Placebo effect  tendency of people to respond favourably to any
treatment
Non randomized concurrent control group
• Non random from the disease population
• 2 groups, 2 different treatments

Problems / bias
• Placebo effects
 Systemic review
• Combined result from 2 – 3 researches together to get a meta
analysis diamond

• Combine all results and values  to get avg

Problems & bias

• Publication bias 
PICO
• How to well construct the research question
• Fundamental building block of clinincal research
• To formulate research questions

• P  POPULATION, PATIENT OR PROBLEM

• I  INTERVENTION (TREATMENT, DIAGNOSITC TEST OR
EXPOSURE)
• C  COMPARISION OR CONTORL (PLACEBO
• O  OUTCOME (RESULT)

Example
• In adults with chronic periodontitia (P) does laser therapy
(I) compare with scaling & root planning (C) lead to
greater reduction in pocket depth & improvement in
Example
• Does daily use of herbal mouthwash reduce the
incidence of gingivitis in adults more effectiviely than
standard antiseptic mouthwash over a period of 6
months

• P  ADULTS
• I  HERBAL MOUTHWASH
• C  ANTISEPTIC MOUTHWASH
• O  REDUCE INCIDENCE OF GINGIVITIS
Finer
• Criteria to evaluate the quality of a research question

• F  FEASIBLE (Study should be realisitc considering time, budget,

expertise, equipment, sample, access to data)

• I  INTERESTING (research should be engaging & hold the interest of

researchers, clinician, target audience

• N  NOVEL (add value to exisiting value, new insights, new treatments

methods )

• E  ETHICAL (should comply with etthical boundaries) (all papers

involving human subject must be reviewd and passed by the
instituional commity)
Example
• Does daily use of herbal mouthwash reduce the incidence of gingivitis
in adults more effectiviely than standard antiseptic mouthwash over a
period of 6 months

• F  can be conducted in clinic with both mouthwashes available (1)

• I  it is interesting for both clinician and audience (non chemical

alternate for mouthwash) (1)

• Novel  explore efficiacy of natural herbal, adding to limited research

to the herbal products in dentistry (1)

• Ethical  minimal harm to the subject (1)

 Data
presentation
Box & whisker
plot / Box plot
• Are used in statistics to graphically display various pareameters
at a glance
• The data must have metric scale level  eg:- age, temp
• Used to compare & contrast two or more group  eg:- salary of
men & women
• Divides / represent data in quartiles  25% each
25% 25% 25%
25%

In boxplot these can be read

• Median
• Interquartile range
It shows
• Min
• Median  line in middle reprsents the median (middle point of
data)(50% of the data, also represent Q2 (u need data values to
calculate median)

• MAX

• Q1 / LOWER QUARTILE  median of bottom half of the values

(25% or ¼ mark in data)

• Q3 / UPPER QUARTILE  median of upper half of the values (75 %

or ¾ mark of data)
Example
• Years of tteching experience
• Data  3,3,7,8,8 | 10,11,12,15,18

• Min = 3
• Max = 18
• Median = 8+10 / 2 = 9
• Q1 = median of lower quartile = 7
• Q2 = median of upper quartile = 12
EXAMPLE
• Study collected data of 100 pts on scale of 1-10 post 24hrs of extraction
without any pain control

• Min = 2
• Max = 10
• Q1 = 3
• Q2 / median = 5
• Q3 = 7

Range
• MAX – MIN
• 10 – 2 = 8

Interquartile range (IQR)

• Q3 – Q1
Scatter plot
• Graph used to display the relationship b/w two quantatative
variables

Explanatory variable / independent variable

• Variable that explains the way other variable responds
• Placed in x-axis

Response variable / dependent variable

• Placed on y axis
• Correaltion  one variable has realtion to the other, but this does not mean
causation

Types of correaltion
1. Negative linear corealtion
• X increases & y decreases

2. Positive linear corelation

• X increases & y increases (both increase)

3. No corealtion
• If there is no linear pattern

Relation can be strong, moderate & weak

a) Strong  points clustered together to the line

b) Moderate  points clustered bit spread out to the line
Co-relation coffiecient
• Tell how strong or weak corealtion is
• Denoted by  r
• r = 1  perfect positive co-relation
• r = 0  no co-relation
• r = -1  perfect negative co relation
Forest plot
• Graph that compares information from many scientific or clinical
studies studying same thing
• Can be used to summarize information from individual studies in
a meta-analysis
Infection control
 Times

• Hand wash  15secs

• Flushing waterlines / ultrasonic  20 - 30 secs
 Routes of transmission
1. Direct contact
• Via  infected person

2. Indirect contact
• Via fomite  clothing, instrument, furniture

3. droplets/aerosols
• Via air

4. Parenteral contact
• Needle stick injury  i/v, i/m, s/c
1. Hepatitis  all in above slides

2. HIV
• 0.3 %  risk of transmission
• RNA virus
• Diagnosed when  HIV antibodies found in blood after elisa test
• No vaccine
• Post-exposure prophylaxisis  anti-virals
3. TB
• Active tb  easily transmission  through nuclei inhalation
• History of travel outside the usa
• Active tb  not seen for elective dental care
• In emergency  take precautions
• Health workers should have tuberculin test once / year

Diagnosis
• Symptoms  cough, night sweats, ulcer on tongue
• Sputum culture
• Chest xray  cavitation in lungs
• +ve tuberculin skin test
 Personal protective equipment (PPE)
Gloves
• Latex  when touching contaiminated
• Utility  used to wash & rinse instruments & cloths during sterilization
(not used in surgery / procedures)

Masks
• Per / pt

Protective glasses
• Dentist at most risk for eye injury

Gowns
• Per / day
 Occupational safety & health administration (OSHA)
• Concerned about everything inside the office

• Protect the health porefessional from the occupational hazards

• All workers mus be offered  free HBV vaccines
• Needle stick injury  report, evaluation, follow up (paid by
employer)
• Cloths worn at work can not be washed at home
• Hazard communication standard  HAZCOM
 Environmental protection agency (EPA)
• CONCERNED ABOUT EVERYTHING OUTSIDE THE OFFICE

• Established maximum exposure levels for mercury vapours  0.1

microgram / kg body weight

• Regulates the transporation of dental waste outside the office

• Requires  <500ml of heterotrophic bacteria per ml of

water
 Sterilization

• Destruction of all life forms including the bacterial, viruses & spores

1. Glutaraldehyde
• Bath in cold solution
• For heat sensitive items  rubber, plastice
• Take long time

2. Pressure sterilization / autoclave

• 121 degrees at 15 psi for 20mins
• Moist heat destroys bacteria by  denaturation of proteins
• Biological monitors  test strips containing spores to test
effectivenessof autoclave (every week)
• Process indicators  strips, change colour when specific conditions
3. Dry heat sterilization
• No mositure
• Only heat
• 160 degrees for 60mins
• Only  glass & metal instruments
• Destroys bacteria by  coagulation of proteins
• Best preservation for  cutting edges(no dull), does not
corrode

4. ethylene-oxide
• Low temp
• Penetrate materials to sterilize
• Pre-packed materials  PSP plates
•
 Disinfection
• Spores not destroyed in this
• TB is destroyed in this
• Letting it sit for  10mins
 Antiseptic
• Used on living tissue  reduce bacterial load
1. Alcohol
• Denaturation of proteins
• Most common

2. Chlorhexadine (CHX)
• Substanivity - contious effects

3. Detergents
• Help loosen & remove microbes from surface with rinsing

4. Quatnary ammonium compounds (quats)

• Most potent
• Disrupts cell membrane
• Lethal to wide organisms
 Waste disposal
1. Sharps bin / red plastic container
• For sharp items  blades, needles

2. infectious waste
• Gloves, gauze, gowns, infected tooth
• Disposed in  separate waste bins marked as biohazard

3. non-infectious wastes
• Not infected with saliva or blood
• Plastic covers on operatory chairs
• Cups
• Bibs
 Spaulding classification system
Critical
• Contacts  soft tissue or vasculature
• Requires  sterilization
• Anything that penetrates / or contaiminated by blood

Semi-critical
• Contacts  mucosa
• Requires  high level disinfection or sterilization if heat stable
• Mouth mirror, twezzers

Non critical
• Contacts  skin
• Requires  disinfection
Material &
equipment
safety
 Mercury
• Inhalation is the  biggest risk

If spilled in the clinic

• Use  special vaccume system
• Then apply  sulphar powder on floor

Acute mercury toxicity

• Muscle weakness (hypotonia)
• Loss of hair (alopecia)
• Weigh loss
• Gi disorders
• Exhausion
 Airborne particles
Splatter / spatter
• Visible  >50 μm
• Fall with in  3 meter
• Can carry blood-borne pathogens

Aerosols
• Invisible  < 50 μm
• Remain floating in air for hours
• Carry on respiratory infection (small nuclei’s)  tb
 Noise control
• Hearing loss develops slowly overtime
• Can be caused by  > 90 dB
 Water lines
• Requires  <500ml of heterotrophic bacteria per ml of
water
• Not recommended to flush lines at the beginning of clinic 
makes no difference

Anti-retraction valves
• Prevent the retraction of fluid from the patient to the handpiece &
water spray hose  Which can passed on to next pt
 Material safety data sheet (MSDS)
• Manual Made by the manufacturer that details the hazards or
particular chemicals & how to deal with spills
• Made & prepared by the manufacturer  provided to the staff by
the employer

National fire protection association colour & number system

• Blue  health hazard
• Red  fire hazard
• Yellow  reactivity of the chemical (instability)
• White  required PPE (any other in white) (specific)

• Numbers  0-4 (least to most dangerous)

Insurance terms
& health care
system
 Terms
• Beneficiary  person with insurance
• Benefactor  insurance company
• Benefits  wht are the benefits  covered in the insurance

• Premium  montly payment to the company

• Copayement  fixed amount u pay when see a doctor
• Deductible  amount u pay before the insurance is used or starts
covering
• Coinsurance  % of the charge u pay
• Out of pocket maximum  most u pay out of pocket until the
insurance covers 100%
 Third party payers
• Insurance companies
• When third party negotiated the payement b/w first 2

Usual, customary & reasonable (UCR)

• Reasonable fees based on the geographical location

Table of allowance
• Lists a maximum amount a plan will pay for the each procedure,
but allows dentist to charge more if they want

Fee schedule
• The amount the dentist has agreed on and insurance will pay in
full
 Payment plans
Fee for service
• Amount paid / procedure or service
• Leading payer for dental treatment

Capitation plan (HMO)

• Per capita = flat fee for each pts seen
• Value of service is more then the payment = loss
• Value of service less the the payment = gain

Sliding scale fee

• Cost of treatment adjusted based on the pts income & ability to pay

Balanced billing
• Dentist charges the pt the remaining fee b/w the total fee & wht the insurance covered /
paid

Propective reimbursment
 Fraud
Unbundling
• Seperating of the dental procedure into its component part
• Sending to insurance  alag alag kr k
• Doctor commiting the fraud

Bundling
• Combining of the distinct dental procedures
• Eg:- crown buil-up & placing crown
• They both are different procedures and should be charged alag
alg but insurance says its counted 1 as it is done to place the
crown
• Insurance in comiting thr fraud
Upcoding
• Reporting a more complex or higher cost procedure than that was done
• Eg:- done pulpotomy but reported RCT
• Dentist resposnible

Down coding
• Changing a procedure code from higher cost to lower cost than what was
reported
• Eg:- did 3 surface composite but they changed it to 1 surface composite
• Insurance company responsible

Overbillling
• Charging more then ethically or legally acceptable
• Dentist said crown cost 500 but insurance paid 400 and dentist then
waived 100 but did not report it to the insurance company
US health
care
Managed care
1. Health maintanence organization
• Prepaid health plan
• Private insurance option for health or dental insurance coverage
• Made of gorup of medical insurance providers who work on specific plans
• Dentist are in contract with them and work on  capitation plan

2. Preferred provider organization (PPO)

• Subscription based plan
• Providers contract with employer or insurance company to provide services
in less amount
• Less then usual fees and higher volume of pts

Dental managed care

• Open panel  can see any pt
• Closed panel  can only see pt members of the managed care organization
 Department of health and human services (HHS)
• Principle agency of us government protecting the health of all
americans
• Suspected health abuse in elders  reported to HHS
• All the remaining agencies are division of hhs

1. Adminitration for children & families (ACF)

• Head start  provides comprehensive early childhood education,
health, nutrition
• Parental involvment services to low income families & children
 Centers for medicare & medicaid services (CMS)
• GOVERNS  HIPPA

Medicare
• For elderly  65 & elder (or with disabilitys)
• Does not cover dental care
• Only covers if needed for health  eg:- extraction before radiation therapy

Medicaid
• Joint federal & state programme
• For people with low income  poor

• Early periodic screening diagnostic & treatment (EPSDT)  requires state to take
action to ensure that children under 21 can access care
CHIPS  children health insurance programme
• Children whose families income is high for medicaid but low for
private insurance
Health resources & services administration
(HRSA)
National health service corps (NHSC)
• Provides loan repayment for health professional who work in
under-served communities

Ryan white care act

• Provides funds for medical & health care for people with 
hiv/aids
 Centers of disease control & prevention (CDC)
• Provides oral health survillence, dental infection control,
community water fluoridation, cancer & tobacco realted issues, &
support for state oral health programmes
• Community level
• Epidemiology
• Disease prevention
• Health awareness
 Food & drug administration (FDA)
• Evaluate food, drugs & medical devices  efficacy & safety
 Indian health servcie
• Improves health status of american indians & alaska natives
•
 National institute of health (NIH)
• BIOMEDICAL & PUBLIC HEALTH RESEARCH
 Agency for healthcare research & quality (AHRQ)
• Quality & access to care research

• Quality  assessment, assurance