ACUTE GINGIVAL LESIONS

1. INTRODUCTION

2. CLASSIFICATION:-

- Manson’s classification

3. VARIOUS TYPES OF ACUTE GINGIVAL LESIONS

- epidemiology and prevalence

- etiology

- Predisposing factors

- Clinical features

- Histopathology

- Treatment

4. SUMMARY

5. REFERENCES:-
INTRODUCTION

Acute lesions are by definition of sudden onset limited duration

and with well defined clinical features, by contrast with chronic

gingivitis which frequently not painful, Acute gingival lesions are

usually easier to diagnose. There are some pathological conditions

that can affect other parts of oral Mucosa, as well as gingivae, which

is impossible to classify because a etiology is uncertain e.g. erythema

Multiforme, or because they may be chronic with Acute episodes e.g.

fungal conditions, syphilis, T.B. may occasionally involve the gingiva

but lesions are widespread involving many parts of mouth.

ACUTE NECROTISING ULCERATIVE GINGIVITIS

SYNONYMS

- ulcero membranous gingivitis

- ANUG.

- Vincent’s gingivitis

- Vincent’s gingivo stomatitis.

- Necrotising gingivostomatitis.

- Trench Mouth (Pickard 1973, Johnson and Engel 1986, Noming

and Cohen 1995)

Vincent first described the mixed fusospirochetal microbiota of the so

called ‘Vincent’s Angina’ characterized by Necrotic Areas in the

tonsils (Vincent 1989)

Acute Necrotising ulcerative gingivitis is a distinct and specific

disease. This disease entity has been described as far back as the

days of Hippocrates is known by many synonyms such as Trench

Mouth, Vincent’s Disease and Vincent’s gingivo stomatitis. With the

advent of Antibiotics and with improved Nutritional status the

incidence has decreased and even become extinct in developed

countries. However with the increasing incidence of severe immune

deficiency states such as AIDS the lesion has become more well

recognized and often encountered in developed countries.

In developing countries ANUG remains a commonly diagnosed

clinical lesions. This is because of the existing poor nutritional status;

stressful living conditions, poor oral hygiene. In recent years there

has been increasing recognition for the need to further study ANUG;

particularly in a view of its contribution to the incidence of cancrum

oris – which has been described as a “neglected third world disease”

children in sub- Saharan Africa.

History:- ANUG is a condition that was described as far back as the

4th century B.C by Xenophon. It was 1st described among Greek

soldiers and was characterized by sore mouth and foul smelling

breath.

- John Hunter in 1778 described the clinical features of the

condition and differentiated it from scorbutic gingivitis

- ANUG was seen as epidemic in the French army during the 19 th

century.

- In 1890 plant and Vincent attributed its origin to fusiform Bacilli

and Spirochetes. Terms included Trench mouth, Vincent’s

infection, Vincents stomatitis, spirochetal gingivitis, ulcerative

gingivitis, acute ulcero membranous gingivitis.

Epidemiology and Prevalence:-

- ANUG often occurs in groups in an epidemic pattern.

- Prevalence of NUG appears to have been rather low in U.S.A.

and Europe before 1914. During the World I and II numerous

‘epidemics’ broke out among the Allied troops, but German

soldiers did not seem to have been similarly affected.

- In a study conducted at a dental clinic in Prague, Czech

Republic, following incidence of NUG was reported

0.08% - Between 15 & 19

0.05% - Between 20 & 24

0.02% - Between 25 & 29 (skach et al 1970)

 - NUG occurs in all ages with highest incidence reported between

20 and 30 (Smith et al 1932) and ages 15 and 20 (Skach et al

1970)

- It has been reported in children from low socio economic groups

in underdeveloped countries (Jimener et al 1975)

- NUG is more common in children with down syndrome than in

children with mental deficiencies (Brown et al 1973)

- During World war II upto 14% of the Danish military personnel

encountered NPD (Puidborg 1951)

- In 1960’s NPD was found in 2.5% of 326 U.S students during the

1st college year, but over the next year more students became

affected, with a total of 6.7% demonstrating the disease during

the 1st 2 college years (Gidson 1964)

CLASSIFICATION

According to Manson

a) Traumatic lesions of gingiva

- Physical Injury

- Chemical Injury

b) vlral Infections

- Acute herpetic gingivo stomatitis.

- Herpangina (a disease caused by Cox sackie)

 - Hand foot and Mouth Diseases.

- Measles.

- Herpes varicella/zoster virus infections

- Glandular fever.

c) Bacterial Infections:-

- ANUG

- Tuberculosis

- Syphilis.

d) Fungal Diseases

- Candidiasis.

e) Gingival abscess

f) Apthous ulceration.

g) erythema Multiforme.

h) Drug allergy and contact hypersensitivity.

Pathogenic potential of microorganism:-

Bacteria can invade epithelium (Heylings et al 1967).

Spirochetes can invade the vital connective tissue (listgarten 1965).

The pathogenic potential is further substantiated by the fact that both

fuso bacteria and spirochetes can liberate endotoxins (Mergenhagen

et 1961, Hofslad 1970) This may be by Direct or Indirect effect.

Indirectly – endotoxcins can contribute to tissue damage in several

ways –

1. They can function as Antigens and elicit Immune Response.

2. They can activate complement directly through the alternative

pathway and thereby liberate chemotoxin, but they also can

activate macrophages, B & T lymphocytes and influence the

hosts immune reactions by interfering with cytokine produced

by these cells.

Definition:-

1. Necrotizing ulcerative gingivitis is inflammatory destructive of the

gingiva, which presents characteristic signs and symptoms.

2. ANUG is a disease with rapid onset characterized by painful,

necrotic, ulcerative gingival lesions.

a) Etiology:-

i) The Role of Bacteria:-

- NUG is caused by specific Bacteria, namely a fusiform Bacillus

and spirochaetal organism (Plaut 1894 & Vincent 1896)

- Rosebury (1950) and colleagues described a fuso spirochetal

complex consisting of T.Microdentium, intermediate

spirochetes, vibrios, fusiform Bacilli, filamentous organisms, in

addition to several Borellia species.

 - Loesche et al 1982 described a predomint flora and variable

flora associated ANUG. Constant flora is composed of provotella

intermedia, in addition to fuso bacteria, treponemas and

selenomonas species.

The variable flora consists of heterogeneous ray of Bacterial

types.

- Chung et al 1983 found increased Immunoglobulin (IgE and IgM)

antibody titers for intermediated size spirochetes and prevotella

intermedia compared with titers in those with chronic gingivitis

and healthy controls.

- Cogen et al 1983 described a depression in host defense

mechanism, particularly in PMN chemotaxis and phagocytosis.

ii) Local predisposing factors:-

- Pre-existing gingivitis:- It may also occur in disease free

mouths. It always occurs superimposed on preexisting chronic

gingival Disease and periodontal pockets.Deep periodontal

pockets and pericoronal flaps are particularly vulnerable areas

because they offer a favorable environment for the proliferation

of anaerobic fusiform Bacilli and spirochetes hence called

Incubation Zones.

- Areas of gingiva traumatized by opposing teeth in malocclusion,

such as palatal surface behind the maxillary incisors and labial

 gingival surface of the mandibular incisors are frequent sites of

NUG.

- Pindborg et al 1951 & Goldhaber 1957 reported that 98% of the

patients with NUG were smokers and that the frequency of this

disease increase with an increasing exposure to tobacco smoke.

b) Debilitaling Disease:-

This may predispose the development of NUG. These disease

include chronic diseases such as syphilis and cancer, severe GIT

disturbances like ulcerative colitis. Blood dyscrasias like leukemia

(Bregman et al 1992) AND aids (Drinkard et 1991, Glick 1994,

Horning 1995)

- Nutritional deficiency resulting from debilitating disease may be

an additional predisposing factor.

Mechanism:-

Psychosomatic factors:

- The disease often occurs in association with stress situations

e.g. induction into armed forces or school examination (Giddon

et al 1964) as well as increased adrenocortical secretion.

(Shannon et al 1964) are common in ANUG patients.

Mechanism of Action:- According to cohen-cole et al 1983. Cohen

and coworkers have suggested that a psychiatric disturbance may

lead to activation of the hypothalamic pituitary adrenal axis. This

results in elevation of serum and urine cortisol levels, which is

associated with a depression of lymphocyte and

polymorphonuclear leukocytes function that may predispose to

acute necrotizing ulcerative gingivitis.

Other Mechanism:-(Kardachi & Clarke 1974) – stress could reduce

Blood flow to the gingiva arteriorles, stimulated by the sympathetic

Nervous system CLINICAL FEATURES:- It often occurs as an acute

episode; it under goes a diminution in severity leading to sub Acute

stage with milder clinical symptoms.

- Disease may subside spontaneously without treatment. Such

patients generally have history of repeated remissions and

exacerbations. Recurrence in this is frequent.

Oral Signs:-

- lesions are punched out crater like depression at the crest of the

interdental papillae, subsequently extending into marginal

gingival and rarely to attached gingiva and oral mucosa.

- Surface of gingival craters in covered by a gray

pseudomembranous slough, demarcated from the remainder of

the gingival mucosa by a pronounced linear erythema

- In some instance, the lesions are demarcated of the surface

pseudomembrane, exposing the gingival margin, which is red,

shiny and haemorrhagic.

 - Spontaneous gingival hemorrhage or pronounced bleeding on

the slightest stimulation.

- Fetid odor

- Increased Salivation.

Symptoms:-

- Lesions are sensitive to touch.

- Constant radiating, gnawing pain which is intensified by eating

spicy or hot foods and chewing.

- Metallic foul taste,

- Pasty saliva.

Extraoral and systemic signs and symptoms:-

- Local lymphadenopathy.

- Slight elevation in temperature.

- Marked systemic complications like high fever, increased pulse

rate, leucocytosis, loss of appetite and general lassitude.

- Insomnia.

- Constipation

- GIT disorders.

- Headache

- Mental depression.

- In rare cases, severe sequel such noma or gangrenous

stomatitis have been described (enwon et al 1972)

CLINICAL COURSE:-If untreated, NUG may lead to NUP with a

progressive destruction of the periodontium and denudation of the

roots.

A) Pindborg et al 1966 have described the following stages in

progress of NUG.

i. only the tip of the interdental papilla affected.

ii. lesion extends to marginal gingiva and causes punched out

papilla

iii. Attached gingiva is affected

iv. Bone is exposed.

B) Horning and cohen et al 1995 extended the staging of these oral

necrotizing disease as follows.

Stage 1 – Necrosis of tip of the interdental papilla 93%

Stage 2 – Necrosis of the entire papilla (19%)

Stage 3 – Necrosis extending to gingival Margin (21%)

Stage 4 – Necrosis extending also to the attached gingiva (1%)

Stage 5 – Necrosis extending into buccal or labial mucosa (6%)

Stage 6 – Necrosis exposing alveolar Bone (1%)

Stage 7 – Necrosis perforating skin of check (0%)

Stage 1 is NUG
Stage 2 may be either NUG or NUP because attachments loss have

occurred.

Stage 3 & 4 are NUP

Stage 5 & 6 are necrotizing stomatitis.

Stage 7 is Noma.

Histopathology:-

- it involves both stratified squamous epithelium and underlying

connective tissue.

- The surface epithelium is destroyed and is replaced by a

meshwork of fibrin, necrotic epithelial cells, PMN’s and various

types of microorganisms.

- The underlying connective tissue is markedly hyperemic, with

numerous (excess of blood in a part) engorged capillaries and

a dense infiltration of PMN’s.

Relation of Bacteria to lesions:-

List garden – 1965 described the following 4 zones which blend with

each other and may not all be present in every case.

Zone 1 :- Bacterial Zone, the most superficial, consists of varied

Bacteria, including a few spirochetes of the small, medium and large

types.

Zone 2:- Neutrophil Rich zone contains numerous leukocytes many

spirochetes of various types, between the leucocytes.

Zone 3:- Necrotic Zone consists of disintegrated tissue , fibrillar

material, remnants of collagen, and numerous spirochetes of the

medium and large types with few other organisms.

Zone 4 :- Zone of spirochetal Infiltration:-

Consists of well preserved tissue infiltrated with medium and large

spirochetes, without other organisms.

Bacterial flora showed that swears from the lesions present scattered

Bacteria, predominantly spirochetes and fusiform Bacilli,

desquamated epithelial cells and occasional PMN’s.

electron microscopic study showed that spirochetes may be classified

into small (7% to 39% of the total spirochetes),Medium (43.9% to

90%) and large (0 to 20%). (Listgarten et al 1967). It was also

suggested that medium sized spirochetes are present in greater

numbers in pooled scrapings from lesions of NUG and are found in

greater percentage in deeper portion of the lesions.

Treatment:

1. Non Ambulatory patient – With symptoms of generalized

systemic complications.

2. Ambulatory patient – With no serious systemic complications

1. Treatment for Non Ambulatory Patients

Day 1
a. Local treatment limited to gently removing the necrotic

pseudomembrane with a pellet of cotton saturated with hydrogen

peroxide [H2O2.]

b. Advised bed rest and rinse the mouth every 2 hours with a

diluted 3% hydrogen peroxide [H2O2.]

c. Systemic antibiotics like penicillin or metronidazole can be

prescribed.

Day 2

a. If condition is improved, proceed to the treatment described

for ambulatory patients. If there is no improvement at the end of

the 24 hours, a bedside visit should be made. The treatment

include again gently swab the area with hydrogen peroxide,

instructions of the previous day are repeated.

Day 3

a. Most cases, the condition will be improved, start the

treatment for ambulatory patients.

2. Treatment for Ambulatory Patients

1st visit

A topical anesthetic is applied and after 2 or 3 minutes the

areas are gently swabbed with a cotton pellet to remove

pseudomembrane and non attached surface debris. After the

 area is cleansed with warm water the superficial calculus is

removed with ultrasonic scalers. Patients with moderate or

severe necrotizing ulcerative gingivitis and local

lymphadenopathy, are placed on antibiotic regime of penicillin

500 mg thrice daily, for penicillin sensitive patients

erythromycin or metronidazole 200mg or 400mg twice daily for

seven days.

Sub gingival scaling and curettage are contraindicated at this

time because of possibility of extending the infection to deeper

tissues.

Instruction to the patient :

1. Avoid smoking, alcohol.

2. Rinse with 3% hydrogen peroxide and warm water for every two
hours.
3. Confine tooth brushing to the removal of surface debris with
a bland dentifrice, use of interdental aids and chlorhexidine
mouth rinse are recommended.
2nd Visit
Scalers and curettes are added to the instrumentarium,
shrinkage of the gingiva may expose previously covered calculus
which is gently removed. Same instructions are reinforced.
3rd Visit
Scaling and root planing are repeated, plaque control
instructions are given. Hydrogen peroxide rinses are discontinued.
4th Visit
 Oral hygiene instructions are reinforced and thorough scaling
and root planing are performed.
5th Visit
Appointments are fixed for treatment of chronic gingivitis,
periodontal pockets and pericoronal flaps and for the elimination
of all local irritants.
Patient is placed on maintenance programme.

Further Treatment consideration:-

1. Gingivoplasty:- If teeth are irregularly aligned healing

sometimes results in formation of shelf like gingival margin,

which favors the retention of plaque and recurrence of gingival

Inflammation. This can be eliminated by gingivoplasty or

electro surgery.

2. Surgical procedures:- Tooth extraction or periodontal surgery

should be postponed until 4 weeks after the acute signs and

symptoms of NUG have subsided. If emergency Rx is required

prophylactic chemotherapy with systemic penicillin.

3. Role of drugs:- Escharotic drugs such as phenol, silver nitrate

and tannic acid should not be used. They are Nercotizing

Agents that alleviate the painful symptoms by destroying the

nerve endings in the gingiva. They also destroy the young cells

necessary for repair and delay healing. Their repeated use

results in loss of gingival tissues.

 4. Systemic Antibiotics:- Only in patients with toxic systemic

complications.

5. Supportive systemic treatment:-

- copious fluid consumption

- Analgesics

- Bed rest.

6. Nutritional supplements:-

- Vitamin B and C.

Primary Herpetic Gingivo Stomatitis.

It is a viral infection of the oral cavity caused by the herpes

simplex virus type 1 (HSV 1). It occurs most often in infants and

children younger than 6 years of age (Scott et al 1941) but it is also

seen in adolescents and adults. It occurs with equal frequency in

male and female patients.

C/F

Oral signs:-

- It appears as a diffuse, shiny erythematous involvement of the

gingiva and the adjacent oral mucosa with varying degrees of

edema and gingival Bleeding.

- In its initial stage it may appear as discrete, spherical gray

vesicles dispersed in different areas. E.g. labial and Buccal

 Mucosa, soft palate, pharynx and tongue. After approximately

24 hours the vesicles rupture and form painful small ulcers with

a red, elevated halo like margin and a depressed yellow, and

grayish white central portion.

- Diffuse, edematous, erythematous enlargement of the gingiva

with a tendency towards bleeding is seen.

- Course of the disease is 7-10 days. The diffuse gingival

erythema and edema that appear early in me disease persist for

several days after ulcerative lesions have healed. Scarring does

not occur in the areas of healed ulceration.

Oral symptoms:-

- Generalized soreness of the oral cavity which interferes with

eating and drinking.

- The ruptured vesicles are sensitive to touch, thermal changes

and foods.

Extra Oral and systemic signs and symptoms:-

- Involvement of the lips, face (herpes labialis, cold sore) with

vesicles and surface scale formation may accompany the intra

oral disease.

- Cervical Adenitis, fever as high as 101 – 105 F and generalized

malaise are common.

History:-

The condition frequently occurs after a episode of febrile

disease such as pneumonia, meningitis, influenza and typhoid. It also

tends to occur during periods of anxiety, strain or exhaustion.

Location of the virus is in the gasserian ganglion. The virus may

descend to the lip through the trigeminal nerve, which may explain

why the location of the blister on the lip is usually seen.

Histopathologic:-

- Epithelium of gingiva is thinned out or atrophied due to

Balloning degeneration. The virus targets the epithelial cells.

Balloning degeneration consists of acantholysis, nuclear clearing

and nuclear enlargement. These cells are called Tzanck cells

- Vesicles formed rupture to form a discrete ulceration, which

appears to have a central portion of acute inflammation

characterized by ulceration and varying degrees of purulent

exudates, surrounded by a zone rich in engorged blood vessels.

- Vesicles characterized by extra and intra cellular edema and

degeneration of epithelial cells.

- Smear taken from fluid shows under election microscope the

presence of intra nuclear virus particles - Lip schutz Bodies.

 There are round esinophilic inclusion Bodies are found in nuclei

of epithelial cells.

Diagnosis:-

- Patients history and clinical findings. Laboratory diagnosis include

a. Direct smear:- Material is obtained from the base of the lesions

and smeared and stained. Presence of multi nuclear giant cells,

containing intra nuclear eosinophilic inclusion Bodies. However

this cannot distinguish from other infections like CMV, varicella

zooster virus.

b. Innoculation of the virus from a suspected site, to tissue

culture.

c. Virus can be determined by an election microscopic

examination and specific HSV Antigens can be detected in cells

from the lesions by Immuno florescence.

Treatment Various medications have been used in the

treatment of this condition including;

Local applications – using 8% zinc chloride, Talbot’s iodine, phenol,

riboflavin, thiamine etc. Chlortetracycline (aureomycin) has

been successfully used as a mouthwash applied topically in a

3% ointment or administered systemically in the form of 250mg

capsules

Palliative treatment – makes the patient comfortable until the

disease runs its course (7-10 days).

Plaque food debris and superficial calculus are removed to reduce

gingival inflammation.

Relief in pain is obtained with diclonine hydrochloride – a topical

anesthetic mouth wash, which is available in a 0.5% solution

that maybe diluted 1:1 with water.

Supportive treatment: Copious fluid intake and systemic

antibiotic therapy for management of toxic systemic

complications. For relief of pain, systemically administered

aspirin is usually sufficient.

Pericoronitis

Definition: It is an acute infection which refers to inflammation of

gingiva and surrounding soft tissues of an incompletely erupted

tooth. It occurs most frequently in the mandibular third molar

area.
Types- Acute, sub acute or chronic.

Clinical features:
Signs and symptoms: Include markedly red, edematous
suppurating lesion that is extremely tender with radiating pain to
the ear, the throat and floor of the mouth.The patient is extremely
uncomfortable because of the foul taste and inability to close the
jaws. In addition to the pain, swelling of the cheek in the region of
the angle of the jaw is seen.

Acute pericoronitis: It is identified by varying degrees of involvement

of pericoronal flap as well as with systemic complications. An

influx of inflammatory fluid and cellular exudates results in

an increase in bulk of the flap which interferes with complete

closure of the jaws. The flap is traumatized by contact with

the opposing jaw and inflammatory involvement is

aggravated.

Lymphadenitis is a common finding; the patient may also have

toxic systemic complications such as fever, leukocytosis and malaise.

Complications

 The involvement may become localized, in the form of

pericoronal abscess.
 If it occurs in a partly erupted vital tooth it may give rise to
cyst formation.
 It may spread posteriorly into the oropharyngeal area and
medially into the base of the tongue, making it difficult for the
patient to swallow.
 Depending on the severity there is involvement of the
submaxillary, cervical, deep cervical and retropharygeal lymph
node.
 Peritonsillar abscess formation, cellulitis and Ludwig’s angina
are infrequent but nevertheless potential sequelae of acute
pericoronitis.

Treatment:The treatment of pericoronitis depends on:

 Severity of the inflammation .

 The systemic complications and ,

 The advisability of, retaining the involved tooth .

First visit

1. The area is gently flushed with warm water to remove

superficial debris and exudate followed by application of topical

anesthetic agent.

2. The flap is reflected with a scaler and the underlying debris is

also removed and the area is flushed with warm water.

3. Instructions to the patient include hourly rinses with a solution

of a tea spoonful of salt in a glass of warm water, rest, copious

fluid intake and administration of systemic antibiotics, if toxic

symptoms are present.If the gingival flap is swollen and

fluctuant an anteroposterior incision to establish drainage is

 made with a No. 15 bard parker blade, followed by insertion of

¼ inch gauze wick.

In the next visit, determination is made as to whether the

tooth is to be retained or extracted . This decision is governed by

the likelihood of further eruption into a good functional position.

If it is decided to retain the tooth, the necessary surgical

procedures are performed using a periodontal knife or electro

surgery. Under anesthesia, a wedge shaped incision is made to

section a tissue that includes the gingival flap with the tissue

distal to the involved tooth as well. After the tissue is removed, a

periodontal pack is placed.

SUMMARY:-

1. Acute gingival lesions are classified as acute necrotizing

ulcerative gingivitis (ANUG) primary herpetic gingivostomatitis,

and pericoronitis.

2. ANUG is an inflammatory, destructive disease of the gingiva,

which presents with characteristic signs and symptoms.

3. Oral lesions are characterized by punched-out, crater like

depressions at the crest of the Interdental papillae,

subsequently involving marginal gingiva and rarely attached

gingiva.These craters are covered by greyish

pseudomembraneus slough.Patients with ANUG complain of a

 constant radiating, gnawing pain and metallic taste with

excessive amount of pasty saliva.

4. Etiological factors responsible for ANUG are divided into :

- Role of bacteria (fusospirochetal complex)

- Local predisposing factors like pre existing gingivitis, injury to

the gingiva and smoking.

- Systemic predisposing factors like nutritional deficiency,

debilitating diseases and psychosomatic factors

5. Primary herpetic gingivostomatitis is a viral infection

characterized by diffuse erythema and vesicular eruptions.

6. Pericoronitis is an acute infection, which refers to inflammation

of the gingiva and the surrounding soft tissues of an

incompletely erupted tooth. (Mostly in mandibular III molar

area).

REFERENCES

1. J.D. Manson & Bmeley, Outline of Periodontitis, Third Edition

2. Yoji Murayama, Hidemikurihara and Thomas E. Van Dyke,

Acute Necrotizing Ulcerative Gingivitis, Risk Factors involving

Host Defense Mechanisms, Periodontol 2000, Vol. 6, 1994.

3. Loesche WJ, Syed SA, Langhorn BE. The bacteriology of

acute necrotizing ulcerative gingivitis. J. Periodontol, 1982: 53:

223.
4. Carranza and Newman, Clinical Periodontology W.B.

Saunders, 9th Edition.