Acute Ging Lesions

8/12/2019 Acute Ging Lesions

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INTRODUCTION

ACUTE LESIONS.sudden onset, limited duration and with well-

defined clinical features;

There are some pathological conditions that can affect the oral mucosa,

including the gingiva, which are impossible to classify precisely either because

the etiology is uncertain, e.g. erythema multiforme, or because they may be

chronic with acute episodes, e.g., the fungal disease candidosis, gonorrhoea, &

other infectious disease

But the lesions are widespread, involving many parts of the mouth as well as

other parts of the body.


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GINGIVAL LESIONS TO BE DESCRIBED ARE:

1) Traumatic lesions, both physical and chemical.

2) Acute necrotizing ulcerative gingivitis.

3) Acute herpetic gingivo stomatitis.

4) Candidiasis.

5) Gingival abscess.

6) Aphthous ulcers.

7) Drug allergy and contact hypersensitivity.

8) Pericoronitis.


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TRAUMATIC LESIONS Physical injury can be mechanical or thermal.

A carelessly used tooth brush or a sharp piece of food such as fish- bone, hot

food or drink are the most common cause of injury.

Occasionally the cause is more bizarre, E.g., a cigarette burn, a pencil pushed

into the mouth, a hair- grip, a musical instrument.

Chemical causesof damages include aspirin , escharotics such as silvernitrate, even hydrogen peroxide solution used too strong and too frequently.

Careless use of a caustic by the dentist, e.g., phenol, trichloracetic acid.


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TRAUMATIC LESIONS

TREATMENT : Frequently the wound heals without any active intervention. The patient should avoid irritant foods or hot drinks.

Rinsing with cold water or a very dilute saline solution might be soothening.

Strong antiseptic should be avoided.

Troches containing a topical anaesthetic, e.g. Benzocaine lozenge, can berecommended and some analgesic such as aspirin or paracetamol prescribed.

If the cause of the injury is still there, e.g. a fish bone, it should be removed as

gently as possible.

If there is secondary infection, an antibiotic should be prescribed.

It can be helpful to protect the wound with a bland dressing such as

carboxymethyl cellulose gelatin paste (ora base) which is spread gently over

the wound several times a day.


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ACUTE NECROTIZING ULCERATIVE

GINGIVITIS

Acute necrotizing ulcerative gingivitis (ANUG) is an inflammatory

destructive disease of the gingiva, which presents characteristic signs and

symptoms.


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HISTORY

Because of the description by Vincent of the organisms associated with the

disease it is also called as Vincent's infection. It may vary from an acute reaction with painful ulcerative, necrotic and

membranous lesions, to chronic infections with few symptoms.

In the 1890 Plaut and Vincent suggested that it was caused by a

fusospirochetes.

It was recognized as far back as the fourth century B.C. by Xenophon who

mentioned that Greek soldiers were affected with sore mouth and foul

smelling breath.


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In 1778 John Hunter described the clinical findings and differentiated it from

scurvy and chronic destructive periodontal disease.

In 1886 Hersch discussed some of the feature associated with the disease,

such as enlarged lymph nodes, fever, malaise and increased salivation.

During world war I, it was important because of its high prevalence among

soldiers. It was known as trench mouth, and was considered contagious. Today although the condition is no longer considered communicable, the

pathogenic mechanism are still some what unclear, since ANUG is a complex

disease and not a simple infectious process.


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ACUTE NECROTIZING ULCERATIVE

GINGIVITIS Other terms for this condition include

Vincent's infection,

Stomatitis ulcerosa,

Acute ulcero membranous gingivitis.

Trench mouth, Putrid stomatitis,

Ulcerative gingivitis,

Fetid stomatitis,

Acute septic gingivitis,

Vincent's stomatitis,

Plaut vincent stomatitis,

Spirochetal stomatitis


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PREDISPOSING FACTORS

LOCAL: Pre- existing gingivitis, injury to the gingiva, and smoking are important

predisposing factors.

Deep periodontal pockets and pericoronal flaps are particularly vulnerable

areas for the occurrence of the disease.


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PREDISPOSING FACTORS SYSTEMIC PREDISPOSING FACTORS: NUTRITIONAL DEFICIENCY:Necrotizing gingivitis has been produced

by giving animals nutritionally deficient diets.

Animals receiving diets deficient in vitamin B. complex ..

Clinical observationsthat low vitamin intake or vitamin C deficiency..

ANUG.

DEBILITATING DISEASE: Debilitating systemic disease such as metallic intoxication, cachexia caused by

syphilis and cancer, severe gastro intestinal disorders such as ulcerative colitis,blood dyscrasias such as leukemias and anemia, influenza, the common cold,

and AIDS predispose to the development of ANUG.

Mayo and associates produced ulcero necrotic lesions in the gingival margins of

hamsters exposed to total body irradiation. These lesions could be prevented by

systemic antibiotics.


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Pindborg.98% percent of his ANUG patients were smokers and that the

frequency of this disease increases with an increasing exposure to tobacco

smoke.

It has not been established whether this correlation occurs because

(1) tobacco smoke has a direct toxic effect on the gingiva,

(2) vascular or other changes are induced by nicotine or other substances, or

(3) smoking and ANUG are both reflections of stress.

Iatrogenic. Over hanging margins of restorations, ill fitting crowns, inlays or

prosthetic appliances have also been reported to cause ANUG so also the

inadequate contact areas resulting from Dental caries or faulty restorations

and food impaction.


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PSYCHOSOMATIC FACTORS:Psychological factors appear to beimportant in the etiology of AN UG.

The disease often occurs in association with stress situations

Psychological disturbances as well as increased adrenocortical secretion, are

common is patients with the disease.

Significant correlation between disease incidence and two personality trails,

dominance and abasement, suggests the presence of an ANUG - prone

personality. The mechanisms where by psychological factors create or predispose to

gingival damage have not been established.


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Cohen - Cole and coworkers suggested that

Psychiatric disturbance and the impact of negative life events(e.g., anxiety, depression, psychopathic deviance and stress)

Activation of the hypothalamic pitutary ardrenal axis.

Elevation of serum and urine cortisol levels, associated with a depressionof lymphocyte and PMN function

Predispose to ANUG.


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CLINICAL FEATURES

The onset of acute forms of the disease is usually sudden, with a superficial

pressure type pain, tenderness, profuse salivation, a peculiar metallic tasteandspontaneous bleedingfrom the gingival tissues.

The patient commonly experiences a loss of the sense of taste, the teeth aresensitive to premature contact, thought to be slightly extrudedor to have awoody sensation.


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DIAGNOSTIC FEATURES

PRIMARY: 1) Interproximal necrosis and ulceration (punched out cratered papillae).

2) Painful gingivae with constant, radiating, gingival pain.

3) Bleeding (spontaneons on slight Provocation).


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DIAGNOSTIC FEATURES

SECONDARY: 4) Pseudomembranous.

5) Fever, malaise, Lymphadenopathy.

6) Fetid odor.

The first three are necessary for reliable diagnosis.

The rest are often present and are additional signs and symptoms but are of

themselves not diagnostic.


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DIAGNOSTIC FEATURES ORAL SIGNS: Punched out, crater like depressions at the crest of the interdental papillae,

Rarely covering the entire width of attached gingiva.

The surface of the gingival crater is covered by a gray,

pseudomembraneous slough.

In some cases, the lesions are denuded of the surface pseudomembrane

exposing the gingival margin, which is red, shiny and hemorrhagic.


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DIAGNOSTIC FEATURES

EXTRAORAL AND SYSTEMIC SIGNS AND SYMPTOMS: Patients are usually ambulatory.

Mild and moderate stages of the disease..local lymphadenopathy and a

slight elevation in the temperature.

Severe cases..marked systemic complications such as high fever, increased

pulse rate, leucocytosis, loss of appetite, generalised lassitude.

Systemic reactions are most severe in children.

These are insomnia, constipation, gastro intestinal disorders, headache.

In rare cases severe sequelae such as Noma or Cancrum oris, Peritonitis,

Toxemia, Fatal brain abscess, Septicemia, Even death may occur.


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SITE AND EXTENT OF INVOLVEMENT

Involvement may be limited to a single tooth or group of teeth or may be wide

spread throughout the mouth.

Involvement of the incisor region and third molar flaps seem to occur most

frequently.

Rare in edentulous mouths but isolated spherical lesions occasionally occur on

the soft palate.

It may spread to other parts of the oral mucosa and adjacent marginal

surfaces of the tongue.

Tonsils should always be examined, since these organs may be affected

ALTERATIONS IN TISSUE FORM WITH


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ALTERATIONS IN TISSUE FORM WITH

REPEATED ATTACKS Slight proliferation of the gingiva adjacent to the necrotic area may take

place.

Repeated attacks,..interdental tissue may become cratered.

When deep interdental craters occur and when roots are closely

approximated the septum may be lost resulting in the formation of a deep

cleft or reverse architecture.

Even when the disease process is arrested the deformity of revere architecture

may remain.

Such gingival and osseous deformities may require surgical correction.


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ANUG

CLINICAL COURSE: The clinical course is indefinite.

If untreated,.. ANUG may result in progressive destruction of the

Periodontium, denudation of the roots and increase in the severity of toxic

systemic complications.

It often undergoes a diminution in severity, leading to subacute stage with

varying symptoms.

The disease may subside spontaneously without treatment, such patients

generally have a history of repeated remissions and exacerbations.


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HISTOPATHOLOGY

Microscopically the lesion appears as a nonspecific acute necrotizing

inflammation at the gingival margin, involving both the st. squamous

epithelium and the underlying connective tissue.

Even in non ulcerated areas there is general lack of keratinization of gingivaltissues.

This is the zone that appears clinically as the surface pseudomembrane.


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HISTOPATHOLOGY

Schaffer using light microscopy, failed to find bacteria penetrating vitaltissues.

Listgartenon the other hand utilizing electron microscope was able toidentify spirochetes between viable epithelial cells.

The maximum depth of bacterial infiltration into the lamina propria ranged

from 155 to 144 microns from the nearest epithelial basal lamina.


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IMMUNOLOGIC FINDINGS

In ANUG both the cellular and humoral responses are affected.

Serum .patients with acute phase.elevated IgG and IgM antibody

titers to intermediate sized oral spirochetes and elevated IgG titers to P.

gingivalis & B. melaninogenicus

The histopathologic changes, the large no. of bacteria with in the tissues, and

the elevated levels of antibodies suggest the possibility of an immune complex

type of disease.

At a cellular level the patients have reduced PMN chemotaxis and

phagocytosis.

RELATION OF BACTERIA TO THE


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CHARACTERISTIC LESION

Light microscope: It appears that the exudate on the surface of the necrotic lesion contains

microrganisms that morphologically resemble cocci, fusiform bacilli and

spirochetes.



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CHARACTERISTIC LESION Listgarten. following zones (seen under electron microscope) which blend

with each other and may not all be present in every case. Zone I:Bacterial zone.most superficial,. consists of varied bacteria,

including a few spirochetes of the small, medium and large sized.

Zone II:Neutrophil rich zone .contains numerous leukocytes, mainlyneutrophils with bacteria, including many spirochetes of various typesbetween the leukocytes.

Zone III:Necrotic zone consists of disintegrated tissue cells, remnants ofcollagen fibers, fusiform shaped bacteria and numerous spirochetes of the

intermediate size and large types, with other organisms.

Zone IV:Zone of spirochetal infiltration consists of well preserved tissueinfiltrated with intermediate sized and large spirochetes with out other

organisms



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CHARACTERISTIC LESION

Bacterial Flora: Spirochetes have been found as deep as 300 microns from the surface. The mean fusiform bacillus count in the saliva of patients with ANUG is

higher than that in the saliva of normal persons.

Fusobacterium species account for the majority of the total fusiform bacilli in

both groups.


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DIAGNOSIS

Diagnosis is based on clinical findings. A bacterial smear may be used to confirm the clinical diagnosis, but it is not

necessary nor definitive, because the bacterial picture is not appreciably

different from that in marginal gingivitis, periodontal pockets, pericoronitis

or herpetic gingivostomatitis.

Microscopic examination of the biopsy specimen is not sufficiently specific to

be diagnostic.


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DIFFERENTIAL DIAGNOSIS

NUG should be differentiated from Acute herpetic gingivostomatitis, Ch.

periodontal pockets, Desquamative gingivitis, Streptococcal

gingivostomatitis, Diphtheritic lesions, Gonococcal gingivostomatitis,

Apthous stomatitis, Syphilitic lesions, Tuberculous gingival lesions,

Candidiasis, Agranulocytosis, Vincent's Angina, Dermatoses, Pemphigus,

Erythema multiforme and lichen planus.


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AGRANULOCYTOSIS: Is characterized by ulceration and necrosis of the gingiva resembling ANUG.

There is increase in agranulocytes.

Blood studies serve to differentiate between NUG and the gingival necrosis

in agranulocytosis.


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APTHOUS ULCERATIONS: Clinically they are fibrin covered ulcerations of varying size and surrounded

by a red halo, quick development and lymph nodes painfully swollen.

Etiology still unknown stress trauma may in some cases be eliciting factors.


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TUBERCULOUS GINGIVAL LESIONS: Infectious granulomatus disease

Caused by Mycobacterium tuberculosis.

Lesions of gingiva are secondary to pulmonary infection.

A break in the surface of the mucosal tissue is required for inoculation of

organisms carried in the sputum.

Hence frequently found in areas of trauma.

Tuberculous gingivitis is a unusual form which may appear as diffuse,

hyperemic, nodular or papillary proliferation of the gingival tissues.


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ANUG IN LEUKEMIA: ANUG may be superimposed on gingival tissue alterations caused by

leukemia.

Leukemia is one of the conditions that would have to be ruled out.

In some forms of leukemia especially acute necrotizing ulcers may occur in the

oral mucosa, apparently as an exacerbation of an existing chronic

inflammatory condition.


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THE ROLE OF BACTERIA


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Opinion still differ regarding whether bacteria are the primary causative

factor in ANUG.

Studies.One week of metronidazole treatment caused a prompt resolution

in clinical symptoms and significant reduction in the plaque flora following

the resolution of the infection.

This supports a role for the anaerobic species.

Attempts to transmit the disease from animal to another or to producenecrotic lesions in experimental animals have failed.

McDonald et al, (1956) found a combination of four different bacteria.



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Further experiments indicated that among the four, B. melaninogenicus was

the true pathogen. It may under certain conditions produce an enzyme which degrades native

collagen.

The large masses of Gram negative bacteria liberate endotoxins..produce

tissue destruction both by direct toxic effects and indirectly by activating and

modifying tissue responses of the host.

Through direct toxic effect,..endotoxins may lead to damage of cells and

vessels.

Endotoxins can contribute to tissue damage in several ways.


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COMMUNICABILITY


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COMMUNICABILITY

Attempts have been made to spread ANUG from human to human without

success.

Both a predisposed host and the presence of appropriate bacteria are necessary

for the production of this disease.

ANUG is an endogenous infectious disease and there fore not communicable.

EPIDEMIOLOGY AND PREVALENCE


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EPIDEMIOLOGY AND PREVALENCE

ANUG occurs at all ages, with the highest incidence reported between ages

15-35 years old. It is not common in children of the western developed countries but it has

been reported in children from low socioeconomic groups in underdeveloped

countries.

In India 54% and 58% of the patients in two studies were under 10years old.

It has been reported in several members of the family in low socioeconomic

groups.

ANUG is more common in children with Down's syndrome than in other

retarded children.

A most often diagnosis is made confusing it with primary herpetic

gingivostomatitis.


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TREATMENT


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TREATMENT

The oral hygiene is evaluated.

The presence of periodontal pockets, pericoronal flaps and local irritants is

determined.

A bacterial smear may be made from the material in the involved areas.

AFTER THE DIAGNOSIS IS ESTABLISHED, the patient is treated as

i) Nonambulatory patient OR ii) Ambulatory patient.

NON AMBULATORY PATIENTS


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NON-AMBULATORY PATIENTS

These are patients with symptoms of generalized toxicity such as high fever,

malaise and lassitude.

Bed rest is often necessary and extensive office treatment should not be

undertaken until the systemic symptoms subside.

DAY ONE: - Gently remove the necrotic pseudomembrane with a cotton pellet saturated

with hydrogen peroxide.

- Bed rest should be advised - Mouth rinse every 2 hrs with equal mixture of warm water and 3%hydrogen

peroxide.



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For systemic antibiotic action

a) Pencillin 250 qid or 500mg bid.

Erythromycin for penicillin sensitive patients.

b) Metronidazole 250 or 500 mg three times daily for 7 days.

The patient is to report to the dentist after 24 hours.

There may be a severe reaction to the antibiotic, and the hydrogen peroxide

mouth wash may produce diffuse erythema, ulceration of the mucosa and

swelling of the tongue.



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DAY TWO:If condition has improved, proceed to the treatment described forambulatory patients.

If no improvement ,a bed side visit should be made again.

Swab the involved gingiva with hydrogen peroxide, check the temperatureand for the oropharyngeal involvement.

Ask the patient to come after 24 hrs.

DAY THREE:Most of the patients Improve by this time and the treatmentof ambulatory patients is started.

AMBULATORY PATIENTS


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AMBULATORY PATIENTS

In these patients, there are no serious systemic complications.

DAY ONE:Treatment is confined to the acutely involved areas which areisolated and dried.,

-A topical anaesthetic is applied and then gently swab to remove the

pseudomembrane and non attached surface debris.

-After the area is cleaned with warm water, the superficial calculus is

removed with ultrasonic scalers

-Sub gingival scaling and curettage are contraindicated because the infection

may extend into the deeper tissues and may also cause bacteremia.

-For extensive treatment such as extractions and perio surgeries the patient

has to be symptom free for a period of 4 weeks so as to minimise the likelihood

of exacerbation of the acute sypmtoms.

AMBULATORY PATIENTS


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AMBULATORY PATIENTS

INSTRUCTIONS TO THE PATIENT:a) That the treatment is not complete when the pain stops.

b) Avoid tobacco, alcohol and condiments.

c) Rinse with a glassful of an equal mixture of 3 per cent hydrogen peroxide

and warm water every 2 hours.

d) Avoid exertion, prolonged exposure to sunlight.

e) To continue the oral hygiene instructions.

AMBULATORY PATIENTS


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AMBULATORY PATIENTS

DAY TWO: The patient's condition is usually improved.

-Gingival margins are erythematous but with out psuedomembrane.

-Scalers and curetters are added to the procedures of day one.

-The instructions to the patient are the same as on the previous day.

-If patient complains of hydrogen peroxide mouth wash, ask him to use warm

water alone.


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AMBULATORY PATIENTS


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AMBULATORY PATIENTS

DAY FIVE:,Comprehensive treatment of the chronic periodontal problemshould be started.

-Chronic gingivitis, elimination of all forms of local irritation.

-Elimination of periodontal pockets, pericoronal flaps.

-Patient with out gingival disease other than the acute involvement are called

after a week. If condition is satisfactory than he/she is recalled after a month.

At which time the subsequent recall visits are scheduled according to the

patient's needs.

GINGIVAL CHANGES WITH HEALING


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GINGIVAL CHANGES WITH HEALING

The characteristic lesion of ANUG undergoes the following changes in thecourse of healing in response to treatment.

1. Removal of the surface pseudomembrane exposes the underlying red,hemorrhagic crater like depressions in the gingiva.

2. In the next stage the bulk and redness of the crater margins are reduced, butthe surface remains shiny.

3. This is followed by the early signs of the restoration of normal gingivalcontour and color.

4. In the final stage the normal gingival color, consistency, surface texture, andcontour are restored.

5. Portions of root exposed by the acute disease are covered by healthy gingiva.6. When the menstrual period occurs in the course of treatment, there is atendency toward exacerbation of the acute signs and symptoms, giving theappearance of a relapse.

7. Patients should be informed of this possibility and spared unnecessary

anxiety regarding their oral condition.

FURTHER TREATMENT CONSIDERATIONS


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Surgical procedure;Extractions and surgeries should be postponed four weeksafter the acute signs and symptoms have subsided.

If emergency surgery is required in the presence of the acute symptoms

prophylactic chemotherapy with penicillin or other antibiotics. is indicated to

prevent worsening or spreading of the acute disease.



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Contouring the gingiva as an adjunctive procedure.

This can be done by reshaping the gingiva with a periodontal knife or with

electrosurgery.

Shallow craters can be removed by gingivectomy, while deep defects require

flap surgery.

Thinning of thick flap margins and correction of form to achieve optimal

interproximal coverage and contour are important but demanding technically.



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SUPPORTIVE SYSTEMIC TREATMENT: Copious fluid consumptionand administration of analgesics for relief of pain.

NUTRITIONAL SUPPLEMENTS:The rationale for these are based on thefollowing.

Disease seen in animals having nutritional deficiency

Difficulty in chewing raw fruits and vegetables due to painful conditions

could lead to the selection of a diet inadequate in vitamins B and C.

Isolated clinical studies report fewer recurrences of ANUG when treatment is

supplemented with vit B and C.

Nutritional supplements may be discontinued after 2 months.



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SEQUELAE OF INADEQUATE TREATMENT A) PRESISTANT OR UNRESPONSIVE CASES: If the dentist finds it necessary to change from drug to drug to relieve a

stubborn case of ANUG,

i) All local drug therapy should be discontinued so that the condition may be

studied in an uncomplicated state.

ii) Careful D/D is undertaken to rule out disease that resemble ANUG.

iii) Special attention is given by instructing the patient in plaque control before

under taking comprehensive local treatment.



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RECURRENT ANUG :.

i) Inadequate local therapy:Treatment is discontinued after the acute phasewith out eliminating the chronic gingival disease and perio pockets.

This persistent chronic inflammation causes degenerative changes that

predispose the gingiva to recurrence of acute Involvement.

ii) Pericoronal flap:Recurrent acute involvement in the mandibular anteriorarea is often associated with persistent pericoronal inflammation arising fromdifficult eruption of third molars.

The anterior involvement is less likely to recur after third molar situation is

corrected.



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iii) Anterior overbite:It is a contributing factor in the recurrence of disease inthe anterior region.

When teeth impinge on the labial gingival margin or the mandibular teeth

strike the palatal gingiva, the resultant tissue injury predisposes the gingiva

to recurrent acute disease.

Correction of the overbite is necessary for the complete treatment of ANUG.

iv) Inadequate plaque controland heavy use of tobaccoare also commoncauses of recurrent disease.

INDICES IN ANUG


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INDICES IN ANUG

To assess the relative effectiveness of various drugs. ..

Wade et al, developed a method of assessment which included clinicalphotographic and bacteriological evalutions, as well as recording of the time

required to eliminate soreness and to stop bleeding.

BACTERIOLOGICAL IMPROVEMENT INDEX:-It is obtained byallocating bacterial smears from the severest ulcer to one of 3 groups

representing typical, atypical or no bacteriological evidence of the infection.

-At the second visit a similar assessment from the same papilla was

undertaken and change of group provided the figures for the index.

ULCER IMPROVEMENT INDEX:This expressed any reduction in thenumber of ulcers after medication as a percentage of the number present

initially.

ACUTE HERPETIC


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ACUTE HERPETIC

GINGIVOSTOMATITIS The two strains of herpes simplex virus (HSV) ..

HSV 1 is more frequently associated with oral lesions

HSV 2 is usually isolated from the genital area.

AHGS .. HSV 1

Prevalence


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Prevalence

Acute herpetic gingivostomatitis occurs more frequently in infants and

children younger than 6 years of age, but it is also seen in adolescents and

adults.

It occurs with equal frequency in males and female patients.

The initial infection with HSV is asymptomatic in 80% to 90% of patients.

Primary infection

Secondary infection

Clinical Features


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Clinical Features

ORAL SIGNS: Diffuse, erythematous, gingiva and

the adjacent oral mucosa with

varying degrees of edema and

gingival bleeding. Initial stage..discrete spherical

gray vesicles, which may occur on the

gingiva the labial and buccal

mucosa, the soft palate, the pharynx

the sublingual mucosa, and the

tongue.

After approx 24,hrs vesicles rupture and form painful small ulcers with a red


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Af pp x , p f p f

elevated, halo-like margin and a depressed yellowish or grayish white central

portion.

The course of the disease is limited to 7 - 10 days. The diffuse gingival erythema and edema that appear early in the disease

persist for several days after the ulcerative lesion have healed.

Scarring does not occur in the areas of healed ulceration.


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ORAL SYMPTOMS: Generalized 'soreness' of the oral cavity which interferes with eating and

drinking.

Ruptured vesicles are the focal sites of pain and are particularly sensitive to

touch, thermal changes, foods such as condiments and fruit juices and the

action of coarse foods.

In infants the disease is marked by irritability and refusal to take food.


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EXTERNAL AND SYSTEMIC SIGNS AND SYMPTOMS: Herpetic involvement of the lips or face (herpes labialis cold sore) with vesicles

and surface scab formation may accompany the intra-oral disease.

Cervical adenitis, fever as high as 101 to 105 F (38.3 to 40.6 c) and generalized

malaise are common.


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HISTOPATHOLOGY


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HISTOPATHOLOGY

The discrete ulcerations..have a central portion of acute inflammation with

varying degree of purulent exudate surrounded by a zone rich in engorged

blood vessels.

The microscopic picture of the vesicles is characterized by extra and

intracellular edema and degeneration of the epithelial cells.

The cell cytoplasm appears liquified and clear.

The nucleus degenerates.

The vesicle formation results from fragmentation of the degenerated epithelial

cells.

HISTOPATHOLOGY


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The fully developed vesicle is a cavity in the epithelial cells with occasional

PMNS.

The base of the vesicles is formed by edematous epithelial cells of the basal

and prickle cell layers.

The superficial surface of the vesicle is formed by compressed upper layer of

prickle cells of the stratum granulosum and the stratum corneum.

Occasionally rounded eosinophilic inclusion bodies may be a colony of virus

particles, degenerated protoplasm remnants of the affected cell or a

combination of both.

DIAGNOSIS


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G OS S

Diagnosis is usually established from the

1. patient's history.

2. clinical findings.

3. laboratory confirmatory tests.

Laboratory Confirmatory Tests


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y y

Direct smears: If vesicle is intact, the top is removed and the fluid is allowed to escape.

The base of the lesion is scraped with a sharp instrument, and the material

obtained is smeared on a glass, allowed to dry and stained.

The finding of multinucleated cells with swelling, ballooning and

degeneration is adequate for diagnosis.

Immuno fluorescent antibody techniques have also been used successfully.

ISOLATION OF THE VIRUS


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This can be done in tissue culture or in the chorioallantoic membrane of a

chick embryo

For the analysis in tissue culture, material obtained from the lesion on a

sterile cotton- tipped applicator is sent to the laboratory in skimmed milk.

For the analysis in chick embryo, the material removed from the suspected

lesion is placed in salivary solution or thioglycolate medium.

Small amounts of the material are injected into 10 day old embryonated eggs,

after 48 hours, the egg is opened and the chorioallantoic membrane is

inspected for pocks or viral colonies.

ANTIBODY TITRATIONS :


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If a specimen of blood collected when the patient is first seen, is examined for

neutralizing antibodies, non can be found.

Successive specimens taken during the convalescent period show a rising titerof neutralizing antibodies that remain high permanently.

BIOPSY: Stained sections of the vesicles of acute herpetic gingivostomatitis,

herpeszoster and varicella ( chickenpox) reveal eosinophilic intranuclear

inclusion bodies with peripheral cells.

HEMATOLOGIC STUDIES: It has not been possible to demonstrate alterations in the hematologic picture

of patients with acute herpectic gingivostomatitis.

Differential diagnosis


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g

Acute necrotizing ulcerarive

gingivitis

Acute herpetic gingivostomatitis

Bacteria.most probably fusospirochetes Viral etiologyNecrotizing condition.Punched out gingivalmargin. Diffuse erythema and vesicular eruptionPseudomembrane peels off, leaving raw areas. Vesicles rupture and leave slightly depressed oval orspherical ulcer.Marginal gingiva affected Diffuse involvement of gingiva, may include buccalmucosa and lips.Occurs mostly in adults , Relatively uncommon inchildren.

Occurs more frequently in children

No definite duration Duration of 7-10 days.No demonstrated immunity An acute episode results in some degree of immunity.Contagion not demonstrated Contagious

2) ERYTHERMA MULTI FORME:


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The vesicles in erythema multiforme are generally more sensitive than those in

AHGS and on rupture demonstrate a tendency toward pseudomembrane

formation. In addition, the tongue in the former condition usually is markedly involved,

with infection of the ruptured vesicles resulting in varying degrees of

ulceration.

Oral involvement in erythema multiforme may be accompanied by skin lesion.

The duration of erythema multiforme may be comparable with that of acute

herpetic gingivostomatitis, but prolonged involvement for a period of weeks is

not uncommon.


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3) STEVEN. JOHNSON SYNDROME:

Is a comparatively rare form of erythema multiforme, characterized by

vesicular hemorrhagic lesions in the oral cavity, hemorrhagic ocular

lesions and bullous skin lesions.


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4) BULLOUS LICHEN PLANUS: Painful condition. .large blisters on the tongue and cheek that rupture and

undergo ulceration, it runs a prolonged indefinite course.

Patches of linear group, lace-like lesions

of lichen planus are often interspersed among the bullous eruptions.

Coexistent involvement of the skin in lichen planus affords a basis for

differentiation between bullous lichen planus and acute herpetic

gingivostomatitis.

5) APHTHOUS STOMATITIS (canker sore):


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Characterized by the appearance of discrete spherical vesicles that rupture

after 1 or 2 days and form depressed spherical ulcers.

The ulcers consist of a saucer-like red or grayish, red central portion and an

elevated rim-like periphery.

The lesions may occur any where in the oral cavity.

Aphthous stomatitis is painful. The duration of each lesion is 7 to 10 days.

As a rule the lesions are larger than those seen in acute herpetic

gingivostomatitis.

Aphthous stomatitis occurs in the following forms:


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p f g f

In occasional aphthaea single lesion occurs occasionally, at intervals thatvary from months to years.

Healing of the lesion is followed by uneventful recovery .

With acute aphthaethere is an acute episode of aphthae, which may persistfor weeks.

During this period, lesions appear in different areas of the, mouth, replacing

others that are healing or healed.

Such acute episodes are often seen in children with acute gastrointestinal

disorders and may also occur in adults under comparable conditions.

Remission of the gastrointestinal disturbance is generally accompanied by

cessation of the acute episode of apthae.

is a perplexing condition in which one or more oral


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Chronic recurrent aphthaeis a perplexing condition in which one or more orallesions are always present.

In rare instances lesions on the genital anal and conjunctival mucosae

accompany the oral aphthae.

The duration of involvement with chronic aphthae may be a period of years.

The etiology of aphthous stomatitis is unknown.

Herpes simplex virus was suspected to be the cause, but antibody and tissue

culture studies discourage this opinion.

COMMUNICABILITY


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Acute herpetic gingivostomatitis is contagious.

Most adults develop immunity to HSV as the result of infection during

childhood, which in most instances is subclinical.

For this reason acute herpetic gingivostomatitis usually occurs in infants and

children.

Herpetic Whitlow


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Common occupational hazard in medical and dental professionals.

Precautions

Herpetic whitlow follows HSV inoculation onto abraded skin on the hands.

C/F.erythema, vesicles and edema on

the skin of the finger.

Frequently, vesicles appear at the margin of uninvolved skin.

TREATMENT


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Treatment of AHGS is mainly supportive and aimed at alleviating pain and

reducing the chance of secondary infection.

Mouthrinses with a 2% lidocaine viscous solution are beneficial and facilitate

drinking and eating of soft foods and oral hygiene. .

A milder anaesthetic action may be obtained by the use of 5% aqueous

diphenhydramine ( Benadryl) solution.

Abundant bicarbonate or saline solution mouth washes provide mechanical

cleansing.

In secondary fungal infections. antimycotic agents (such as Nystatin

suspension 100,000 units Iml)

Acyclovir, selectively inhibits the replication of the virus with out affecting

noninfected cells.

It inhibits HSV type 1 and 2 ,varicella zoster viruses and cytomegalovirus in

vitro.

CANDIDIASIS


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Oral candidiasis (monoliasis).fungal infection, mainly associated with

extremes of age, debilitation, immunodeficiency and prolonged antimicrobial

therapy.

Pearly / bluish white and covers any part of oral mucosa.

The patches of candidiasis resembling

"milk curds" .mouth corners are called perleche.

The white plaques are attached to the underlying

mucosa and when scraped, leave erythematous mucosa with bleeding spots.

Pain is the most common symptom.

Other frequent complaints include a burning sensation of the oral mucosa

especially tongue, loss of taste and the onset of a metallic taste in the mouth.

Classification


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Lehner 1967, Higgs & Well 1972

ACUTE CHRONIC

1. Acute Pseudomembraneous oral

candidiasis (Thrush)

1. Chronic Hyperplastic oral

candidiasis

2. Acute atropic oral candidiais 2. Chronic mucocutaneous candidiasis

- Chronic familial MC candidiasis

- Chronic localised MC candidiasis

- Candidiasis endocrinopathy

syndrome

3. Chronic Atropic Oral Candidiasis

Classification of Primary Oral Candidiasis


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ACUTE CHRONIC CANDIDA

ASSOCIATEDLESIONS

-Pseudomembranous Pseudomembranous Angular Chelitis

-Erythematous Erythematous Denture Stomatitis

Plaque like Median Rhomboid

Glossitis

Nodular

- Axiel et al 1990

ACUTE PSEUDOMEMBRANOUS CANDIDIASIS


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Thrush is found in infants, debilitated older adults and patients with HIV

infection

In the gingivae, tongue, cheeks and throat.

They appear as white, elevated patches

which can be wiped away to leave a raw red base.

The findings of chronic or recurrent oral candidial infection in a otherwise

healthy patients should alert the dental practitioner of defective immunity

(e.g. AIDS) justifying further investigation.

TREATMENT


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1ml Nystatin in suspension (100,000 to 200,000 units/ml) is held in the

mouth for approximately 5 minutes and then swallowed.

This treatment should be repeated four times a day while the disease is still

active and for several days after the signs and symptoms have improved.

Amphotericin B lozenges (10mg) are also being used for 3 to 4 times a day.

In infants a suspension of Nystatin (100, 000 u/ml) can be painted on the

lesions two or three times a day.


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TREATMENT


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If the cause of the abscess is still present it should be removed carefully.

Drainage can be established by hot salt water mouth washes used every 2 hrs.

If the lesion persists, it can be curetted under local anaesthesia or incised if it

is pointing.

If persistent and severe, a systemic antibiotic may be needed.

Any residual pocketing can be removed by thorough subgingival curettage or

localized gingivectomy.

APHTHOUS ULCERATION


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APHTHOUS ULCERS:commonly occur in 10% to 60% of population(Axell and Henricsson, 1985).

Recurrent mouth ulcers are the most common lesions of the oral mucosa.

There are three types of ulcers;

1) Minor apthous ulcers,

2) Major aphthous ulcers and

3)Herpetiform ulcers.

Their common characteristics are that they are painful lesions which appears


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with out any reason, last for several days or weeks, heal and then after a

variable interval, recur. Several related factors have been suggested, such as emotional stress and

hormonal change.

In a number of patients the ulcers appear to be related to the menstrual cycle,the peak incidence being found in the post ovulation period.

There may be a relationship between ulceration and iron deficiency anaemia,

deficiency of folic acid and vitamin B 12.

Cooke (1969) divided the disease in to three forms 1) minor aphthous ulcers 2)Major apthous ulcers 3) Herpetic form aphthous ulcers.


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HERPETIFORM APHTHOUS ULCERS


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Despite their name they are not related to herpes.

They are most frequent in females and occur as a group of pin head ulcers

which may coalesce to form a large painful ulcer.

They can occur on any part of the oral mucosa, including the tongue, palate

and oropharynx in which case they cause dysphagia (discomfort or pain on

swallowing).

TREATMENT


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Treatment of mild cases of RAS (Recurrent aphthous stomatitis) is generally

palliative to reduce pain.

Tetracyclin therapy alters to some degree, the ulcer duration , size, and

associated pain (Graykowski and kingman 1978).

In severe, generalized cases, topical corticosteroids are commonly used to

reduce symptoms and the duration of lesions (Glass et at 1986).

It is usually best to start the corticosteroids during the pre monitory stage

(pimlott and walker, 1983; Rennie et ai, 1985)

kenalog in orabase and 0.05% fluocinonide in orabase have both been

recommended (Pimlott and walker, 1983; Glass et at 1986)

If ulcers do not heal with in the normal 2 to 4 week period, reassessment of

the lesion has to be made, and other diganoses.malignancies and other

ulcerative lesions must be considered, the most important step taken for non

healing ulcers is a biopsy to rule out malignancies.

DRUG ALLERGY AND CONTACTHYPERSENSITIVITY


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HYPERSENSITIVITY

As the number and variety of drugs and chemicals used as food additives

increases, oral manifestations of hypersensitivity become more common.

Adverse reactions are basically of two types:

1) Those following systemic administration of a drug or chemical.

2) Those following direct contact with the oral mucosa.

DRUG ALLERGYTh i b k d b i illi di l l h i


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These reactions can be provoked by penicillin, diazepam, local anaesthetics,

codeine, tetracycline, barbiturates and many other drugs in common use.

Manifestations depend on the type of allergic response provoked ,ranging from

simple drying of the mouth to the most severe response, anaphylactic shock,

which is potentially fatal.

A severe reactionangioneurotic oedema, in which there is swelling of the face

eyelids, lips, tongue and even pharynx.

Also seen utricaria, skin rash, pain in the joints and fever.

In the mouth,.patches of inflammation,

vesicles and ulcers may appear.

CONTACT HYPERSENSITIVITY


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Reactions of the oral mucosa have been reported to chewing gum ,mouth

washes, toothpastes, sweets, cosmetics, topical antibiotics, periodontal

dressings etc. often flavouring agents such as peppermint, menthol, cinnamon,

eugenol are implicated.

Symptoms start with a burning sensation of the oral, mucosa and swelling

and redness of the tongue, lips and gingiva.

The epithelium may peel off to leave very sore ulcerated areas.

The gingivae are characteristically bright red and sensitive and because the

patient can not clean the mouth it can become very unhygeinic.

MANAGEMENT


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The drug or chemical suspected must be immediately with drawn.

Antihistamines, are useful where symptom are mild but more severe reactions

e.g. angioneurotic oedema, may require injection of hydrocortisone

hemisuccinate.

In anaphylactic shock I. M. injection of 0.5 ml of 1: 1000 adrenaline is

necessary .

The mouth can be kept clean by frequent warm water or weak saline mouth

washes.

PERICORONITIS


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The term pericoronitis refers to inflammation of the gingiva in relation to the

crown of an incompletely erupted tooth.

It occurs most frequently in the mandibular third molar area.

Pericoronitis may be acute, subacute or chronic.

PERICORONITIS


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ANATOMIC RELATIONSHIPS:

Occlusal surface of an involved tooth may be partly covered by a flap of

tissue, the operculum which exists during the eruption of the tooth and may

persist afterward.

Various degrees of malposition eruptions may further complicate architecture.


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CLINICAL FEATURES


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Markedly red, swollen, operculum that is exquisitely tender, with radiating

pain to the ear, the throat and the floor of the mouth.

The patient is extremely uncomfortable because of a foul taste and an

inability to close the jaws in addition to the pain.

Swelling of the cheek in the region of the angle of the jaw andlymphadenitis are common findings.

The patient may also have toxic systemic complications such as fever

leukocytosis and malaise.

Pericoronitis


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COMPLICATION


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The involvement may become localized in the form of pericoronal abscess.

It may spread posteriorly into the oropharyngeal area and to the base of the

tongue, making it difficult for the patient to swallow.

Depending upon the severity and extent of the infection, there is involvement

of the submaxillary, posterior cervical, deep cervical and retropharyngeal

lymph nodes.

Peritonsillar abscess formation, cellulitis and ludwigs angina are infrequent,

but neverthless potiential sequelae of acute pericoronitis.

TREATMENT


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Depends on three factors

1) Severity of inflammatory process.

2) Systemic complications.

3) Advisability of retaining the involved tooth.

STEPS IN THE TREATMENT OF PERICORONITIS ARE


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FIRST APPOINTMENT:1) Patient should be medicated with antibiotics as necessary - Penicillin or

erythromycin or Tetracyclines.

2) Chlorhexidine irrigation may be effective.

3) Cleanse the area by lavage and gently curettage and establish drainage.

4) Warm saline rinses.

SECOND APPOINTMENT (24 HRS LATER)5) Remove the gauze, drain and insert new drain for 24 hrs if necessary.

6) Operculectomy or extraction.

Complications of Impacted Teeth


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Operculectomy


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CONCLUSION


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The most difficult part in the treatment of these acute gingival lesions is not

in recognition and treatment, but in patient management.

Maintaining patient co-operation and the participation beyond relief of pain

is the most challenging port of therapy.

Hence the dentist should make the patient understand that the high rate of

disease recurrence result from patient negligence and that they must assume a

major part of the responsibility for the outcome of the disease and its various

sequelae.

A tremendous improvement has been achieved, as a result of constant

research, in various therapeutic modalities for these acute lesions of gingiva.

References


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Carranza 9thEdn

Lindhe

Gant 6thEdn

Periodontics..Genco & Cohen

Periodontology 2000 ANUG as a risk factor

Internet sources


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Documents

Acute Ging Lesions