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.
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.
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 causes of damages include aspirin , escharotics such as silver
nitrate, even hydrogen peroxide solution used too strong and too frequently.
Careless use of a caustic by the dentist, e.g., phenol, trichloracetic acid.
TRAUMATIC LESIONS
Diagnosis..Usually the patient is aware of the accident and may last for a
day or so and be followed by several days of soreness and sensitivity to
further irritation.
A localized area of inflammation and ulceration may form. The wound is
bright red which can be felt by the tongue.
In this case pain persists, the wound may suppurate and this may be
accompanied by lymph gland enlargement and malaise.
Abscess formation may follow if the foreign object is not removed.

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 be
recommended 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.
ACUTE NECROTIZING ULCERATIVE
GINGIVITIS
Acute necrotizing ulcerative gingivitis (ANUG) is an inflammatory
destructive disease of the gingiva, which presents characteristic signs and
symptoms.
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.

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.

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

CLASSIFICATION
On the basis of severity, duration and onset of infection, it is classified as
ACUTE: Most often SUDDEN ONSET
SUB ACUTE: It is relatively mild and more persistent form.
RECURRENT: It is marked by periods of remission and exacerbation.

Sudden onset.following a debilitating disease or acute respiratory tract
infection.
Change in living habits, work with out adequate rest, and psychological stress
. patient's history.
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.


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.
PREDISPOSING FACTORS
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.

PREDISPOSING FACTORS
PSYCHOSOMATIC FACTORS: Psychological factors appear to be
important 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.
PREDISPOSING FACTORS
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 depression
of lymphocyte and PMN function

Predispose to ANUG.
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 taste
and spontaneous bleeding from the gingival tissues.
The patient commonly experiences a loss of the sense of taste, the teeth are
sensitive to premature contact, thought to be slightly extruded or to have a
woody sensation.

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).

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.


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.

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.
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
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.


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.
HISTOPATHOLOGY
BACTERIOLOGIC EXAMINATION:
Smears of material from the involved gingiva show, a vast numbers of
fusobacterium and oral spirochetes, Borrelia vincentii and more recentlyP.
intermedia. .
Various other spirochetes, filamentous organisms, vibrios, cocci, desquamated
epithelial cells, varying numbers of polymorphonuclear leukocytes
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 gingival
tissues.
This is the zone that appears clinically as the surface pseudomembrane.

HISTOPATHOLOGY
Schaffer using light microscopy, failed to find bacteria penetrating vital
tissues.
Listgarten on the other hand utilizing electron microscope was able to
identify 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.


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
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.


RELATION OF BACTERIA TO THE
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, mainly
neutrophils with bacteria, including many spirochetes of various types
between the leukocytes.
Zone III: Necrotic zone, consists of disintegrated tissue cells, remnants of
collagen 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 tissue
infiltrated with intermediate sized and large spirochetes with out other
organisms
RELATION OF BACTERIA TO THE
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.
STAGING OF ANUG
Pindborg
Stage Ionly tip of interdental papilla is affected
Stage II..Marginal gingiva affected with punched out papilla
Stage III.Attached gingiva also affected
Stage IV.Bone also exposed
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.
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.


DIFFERENTIAL DIAGNOSIS
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.

DIFFERENTIAL DIAGNOSIS
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.
DIFFERENTIAL DIAGNOSIS
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.

DIFFERENTIAL DIAGNOSIS
DERMATOSES: No bad breath, skin symptoms present.
1. Lichen planus: Rarely seen in gingiva (less than 10%) . Frequently
accompanies or precedes the skin lesions. White striations can usually be
found at the periphery of the ulcerated areas.
2. Erythema multiforme : Vesiculobullous lesions which rupture in the oral
cavity and leaves surfaces covered with a thick white or yellow exudate.
More generalized form in the oral cavity including lips and pharynx, not
restricted to marginal gingiva alone.
3. Pemphigus: Vesiculo bullous lesion shows Nikolsky's sign
No intra oral site is immune to these lesions.


DIFFERENTIAL DIAGNOSIS
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.

DIFFERENTIAL DIAGNOSIS
ANUG & AIDS:
ANUG is frequently found in patients with AIDS.
In these cases ANUG has the same clinical features, although it reportedly
follows a very destructive course leading to the loss of soft tissue and bone
and to the sequestra formation.

THE ROLE OF BACTERIA
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 produce
necrotic lesions in experimental animals have failed.
McDonald et al, (1956) found a combination of four different bacteria.
THE ROLE OF BACTERIA
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.

THE ROLE OF BACTERIA
Bact can function as antigens and elicit immune reactions.
They can activate macrophages and may influence the host's immune
reactions.
They can stimulate bone resorption.
Titers of antibodies to actinomyces viscosus, and fusobacterium fusiforme
were similar in patients with ANUG and chronic gingivitis.
It supports the clinical finding that ANUG always develops from preexisting
chronic gingivitis.
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
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.

TREATMENT
The treatment of ANUG.ALLEVIATION of acute symptoms and
ELIMINATION of all other periodontal disease.
The treatment of ANUG consists of the following phases:
1) LOCAL: elliminating the local cause
2) SYSTEMIC: a) Supportive treatment: Alleviation of generalized toxic
symptoms such as fever and malaise. b) Etiotropic treatment: The correction
of systemic conditions that contribute to the initiation or progression of the
gingival changes.
TREATMENT
Treatment should follow an orderly sequence.
FIRST VISIT :The dentist should obtain a general impression of the patient's
background, including information regarding recent illness, living conditions,
dietary background, type of employment, hours of rest, and mental stress.
The general appearance, nutritional status, patients temperature and the sub
maxillary and submental areas should be palpated to detect enlarged lymph
glands.
The oral cavity should be examined for the characteristic lesions of ANUG,
and the possible involvement of the oropharyngeal region.

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
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.
NON-AMBULATORY PATIENTS
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.

NON-AMBULATORY PATIENTS
DAY TWO: If condition has improved, proceed to the treatment described for
ambulatory patients.
If no improvement ,a bed side visit should be made again.
Swab the involved gingiva with hydrogen peroxide, check the temperature
and for the oropharyngeal involvement.
Ask the patient to come after 24 hrs.
DAY THREE: Most of the patients Improve by this time and the treatment
of ambulatory patients is started.


AMBULATORY PATIENTS
In these patients, there are no serious systemic complications.
DAY ONE: Treatment is confined to the acutely involved areas which are
isolated 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
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
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.
AMBULATORY PATIENTS
DAY THREE:
- Symptom free.
-Slight erythema in involved areas and slightly painful.
-Scaling and root planing repeated.
-Patient is asked to discontinue the hydrogen peroxide rinses and maintain
oral hygiene.
DA Y FOUR:
Plaque control is checked and corrected if necessary.
AMBULATORY PATIENTS
DAY FIVE:, Comprehensive treatment of the chronic periodontal problem
should 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
The characteristic lesion of ANUG undergoes the following changes in the
course 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, but
the surface remains shiny.
3. This is followed by the early signs of the restoration of normal gingival
contour and color.
4. In the final stage the normal gingival color, consistency, surface texture, and
contour 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 a
tendency toward exacerbation of the acute signs and symptoms, giving the
appearance of a relapse.
7. Patients should be informed of this possibility and spared unnecessary
anxiety regarding their oral condition.

FURTHER TREATMENT CONSIDERATIONS
Surgical procedure; Extractions and surgeries should be postponed four weeks
after 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.

FURTHER TREATMENT CONSIDERATIONS
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.
FURTHER TREATMENT CONSIDERATIONS
SUPPORTIVE SYSTEMIC TREATMENT: Copious fluid consumption
and administration of analgesics for relief of pain.
NUTRITIONAL SUPPLEMENTS: The rationale for these are based on the
following.
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.


FURTHER TREATMENT CONSIDERATIONS
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.
FURTHER TREATMENT CONSIDERATIONS
RECURRENT ANUG : .
i) Inadequate local therapy: Treatment is discontinued after the acute phase
with 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 anterior
area is often associated with persistent pericoronal inflammation arising from
difficult eruption of third molars.
The anterior involvement is less likely to recur after third molar situation is
corrected.

FURTHER TREATMENT CONSIDERATIONS
iii) Anterior overbite: It is a contributing factor in the recurrence of disease in
the 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 control and heavy use of tobacco are also common
causes of recurrent disease.

INDICES IN ANUG
To assess the relative effectiveness of various drugs. ..
Wade et al, developed a method of assessment which included clinical
photographic and bacteriological evalutions, as well as recording of the time
required to eliminate soreness and to stop bleeding.
BACTERIOLOGICAL IMPROVEMENT INDEX:- It is obtained by
allocating 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 the
number of ulcers after medication as a percentage of the number present
initially.

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
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
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
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.

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.

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.

HISTORY
Recent acute infection is a common history of patient
The condition frequently occurs during and immediately after an episode of
diseases as pneumonia, meningitis, influenza and typhoid.
It also tends to occur during periods of anxiety strain or exhaustion and
during menstruation.
Acute herpetic gingivo stomatitis often occurs in the early stage of infectious.
mononucleosis.
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
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
Diagnosis is usually established from the
1. patient's history.
2. clinical findings.
3. laboratory confirmatory tests.

Laboratory Confirmatory Tests
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
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 :
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 titer
of 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

Acute necrotizing ulcerarive
gingivitis
Acute herpetic gingivostomatitis
Bacteria.most probably fusospirochetes,
Viral etiology
Necrotizing condition.Punched out gingival
margin.
Diffuse erythema and vesicular eruption
Pseudomembrane peels off, leaving raw areas. Vesicles rupture and leave slightly depressed oval or
spherical ulcer.
Marginal gingiva affected
Diffuse involvement of gingiva, may include buccal
mucosa and lips.
Occurs mostly in adults , Relatively uncommon in
children.
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:
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.
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.

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):
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:
In occasional aphthae a single lesion occurs occasionally, at intervals that
vary from months to years.
Healing of the lesion is followed by uneventful recovery .
With acute aphthae there is an acute episode of aphthae, which may persist
for 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.

Chronic recurrent aphthae is a perplexing condition in which one or more oral
lesions 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
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
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
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

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
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
ACUTE CHRONIC CANDIDA
ASSOCIATED
LESIONS
-Pseudomembranous Pseudomembranous Angular Chelitis
-Erythematous Erythematous

Denture Stomatitis
Plaque like Median Rhomboid
Glossitis

Nodular
- Axiel et al 1990
ACUTE PSEUDOMEMBRANOUS CANDIDIASIS
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
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.
GINGIVAL ABSCESS

Abscess confined to the gingivae is termed as gingival abscess.
Often associated with physical damage to the gingival by a fish-bone, etc.
with subsequent infection of the wound, but it can also arise with in the wall
of a gingival pocket where drainage has been impeded.
Localized, shiny red swelling which is painful.
Associated teeth are sensitive to percussion.
The abscess may spread into the underlying tissue to form a periodontal
abscess.
TREATMENT
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
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
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.

MINOR APTHOUS ULCERS (MIKULICZ'S
APHTHAE)

These are the most common type, one or several small ulcers occur on non-
keratinized oral mucosa, especially the lips, cheeks, vestibule, margins of the
tongue.
They are shallow ulcers less than 10 mm in length with a surrounding zone of
inflammation and slight swelling.
They may be very painful .
The ulcers may last 4-14 days, heal with out scarring and recur after weeks or
months.
They are found in the age group 10-40 years, slightly more frequently in
females than males.
MAJOR APTHOUS ULCERS
These are much less common than the minor variety.
They are larger (up to 30mm) last as long as 40 days, are much more painful.
Some times they recur so rapidly that involvement seems continuous.
They can be found any where on the oral mucosa.
They start as a submucosal nodule which breaks down to form a deep crater
like ulcer with considerable tissue destruction which heals with a scar.
HERPETIFORM APHTHOUS ULCERS
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
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 CONTACT
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 ALLERGY
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
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
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
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
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.

CLINICAL FEATURES
The operculum is often directly traumatized when it is caught between the
crown that it covers and the antagonist tooth during closure.
The crypt like form of the pericoronal tissue favours the proliferation of
micro-organisms
Acute pericoronitis is identified by varying degrees of involvement of the
pericoronal flap and adjacent structures, as well as systemic complications.
The flap is traumatized by contact with the opposing jaw and the
inflammatory involvement is aggravated.
CLINICAL FEATURES
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 and
lymphadenitis are common findings.
The patient may also have toxic systemic complications such as fever
leukocytosis and malaise.


Pericoronitis
COMPLICATION
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
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
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

Operculectomy
CONCLUSION
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
Carranza 9
th
Edn
Lindhe
Gant 6
th
Edn
Periodontics..Genco & Cohen
Periodontology 2000 ANUG as a risk factor
Internet sources