021.acute gingival diseases

acute gingival diseases

1. Dr Jaffar Raza Syed Page 1

Acute Gingival Infections

CLASSIFICATION


a. Traumatic lesions of gingiva:
• Physical injury
• Chemical injury

b. Viral infections:
• Acute herpetic gingivostomatitis
• Herpangina
• Hand, foot and mouth diseases
• Measles
• Herpes varicella/zoster virus infections
• Glandular fever



c. Bacterial infections:
• Necrotizing ulcerative gingivitis
• Tuberculosis
• Syphilis

d. Fungal diseases:
• Candidiasis
e. Gingival abscess
f. Aphthous ulceration
g. Erythema multiforme
h. Drug allergy

2. Dr Jaffar Raza Syed


NECROTIZING ULCERATIVE GINGIVITIS (NUG)

Also known as
►Vincent’s infection
► Trench mouth
► Acute ulceromembranous gingivitis

It is an inflammatory,destructive disease of the gingiva, which presents characteristic
signs and symptoms

►Sudden onset,
►may be followed by an episode of
►Long hours of working withou
►psychologic stress.







NECROTIZING ULCERATIVE GINGIVITIS (NUG)
Acute ulceromembranous gingivitis
It is an inflammatory,destructive disease of the gingiva, which presents characteristic
may be followed by an episode of debilitating diseases or ARTI.
without adequate rest,
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It is an inflammatory,destructive disease of the gingiva, which presents characteristic

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Signs and Symptoms


►Punched out, crater-like depressions at the crest of the interdental
papillae, subsequently involving marginal gingiva and rarely attached gingiva


►grayish pseudomembranous slough


►gingival hemorrhage or pronounced bleeding on the slightest stimulation.


►Fetid odor and increased salivation.


►extremely sensitive to touch

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►constant radiating, gnawing pain that is intensified by eating spicy or hot foods
and chewing


►metallic foul taste


►pasty saliva


►local lymphadenopathy


►elevation in temperature

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Clinical Course

if left untreated, it may lead to destruction of the periodontium, and denudation of
roots (NUP), combined with severe toxic


Etiology
fusospirochetal organisms

►fusiform bacillus
►spirochetes









if left untreated, it may lead to destruction of the periodontium, and denudation of
, combined with severe toxic systemic complications.
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if left untreated, it may lead to destruction of the periodontium, and denudation of

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Local Predisposing Factors

Most important predisposing factors are:

i. Pre-existing gingivitis

ii. Injury to the gingiva

iii. Smoking


Systemic Predisposing Factors

►Nutritional deficiency

►Debilitating diseases

►Psychosomatic factors  activation of the hypothalamic pituitary adrenal axis 
↑ corHsol levels  ↓ lymphocyte and polymorphonuclear leukocytes funcHon

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Relationship of Bacteria to the Characteristic Lesions

four zones

1. Zone I—Bacterial zone:
It is the most superficial zone, consists of varied bacteria, including a few Spirochetes of
the small, medium-sized and large types.

2. Zone II—Neutrophil-rich zone:
Contains numerous leukocytes predominantly neutrophils with bacteria including
spirochetes of various types.

3. Zone III—Necrotic zone:
Consists of a dead tissue cells, remnants of connective tissue fragments, and numerous
spirochetes.

4. Zone IV—Zone of spirochetal infiltration:
Consists of a well preserved tissue infiltrated with spirochetes of intermediate and
large-sized without other organisms.

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Treatment

Treatment for Non-ambulatory Patients


Day 1:
a. gently removing the necrotic pseudomembrane with a pellet of cotton saturated with
hydrogen peroxide (H2O2).

b. Advised bed rest and rinse the mouth every 2 hours with a diluted 3 percent
hydrogen peroxide (H2O2).

c. Systemic antibiotics like penicillin or metronidazole can be prescribed.

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Day 2:
After 24 hours, a bedside visit should be made. The treatment again includes gently
swab the area with hydrogen peroxide, instructions of the previous day are repeated.


Day 3: Most cases, the condition will be improved, start the treatment for ambulatory
patients.

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Treatment for Ambulatory Patients

First visit:
►topical anesthetic
►gently swabbed with a cotton pellet to remove pseudomembrane and
non-attached surface debris.
►area is cleansed with warm water
►superficial calculus is removed with ultrasonic scalers.
►Antibiotics prescription
►Subgingival scaling and curettage are contraindicated

Instructions to the patient
1. Avoid smoking and alcohol.
2. Rinse with 3 percent hydrogen peroxide and warm water for every two hours.
3. Confine toothbrushing to the removal of surface debris with a bland dentifrice,
use of interdental aids and chlorhexidine mouth rinse are recommended.

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Second visit:
►Scalers and curettes are added to the instrumentarium.
►Shrinkage of the gingiva may expose previously covered calculus which is
gently removed.
►Same instructions are reinforced.



Third visit:
►Scaling and root planing are repeated,
►Plaque control instructions are given.
►Hydrogen peroxide rinses are discontinued.



Fourth visit:
►Oral hygiene instructions are reinforced
►thorough scaling and root planing are performed.

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Fifth visit:
►Appointments are fixed for treatment of chronic gingivitis, periodontal pockets
and pericoronal flaps, and for the elimination of all local irritants.
►Patient is placed on maintenance program.

Further Treatment Considerations

1. Gingivoplasty.

2. Systemic antibiotics—only in patients with toxic systemic complications.

3. Supportive systemic treatment—copious fluid consumption and administration
of analgesics and adequate bed rest.

4. Nutritional supplements—vitamin B/C supplements.

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ACUTE HERPETIC GINGIVOSTOMATITIS (AHG)

►viral infection of the oral mucous membrane caused by HSV I and II

►occurs most frequently in infants and children younger than 6 years of age but is
also seen in adults.


Clinical Features

1. appears as a diffuse, shiny erythematous, involvement of the gingiva and
the adjacent oral mucosa with varying degrees of edema and gingival bleeding.

2. In its initial stage it may appear as discrete, spherical, clusters of vesicles dispersed in
different areas, e.g. labial and buccal mucosa, hard palate, pharynx and tongue. After
approximately 24 hours the vesicles rupture and form painful shallow ulcers with
scalloped borders and surrounding erythema.

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3. Diffuse, edematous, erythematous enlargement of the gingiva with a tendency
towards bleeding is seen.

4. The course of the disease is 7 to 10 days.
















3. Diffuse, edematous, erythematous enlargement of the gingiva with a tendency
4. The course of the disease is 7 to 10 days.
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3. Diffuse, edematous, erythematous enlargement of the gingiva with a tendency

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Oral Symptoms

1. Generalized soreness of the oral cavity which interferes with eating and drinking.

2. The ruptured vesicles are sensitive to touch, thermal changes and food.



Extraoral and Systemic Signs and Symptoms

►fever
►loss of appetite
►myalgia
►Cervical lymphadenopathy

►After the primary infection the virus remains
occurs it causes Herpes labialis (cold so

►It is associated with prodrome of
vesicle formation and ulceration

of the oral cavity which interferes with eating and drinking.
2. The ruptured vesicles are sensitive to touch, thermal changes and food.
d Systemic Signs and Symptoms
After the primary infection the virus remains latent in the nerve tissue. If reactivation
occurs it causes Herpes labialis (cold sore).
It is associated with prodrome of tingling and itching on the corners of lip followed by
formation and ulceration
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of the oral cavity which interferes with eating and drinking.
2. The ruptured vesicles are sensitive to touch, thermal changes and food.
in the nerve tissue. If reactivation
on the corners of lip followed by

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Diagnosis
►patients’ history and the clinical findings
►biopsy


Differential Diagnosis
1. Necrotizing ulcerative gingivitis
2. Erythema multiforme
3. Stevens-Johnson syndrome
4. Aphthous stomatitis (Canker sores).


Treatment
►topical lignocaine for pain relieve
►Acyclovir at 15 mg/kg five times a day for 5
►topical antiviral medications such as 5% acyclovir cream or 3%
cream applied three to five times a day




patients’ history and the clinical findings
1. Necrotizing ulcerative gingivitis
4. Aphthous stomatitis (Canker sores).
topical lignocaine for pain relieve
Acyclovir at 15 mg/kg five times a day for 5-7 days
topical antiviral medications such as 5% acyclovir cream or 3% Penciclovir
cream applied three to five times a day
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Penciclovir

17. Dr Jaffar Raza Syed

Recurrent Aphthous Stomatitis (RAS

common condition which is characterized by
►multiple recurrent small, round or ovoid ulcers with circumscribed
►erythematous halo, and yellow or gray floors
►typically presenting first in childhood or adolescenc

►The lesions may occur anywhere in the oral cavity, the
are common sites

►It’s a painful lesion and may occur as a
scattered throughout the mout









Recurrent Aphthous Stomatitis (RAS)
common condition which is characterized by
recurrent small, round or ovoid ulcers with circumscribed
, and yellow or gray floors
typically presenting first in childhood or adolescence
The lesions may occur anywhere in the oral cavity, the buccal and labial
lesion and may occur as a single lesion or as lesions
throughout the mouth
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recurrent small, round or ovoid ulcers with circumscribed margins,
buccal and labial mucosae

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Types

Minor aphthae:

►Is the most common affecting about 80% of patients with RAS
►ulcers are round or oval usually <5 mm in diameter with a
gray-white pseudomembrane and an erythematous halo.
►The ulcers heal within 10-14 days without scarring.



Major aphthae:

►Is a rare severe form of Aphthous ulcer.
►Ulcers are oval and may exceed 1 cm in diameter.
►Ulcers persist for up to 6 weeks and often heal with scarring.

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Herpetiform aphthae:
►least common variety
►characterized by multiple recurrent crops of widespread small, painful ulcers.
►As many as 100 ulcers may be present at a given time,
►each measuring 2-3 mm in diameter.

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Etiology

►Unknown
►linked to RAS are genetic predisposition,
►Hematinic deficiencies,
►Immunologic abnormalities,
►stress,
►food allergy
►gastrointestinal disorders.

►Predisposing factors include hormonal disturbances, trauma, cessation of
smoking and menstruation

Treatment
►topical lignocaine
►Topical steroids like Triamcinolone and Clobetasol
►systemic steroids and Thalidomide to reduce the number of ulcers and recurrences.

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PERICORONITIS

acute infection which refers to inflammation of
of an incompletely erupted tooth.

It occurs most frequently in the mandibular



Types

Acute,
subacute or chronic








acute infection which refers to inflammation of gingiva and surrounding soft tissues
erupted tooth.
It occurs most frequently in the mandibular third molar area.
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gingiva and surrounding soft tissues

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Signs and Symptoms

markedly red, edematous suppurating lesion that is extremely tender with
radiating pain to the ear, throat and floor of the mouth

foul taste and inability to close the jaws.

swelling of the cheek

interferes with complete jaw closure

flap is traumatized by contact with the opposing jaw and inflammatory involvement
is aggravated.

toxic systemic complications such as fever, leukocytosis and malaise

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Complications

Localized  pericoronal abscess or cyst formation

may spread posteriorly into the oropharyngeal area and medially into
the base of the tongue, making it difficult for the patient to swallow

Peritonsillar abscess formation, cellulitis and Ludwig’s angina are the
potential complications



Treatment

The treatment of pericoronitis depends on:
• Severity of the inflammation.
• The systemic complications, and
• The advisability of retaining the involved tooth

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First Visit

warm water flush + topical anesthetic agent

flap is reflected with a scaler and the underlying debris is also removed

hourly rinses instructions

copious fluid intake

systemic antibiotics

If the gingival flap is swollen and fluctuant an antero-posterior incision to
establish drainage is made with a No. 15 bard parker blade

followed by insertion of 1/4th inch gauze wick

In the next visit, determination is made as to whether the tooth is to be retained
or extracted

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