04.acute gingival infections

acute gingival infections

1. ACUTE GINGIVAL INFECTIONS

2. 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. Aphthousulceration
g. Erythemamultiforme
h. Drug allergy

3. CLASSIFICATION

4. Also known as
►Vincent’s infection
►Trench mouth
►Acute ulceromembranousgingivitis
It is an inflammatory,destructivedisease of the gingiva,
which presents characteristic signs and symptoms
►Sudden onset,
►may be followed by an episode of debilitating
diseases or ARTI.
►Long hours of workingwithout adequate rest,
►psychologicstress.

6. Signs and Symptoms
Punched out, crater-likedepressions at the crest of the interdentalpapillae,
subsequently involving marginalgingivaand rarely attachedgingiva
grayish pseudomembranousslough
gingival hemorrhageor pronounced bleeding on the slightest stimulation.
Fetid odorand increased salivation.
extremely sensitive to touch
constant radiating, gnawing painthat is intensified by eating spicy or hot foods and
chewing
metallic foul taste
pastysaliva
local lymphadenopathy
elevation in temperature

7. Etiology
fusospirochetalorganisms
►fusiformbacillus
►spirochetes

8. Clinical Course
if left untreated, it may lead to destruction of the periodontium, and
denudation of roots (NUP), combined with severe toxic systemic
complications.

9. Stages of oral necrotizing disease
by Horning & Cohen
Stage 1-necrosis of the top of the interdental papilla.
Stage 2-necrosis of entire papilla
Stage 3-necrosis extending to the gingival margin.
Stage 4-necrosis extending to the attached gingiva.
Stage 5–necrosis extending to labial & buccal mucosa.
Stage 6-necrosis exposing alveolar bone.
Stage 7–necrosis perforating skin of cheek.

10. Necrotizing Ulcerative Periodontitis

11. Necrotizing stomatitis
NOMA-Cancrumoris

13. Predisposing Factors
predisposing factors are:
Pre-existing gingivitis
Injury to the gingiva
Smoking
Systemic Predisposing Factors
Nutritional deficiency
Debilitating diseases
Psychosomatic factors activation of the hypothalamic
pituitary adrenal axis ↑cortisollevels ↓lymphocyte
and polymorphonuclearleukocytes function

14. Relationship of Bacteria to the Characteristic Lesions
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 neutrophilswith 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 spirochetalinfiltration:
Consists of a well preserved tissue infiltrated with spirochetes of
intermediate and large-sized without other organisms.

15. Treatment
Non-ambulatory Patients
Day 1:
gently removing the necrotic pseudomembranewith a
pellet of cottonsaturated with hydrogen peroxide
(H2O2).
Advised bed restand rinse the mouth every 2 hours
with a diluted 3 percent hydrogen peroxide (H2O2).
Systemic antibioticslike penicillin or metronidazolecan
be prescribed.

16. Treatment
Non-ambulatory Patients
Day 2:
After 24 hours, a bedsidevisit should be made. The treatment
again includes gently swabthe area with hydrogen peroxide,
instructions of the previous day are repeated.
Day 3:
Most cases, the condition will be improved, start the treatment for
ambulatorypatients.

17. Treatment
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
Subgingivalscaling 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 toothbrushingto the removal of surface debris with a bland dentifrice,
use of interdentalaids and chlorhexidinemouth rinse are recommended.

18. Treatment
Ambulatory Patients
Second visit:
►Scalersand curettes are added to the instrumentarium.
►Shrinkage of the gingivamay expose previously covered calculus which is gently removed.
►Same instructions are reinforced.
Third visit:
►Scaling and root planingare repeated,
►Plaque control instructions are given.
►Hydrogen peroxide rinses are discontinued.
Fourth visit:
►Oral hygiene instructions are reinforced
►thorough scaling and root planingare performed.
Fifth visit:
►Appointments are fixed for treatment of chronic gingivitis, periodontal pockets
and pericoronalflaps, and for the elimination of all local irritants.
►Patient is placed on maintenance program.

19. 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

20. ACUTE HERPETIC GINGIVOSTOMATITIS (AHG)
viralinfection of the oral mucous membrane caused by HSV I and II
occurs most frequently in infantsand childrenyounger than 6years of
age but is also seen in adults.

21. Clinical Features
1. appears as a diffuse, shiny erythematous, involvement of the gingivaand
the adjacent oral mucosa with varying degrees of edemaand gingival
bleeding.
2. In its initialstage it may appear as discrete, spherical, clusters of vesicles
dispersed in different areas, e.g. labial and buccalmucosa, hard palate,
pharynx and tongue. After approximately 24 hoursthe vesicles rupture and
form painful shallow ulcerswith scalloped bordersand surrounding
erythema.
3. Diffuse, edematous, erythematousenlargement of the gingivawith a tendency
towards bleedingis seen.
4. The course of the disease is 7 to 10 days.

22. Oral Symptoms
1. Generalized sorenessof the oral cavity which interferes with eating and drinking.
2. The ruptured vesicles are sensitive to touch, thermal changes and food.
Extraoraland Systemic Signs and Symptoms
►fever
►loss of appetite
►myalgia
►Cervical lymphadenopathy
►After the primary infection the virus remains latentin the nerve tissue. If reactivation occurs it
causes Herpes labialis(cold sore).
►It is associated with prodromeof tingling and itchingon the corners of lip followed by vesicle
formation and ulceration

23. Diagnosis
►patients’ history and the clinical findings
►biopsy
Differential Diagnosis
1. Necrotizing ulcerative gingivitis
2. Erythemamultiforme
3. Stevens-Johnson syndrome
4. Aphthousstomatitis(Canker sores).
Treatment
►topical lignocainefor 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

24. Recurrent AphthousStomatitis(RAS)
common condition which is characterized by
►multiple recurrent small, round or ovoid ulcers with
circumscribed margins,
►erythematoushalo, yellow or gray floors
►typically presenting first in childhood or adolescence
►The lesions may occur anywhere in the oral cavity,
the buccaland labialmucosaeare common sites
►It’s a painful lesion and may occur as a single lesion
or as lesions scatteredthroughout the mouth

25. 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 pseudomembraneand an erythematoushalo.
►The ulcers heal within 10-14 days without scarring.
Major aphthae:
►Is a rare severe form of Aphthousulcer.
►Ulcers are oval and may exceed 1 cm in diameter.
►Ulcers persist for up to 6 weeks and often heal with scarring.

26. Herpetiformaphthae:
►least common variety
►characterized by multiple recurrent crops of widespread small,
painful ulcers.
►As many as 100 ulcersmay be present at a given time
►each measuring 2-3 mmin diameter

27. Etiology
►Unknown
►linked to RAS are genetic predisposition,
►Hematinicdeficiencies,
►Immunologic abnormalities,
►stress,
►food allergy
►gastrointestinal disorders
►Predisposing factors include hormonal disturbances, trauma, cessation of
smoking and menstruation

28. Treatment
►topical lignocaine
►Topical steroids like Triamcinoloneand Clobetasol
►systemic steroids and Thalidomideto reduce the number of ulcers and
recurrences.

30. PERICORONITIS
acute infection which refers to
inflammation of gingivaand
surrounding soft tissues of an
incompletely erupted tooth.
It occurs most frequently in the
mandibularthird molar area.
Types
Acute,
subacuteor chronic

31. 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, leukocytosisand malaise

32. Complications
Localized pericoronalabscess or cyst formation
may spread posteriorlyinto the oropharyngealarea and medially into
the base of the tongue, making it difficult for the patient to swallow
Peritonsillarabscess formation, cellulitisand Ludwig’sangina are the
potential complications

33. Treatment
The treatment of pericoronitisdepends on
Severity of the inflammation.
The systemic complications, and
The advisability of retaining the involved tooth

34. First Visit
warm water flush + topical anesthetic agent
flap is reflected with a scalerand 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