Infectious Disease Of Oral Cavity Short Notes

Question 1. Describe Warts.
Answer:

• Common warts are caused by human papillomavirus (DNA viruses) as keratotic papules on the fingers, hands, knees, and rarely on the orofacial region.
• The virus enters the body through maceration and trauma; infects the basal layer leading to viral replication and DNA synthesis. Protein deposition occurs in different genes.
• There is no viremia, and hence systemic immune plays no role in protection. Langer- Hans cells evoke local cell-mediated immunity at the basal layer. Warts are difficult to treat, and spontaneous resolution occurs within 2 years.

.Read And Learn More: Oral Medicine and Radiology Question And Answers

The therapeutic options are:

• Cryotherapy
• Podophyllin
• Intralesional bleomycin.

Question 2. Molluscum contagiosum.
Answer:

• Molluscum infection is common in children, especially children in immunosuppressed and atopic status. The infection is caused by a poxvirus and spread by direct skin contamination.
• The lesions appear as dome¬shaped umbilicated papules commonly on body folds and genitals and rarely on the oral cavity.
• The characteristic histopathological finding is the presence of Henderson-Paterson bodies (intracytoplasmic inclusion bodies).

Molluscum Treatment Option:

• Cryotherapy using liquid nitrogen
• Curettage
• Topical cidofovir.

Question 3. Discuss tetanus
(or)
Lockjaw.
Answer:

• Tetanus is caused by an anaerobic, gram-positive bacterium, Clostridium tetani. The complication of this infection is the muscle spasm and autonomic nervous system disturbance due to the release of a neurotoxin, tetanospasmin by this bacterium.
• In mild cases, local muscle spasms may present. Pharyngeal and laryngeal muscle spasms may cause airway obstruction.
• In severe cases with generalized form, the jaw and face are affected. Trismus, muscle pain, stiffness, and difficulty in swallowing are common.
• The prognosis depends on the speed at which infection spreads. The shorter the incubation period, the prognosis will be poor.

Tetanus Treatment:

• Cleaning and wound debridement to prevent further toxin production.
• The preferred antibiotic is — Metronidazole 500 mg IV 6 hourly for seven days.
• To deactivate the circulating tetanus toxin, and prevent neuronal uptake, antitoxin — Human tetanus immune globulin (TIG) should be administered as IM dose.

Question 4. Actinomycosis
(or)
Cervicofacial actino-mycosis
(or)
Lumpy jaw.
Answer:

• (Action = ray; makes = fungus)
• Actinomycosis is an infectious disease caused by the invasion of tissues by fungus-like bacteria called Actinomyces israelii.
• In many individuals, these anaerobic gram¬positive Actinomyces species are present in polymicrobial flora with other normal commensals, especially in the tonsillar crypts and oropharynx.
• From these sites, the bacteria may enter an opening in the oral mucosa, probably an extracted wound, and cause the characteristic lumpy jaw. Radiotherapy, bisphosphonate therapy, and ulcerative mucosal lesions are the common predisposing factors.
• When the oral mucosal barrier is disturbed, actinomycosis spreads in a slow-progressive mode and crosses the facial planes. The cervicofacial form typically affects tissues surrounding the maxilla, mandible, cheek, chin, and posterior region of the oral cavity.
• It starts as a progressive, painless, and firm-swelling that develops multiple abscesses and draining sinus tracts on the skin surface or oral mucosa. This is followed by a chronic indolent phase in which single or multiple indurations appear which are in woody consistency.
• Central necrosis of the induration occurs with sulfur granules. Pain and trismus are the later complications.
• The sulfur granules are tiny clumps of 0.1-1 mm in diameter in size. Typical microscopic findings include a necrosis and filament gram-positive bacterium that resembles fungi.

Actinomycosis Diagnosis: Bacterial culture.

Actinomycosis Management:

• Actinomycosis needs prolonged treatment with high doses of antibacterial drugs.
• The standard regimen is intravenous penicillin, 18-24 million units/day for 2-6 weeks. The follow-up by treatment is oral amoxicillin for a total period of 6-12 months.

Question 5. Pyogenic granuloma.
Answer:

• Pyogenic granuloma is a reactive or reparative lesion. It is a connective tissue proliferative response to an irritant stimulus like calculus or injury due to foreign materials like denture clasps.
• Other factors like hormones, drugs, gingival inflammation due to defective fillings in the proximal tooth surface, and food impaction have also been suggested as causative agents.

Pyogenic granuloma Clinical Features:

• Gingiva is involved frequently followed by tongue, labial, buccal mucosa, and hard plate.
• It is a sessile or elevated growth, soft in consistency, dark red in the early stage, and later becomes reddish-purple. Bleeding is common for even a slight provocation but no pain.

Gravid Tumor (or) Pregnancy Tumor:

• During the first and third-trimester of preg¬nancy, the estrogen hormone levels will be highly increased.
• Gingival tissues have estrogen receptors which respond to the excess level of the hormone when the associated stimulus is present.
• A pedunculated or sessile, bright-red growth occurs in the gingival which is usually asymptomatic.

Pyogenic granuloma Radiographic Findings: No specific finding for pyogenic granuloma.

Pyogenic granuloma Differential Diagnosis: Fibroma, peripheral giant cell granuloma.

Pyogenic granuloma Treatment:

• Removal of the irritating factor like calculus, or overhanging restorations or followed by surgical excision of the lesion.
• If it is associated with pregnancy, treatment should be carried out after childbirth. Proper oral hygiene procedures should be recommended.

Question 6. Necrotizing ulcerative gingivitis
(or)
Trench mouth
(or)
Vincent’s stomatitis.
Answer:

Acute necrotizing ulcerative gingivitis (ANUG) is a relatively rare clinical entity caused by a heterogeneous mixture of fusospirochetal complex consisting of spirochetes, vibrios, Treponema macrodentium, fusiform bacilli, and Borrelia vincentii.

Necrotizing ulcerative gingivitis Predisposing Factors:

• Stressful conditions induce changes in the gingival tissue, and the causative organisms exert their pathogenic effects on the altered tissues.
• Immunosuppression (especially HIV infection)
• Smoking
• Poor oral hygiene
• Malnutrition.

Necrotizing ulcerative gingivitis Clinical Findings: Gingival ulceration, sharply punched out crate-ring of the interproximal papillae, necrosis, pseudomembrane formation, pain, bleeding, fetid odor, excess salivation, abnormal sensations of the teeth, lymphadenopathy, and fever are the common clinical presentation.

For a clinical diagnosis, three signs and symptoms are essential:

• Acute necrosis and ulceration of interdental papillae
• Pain
• Bleeding.

Necrotizing ulcerative gingivitis Treatment:

• Chlorhexidine (or) hydrogen peroxide mouth rinse for superficial cleaning and debridement.
• Scaling and polishing with the use of topical anesthetics.
• Antibiotics: Amoxicillin (500 mg thrice daily; and metronidazole 400 mg twice daily).

Question 7. Cancrum oris
(or)
Noma.
Answer:

• Noma is a sudden onset of gangrenous infection of the oral cavity which rapidly involves the adjacent hard and soft tissue structures of the face (lip, nose, and cheek) and then stops spreading further.
• There is no specific age group, but the affected individuals are usually malnourished and influenced by some infectious disease which weakens the immune system. The children are frequently affected especially those below 5 years of age.
• The condition starts with acute necrotizing ulcerative gingivitis preferably in the premolar-molar region. There will be pro¬fuse salivation, fetid odor, and purulent discharge.
• The ulcerative lesions may expose the underlying alveolar bone and cause spontaneous shedding of teeth. Within 2-3 days, it causes bluish discoloration of lips and cheek.
• Systemic manifestations include fever, tachycardia, lymphadenopathy, anorexia, edema, and ascites.
• Prevotella intermedia and Peptostreptococ- cus are the microbial agents associated with noma.

Cancrum Oris Complications: Trismus, oronasal fistula, jaw bone sequestration.

Cancrum Oris Treatment:

• Debridement with hydrogen peroxide solution and saline followed by a daily oral rinse of chlorhexidine gluconate (0.12-0.2%).
• Amoxicillin and metronidazole are the choices of antibiotics.
• Supportive therapy with multivitamins and a high protein diet.
• Surgical correction for residual damage later.

Question 8. Discuss oral manifestations of tuberculosis.
Answer:

• Tuberculosis is a granulomatous disease caused by Mycobacterium tuberculosis. Involvement of the oral cavity is infrequent in tuberculous infection.
• Occasionally, primary TB lesion is present in the oral cavity of young individuals as a single, painless ulcer with enlarged regional lymph nodes mimicking oral cancer.
• Secondary oral lesions are rarely present in pulmonary tuberculous patients as a single, large, painful ulcer with an indurated base and irregular margins. These types of lesions occur in elderly patients.
• The tongue is the commonly affected organ (especially the lateral border); however, the involvement of buccal mucosa, palate, and floor of the mouth are also possible.
• Tuberculous gingivitis presents as erythematous gingiva with ulcerated gingival margins with/without pain. It is common among tuberculous-positive children and adolescents.

Tuberculosis Diagnosis: Mantoux skin test, chest X-ray, and biopsy of the oral lesion.

Tuberculosis Treatment:

• Oral tuberculosis lesions are treated as same as systemic tuberculosis.
• A combination drug therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol also known as, 4D- therapy) is the treatment of choice.

Question 9. Infectious mononucleosis.
Answer:

• Infectious mononucleosis is caused by the Epstein-Barr virus, transmitted through saliva. The infection spread through kissing, or by a cough or sneeze, or by sharing food utensils with individuals infected by infectious mononucleosis. It is also called as kissing disease.
• It is also known as glandular fever and is described as a hyperplastic disease of the reticuloendothelial system, lymph nodes, and spleen. Fever, sore throat and malaise are the early symptoms and thrombocytopenia is a later complication.
• Intraoral findings include the erythematous appearance of a soft palate with multiple tiny petechiae. White pseudomembrane covers the tonsils.
• Patients may develop a generalized faint, nonpruritic, maculopapular rash that disappears rapidly.

Infectious mononucleosis Diagnosis:

• Differential count: Increases the number of white blood cells (lymphocytes) and atypical lymphocytes.

Antibody tests:

• Monospot test—To check antibodies to the Epstein-Barr virus. This screening test is based on the agglutination of horse RBCs on exposure to heterophile antibodies. The result is given on the day but is not applicable to diagnose during the first week of illness.
• Paul-Bunnell test—Infected serum is inactivated by a water bath and treated with 0. 85% NaCl. Fresh sheep cells are added. The final serum dilution is 1:20 up to 10,240. Sheep RBCs agglutinate in the presence of heterophile antibodies and incubated at 370°C for 4 hours.
• This is followed by overnight refrigeration. The next day morning, the test tubes are again incubated for 1 hour at 37°C and then lightly turned upside down to observe the agglutination.

Infectious mononucleosis Management: Treatment is nonspecific. Management includes bed rest, proper nutrition, and drinking plenty of fluids.

Question 10. Necrotizing ulcerative periodontitis.
Answer:

• Necrotizing ulcerative periodontitis (NUP) is characterized by extensive soft tissue necrosis and loss of interdental and alveolar bone.
• The microbial component includes Treponema species, Spirochetes, Fusobacterium, Bacteroides melaninogenicus, and P. intermedia.

Necrotizing ulcerative periodontitis Predisposing Factors:

• Immunosuppressed patients especially HIV-positive patients with CD4 count is less than 200 are associated with NUP.
• Severe malnutrition
• Smoking
• Poor oral hygiene
• Necrotizing ulcerative periodontitis starts as blunting or ulceration of the interdental papillae, and progresses rapidly to destroy the alveolar bone.
• Severe pain and spontaneous bleeding will be present.
• Extensive destruction of periodontal tissue may lead to the shedding of teeth within 3-6 months of onset with sequestration.
• Metallic taste, bad breath, and deep jaw pain are the associated symptoms.

Necrotizing ulcerative periodontitis Treatment:

• The acute phase is aimed for pain control:
• Gentle debridement of necrotic tissues
• Chlorhexidine gluconate rinse (0.12%), twice daily
• Soft brushing
• Metronidazole, 400 mg BID for 10 days.
• In the maintenance phase, treatment is directed to eliminate the causative organisms, prevent tissue damage, and to promote healing.

Question 11. Quincy.
Answer:

Quincy denotes the peritonsillar abscess following acute suppurative tonsillitis or abscess in the peritonsillar fossa salivary glands (Weber’s glands).

• The Weber’s glands are the minor salivary glands Junction to clear the debris from the tonsils. Any obstruction in the gland may lead to infection and pus formation. The other possible etiology includes infectious mononucleosis.
• The peritonsillar fossa is composed of loose connective tissue. Any nidus deposited in the region will cause infection and pus formation. The subsequent edema and inflammation may spread to the soft palate, pharyngeal wall, and base of the tongue.
• The incidence of Quincy is frequent in young individuals below 30 years of age.
• The potential complications include pain and difficulty in swallowing, dehydration, fever, foul odor, space infection, trismus, and airway obstruction.

Quincy Treatment:

• Antibiotic sensitivity tests should be performed before selecting the medications. Pus collection is done by fine needle aspiration (FNAC), and the sample should be subjected to a sensitivity test.
• A combination of amoxicillin 500 mg TID, and metronidazole 400 mg BID should be started immediately following diagnosis till receiving the sensitivity report.
• Clindamycin 500 mg BID is an alternate drug.