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Infections of The Oral Mucosa 1 (Slide 10 + 11)
Infections of The Oral Mucosa 1 (Slide 10 + 11)
Viral infections Bacterial infections Fungal infections HIV infection and AIDS
Herpes Viradae
Herpes Simplex 1 Herpes Simplex 2 Varicella Zoster Epstein-Barr Cytomegalovirus (HHV5) Herpes 6 Herpes 7 Herpes 8
Most frequent cause of viral infections of the mouth Primary HSV I Infection (Acute Herpetic Gingivostomatitis)
5 days incubation, then 2 days of prodromal symptoms Acute onset of malaise, fever, and lymphadenopathy. Multiple vesicles and ulcers can occur any part in the oral mucosa and lips 10-14 days to resolve Spread by droplets or lesion contact Majority of cases are subclinical
Herpetic whitlow
Tzank cells
Treatment Supportive Acyclovir in extreme cases Prognosis: self-limited resolves in 10-14 days
HSV remain latent in trigeminal sensory ganglia Virus reactivation associated with: Ultraviolet radiation Trauma Immunosuppression
Vesicles and ulcers recur: most common herpes labialis Intraorally: hard palate and gingiva In small clusters
Varicella-Zoster Virus
Microscopic features: identical to HSV Prognosis for varicella is usually mild in children. vaccine is available. Acyclovir in immunocompromised
Zoster (Shingles)
Same latent state as HSV, in sensory ganglia Predisposing factors: Decreased immunocompetence
Elderly patients Immunosuppressive drugs
Zoster (Shingles)
Unilateral vesicular eruptions Prodromes of pain and parasthesia for up to 2 weeks Trigeminal Nerve:
Complications Post herpetic neuralgia (due to fibrosis around the nerves) Ramsay Hunt syndrome: involvement of geniculate ganglion
Coxsackievirus Enteroviradae
Herpangina
Coxsackie Viruses, Group A, RNA Children Sudden onset of fever, sore throat, nausea, vomiting, diarrhea and lymphadenopathy. Vesicles and ulcers in posterior oral cavity D/D: primary herpes Treatment is symptomatic
Coxsackie A16 Spread in households Oral lesions almost always present Oral lesions resemble herpangina but can be larger 7-10 days.
EBV Young adults Transmitted by saliva Clinically: pharyngitis, LN enlargement Fever, prolonged malaise Non specific oral manifestation Petechei on junction of hard and soft palate Serology: atypical peripheral lymphocytes
EBV
Nasopharyngeal carcinoma Hairy leukoplakia Burkitts lymphoma Oral squamous cell carcinoma?
Measles (Rubeola)
Paramyxovirus Children Prodromal symptoms Koplik spots (white spots on a red background) disappear as skin rash starts
Measles (Rubeola)
Skin rash: start on face, go to trunk Fever Complications Otitis media, pneumonia, encephalitis, brain damage Noma may be a complication in malnourished patients
Cytomegalovirus
Herpes group Rarely causes disease in immunocompetent Subclinical infection is common 40-60% of population Affects immunocompromised individuals
CMV Manifestations
Bacterial infections
Immunsuppression, trauma Chronic gingivitis Association with AIDS Malnutrition and poverty Smoking, fatigue
Clinically Ulceration of interdental papilla and gingival margins Grey-green psuedomembrane, surrounded by linear erythema Halitosis, salivation, lymphadenopathy
ANUG
Psuedomembrane contains: Necrotic debris, exudate, bacteria Persistent form is associated with AIDS ANUG:Important factor to develop NOMA
Orofacial gangrene: severe rapidly destructive Malnourished children, with concurrent infections with measles or malaria
Actinomycosis
Chronic and endogenous, anaerobic, Gram positive Suppurative Actinomyces israelli predominate Soft tissues of the submandibular region Source of infection: infected root canal or third molar Firm swelling (painless) that suppurate Multiple sinuses pointing to skin sulphur granules
Actinomycosis
Actinomycosis
neutrophils
Actinomyces colonies
Histopathology: Granulomatous inflammation Surrounded by granulation tissue Transport of organisms by macrophages Central suppuration
Syphilis
Shallow painless ulcer Indurated base Associated with lymphadenopathy Heals spontanously Dense mononuclear infiltrate mainly plasma cells Heals in 6 weeks
6 weeks later
Secondary syphilis: skin rash and mucous patch Snail track ulcers, flat areas of ulceration that coalesced
Years later
Tertiary :
Gumma:
Necrosis and type IV hypersensitivity Perforation of palate Histopathology: coagulative necrosis surrounded by granulation tissue, giant cells and macrophages due to endarteritis obliterance Followed by:
Atrophic glossitis:
Syphilitic leukoplakia
Congenital Syphilis
Miscarriage, still birth or neonatal infection Collapse of nasal bridge Hutchinson triad: blindness, deafness, dental anomalies Hutchinson incisors (notched teeth)
hard tissue
Tuberculosis
Primary oral infection Secondary oral infection: infected sputum from pulomonary TB
Classical TB ulcer:
Gingival involvement:
Granulomatous inflammation
TB lymphadenitis:
Tuberculous lymphadentitis
Tuberculosis
Granulomas with central necrosis Identification of Acid Fast Bacilli 2 antimicrobial agents: isoniazide and rifampicin, 4-8 months
Treatment:
Leprosy
Tuberculoid Lepromatous
Leprosy
Variable degree of facial deformity Nodules, ulceration, fibrosis Anterior gingiva of maxilla, tongue palate,
Leprosy
Tuberculoid leprosy
Lepromatous leprosy
Gonorrhoea
Neisseria gonorrhea Mainly tonsillar and soft palatal lesions Erythema, vesicles, ulcers, pain