Infections of the Oral Mucosa 1

Dr. Rima Safadi

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

Herpes Simplex Virus

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

Mild circumoral crusting

Primary herpetic gingivostomatitis

Herpes Simplex Virus

Extraoral spread of infection: skin, fingers, nail bed, eyes

Herpetic whitlow

Microscopic features Intraepithelial vesicle

Ballooning degeneration: swollen , eosinophilic cytoplasm, pale vesicular nuclei

Enlarged, multinucleated epithelial cells Tzanck cell: Access to nerve axons

Due to ruptured epithelial cells

Tzank cells

Treatment Supportive Acyclovir in extreme cases Prognosis: self-limited resolves in 10-14 days

Study Box 11.1 (latency of HSV) in your text book

HSV remain latent in trigeminal sensory ganglia Virus reactivation associated with: Ultraviolet radiation Trauma Immunosuppression

Recurrent Herpetic Stomatitis

Asymptomatic or local symptoms Prodrome: no systemic

tingling burning paresthesia

Vesicles and ulcers recur: most common herpes labialis Intraorally: hard palate and gingiva In small clusters

Varicella-Zoster Virus
Chickenpox and herpes zoster (shingles)
Primary Infection: Varicella (Chicken pox) Prodrome: malaise, fever, lymphadenopathy Macules, papules, vesicles, ulcers on skin and oral mucosa

Especially soft palate

Skin lesions are pruritic.

Microscopic features: identical to HSV Prognosis for varicella is usually mild in children. vaccine is available. Acyclovir in immunocompromised

Treatment is supportive Antihistamines, topical lotions

Zoster (Shingles)

Multiple recurrence is rare

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:

Ophthalmic division is most frequently involved Intra or extra oral or both

Complications Post herpetic neuralgia (due to fibrosis around the nerves) Ramsay Hunt syndrome: involvement of geniculate ganglion

Coxsackievirus Enteroviradae

Over 30 types Ones worth mentioning

Herpangina Hand-foot and mouth Acute lymphonodular pharyngitis

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

Hand foot and mouth disease

Coxsackie A16 Spread in households Oral lesions almost always present Oral lesions resemble herpangina but can be larger 7-10 days.

Infectious Mononucleosis (glandular fever)

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

Infectious mononucleosis (glandular fever)

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

Neonatal, transplant, immunosuppressant

CMV Manifestations

Affect salivary glands common but asymptomatic

Xerostomia especially in AIDS

Cause non specific oral ulceration

Atypical peripheral lymphocytes

Bacterial infections

Necrotizing Ulcerative Gingivitis NUG/ ANUG

Endogenous, polymicrobial opportunistic infection Predisposing factors:

Immunsuppression, trauma Chronic gingivitis Association with AIDS Malnutrition and poverty Smoking, fatigue

Overgrowth of fusospirochaetal complex F. fusifornis, T. vincentii

High recurrence rate if underlying cause is untreated

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

Noma (cancrum oris)

Orofacial gangrene: severe rapidly destructive Malnourished children, with concurrent infections with measles or malaria

Immunosuppressed individuals Followed by rapid spread of necrosis from gingiva to cheeck

Usually preceded by NUG

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

Treponema pallidum Primary: chancre : shallow ulcer

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
Hyperkeratosis Followed by: Squamous cell carcinoma

Congenital Syphilis

Miscarriage, still birth or neonatal infection Collapse of nasal bridge Hutchinson triad: blindness, deafness, dental anomalies Hutchinson incisors (notched teeth)

Screw driver teeth

Peg shaped laterals Mulberry molars

Constricted atrophic cusps Globular masses of

Tuberculosis

Mycobacterium tuberculosis Oral infection is not common

Primary oral infection Secondary oral infection: infected sputum from pulomonary TB

Classical TB ulcer:

Painless Chronic Undermined Covered with grey slough On the tongue

Gingival involvement:

Granulomatous inflammation

Granulating gingival lesions

TB lymphadenitis:

Tuberculous lymphadentitis

Tuberculosis

Diagnosis: Biopsy, granulomatous inflammation

Granulomas with central necrosis Identification of Acid Fast Bacilli 2 antimicrobial agents: isoniazide and rifampicin, 4-8 months

Treatment:

Leprosy

Mycobacterium leprae Endemic in tropical areas 2 forms of infection:

Tuberculoid Lepromatous

Oral lesions in lepromatous 50% of patients

Secondary to nasal involvement Maxillary gingiva, palate

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