Gingivostomatitis

Gingivostomatitis is classically caused by primary infection with HSV-1 (rarely HSV-2), typically affecting children aged 1-5 years, often acquired through contact with infected saliva. Pathophysiology involves viral replication in epithelial cells of the oral mucosa causing vesicle formation, which rupture to form painful, shallow ulcers with erythematous bases. Clinically, patients present with high fever, irritability, drooling, refusal to eat/drink (risk of dehydration), painful vesicles/ulcers on the gingiva, hard/soft palate, tongue, buccal mucosa, and lips, and tender submandibular/cervical lymphadenopathy. The condition is typically self-limited, resolving in 7-14 days. After primary infection, HSV becomes latent in the trigeminal ganglion and can reactivate later as herpes labialis (cold sores) triggered by stress, sunlight, or immunosuppression. Diagnosis is usually clinical; Tzanck smear shows multinucleated giant cells, and PCR or viral culture can confirm if needed. Treatment is supportive (hydration, analgesics like topical lidocaine, antipyretics); oral acyclovir may shorten disease course if started early, especially in severe cases or immunocompromised patients. Key differentials include herpangina (coxsackievirus, posterior oropharynx, no gingival involvement), aphthous ulcers (non-vesicular, no systemic symptoms), and hand-foot-mouth disease. A key USMLE testing point is distinguishing primary HSV gingivostomatitis (children, gingiva + oral mucosa, systemic symptoms) from recurrent herpes labialis (adults, lip-only lesions, triggered by stress/UV).