SHORT COMMUNICATION Journal of Oral Medicine, Oral Surgery, Oral Pathology and Oral Radiology;2015;1(1):48-50 48 VALACYLOVIR IN THE MANAGEMENT OF HERPETIC GINGIVOSTOMATITIS AND HERPETIC LABIALIS: CASE REPORT AND REVIEW OF LITERATURE Virender Gombra 1, *, Mandeep Kaur 2 , Shamimul Hasan 3 , Arpita Rai 4 1,3,4 Assistant Professor, 2 Associate Professor, Department of Oral Medicine and Radiology, Faculty of Dentistry, Jamia Millia Islamia. *Corresponding Author: Email: vgombra@jmi.ac.in ABSTRACT Acute herpetic gingivostomatitis (AHGS) is the primary manifestation of herpes simplex-I (HSV-I) infection which causes painful vesicles and ulcers on gingiva and palate. AHGS commonly involves the immobile mucosa of the oral cavity. Recurrent painful oral infections can also occur in immunocompromised and HIV positive patients causing discomfort. Recurrent symptomatic and asymptomatic herpetic labialis may occur because of reactivation of latent virus in sensory ganglia.The objective of this paper is to discuss cases of acute herpetic gingivostomatitis and herpetic labialis and evaluate the effect of valacyclovir in the management of herpetic infections. Keywords: Acute herpetic gingivostomatitis, Herpetic labialis, Valacyclovir. INTRODUCTION Herpetic gingivostomatitis is a viral infection caused by herpes simplex virus (HSV) of the herpetoviridae family. (1) HSV is a double- stranded DNA virus which is a type of human herpes virus (HHV). The herpetic simplex infections are caused by HSV-1 and HSV-2. Orofacial infections are mostly associated with HSV-1, whereas lower body infections are usually associated with HSV-2. (2) The monthly frequencies of recurrence are 0.33 in genital HSV-2 infections, 0.12 in orolabial HSV-1 infections, 0.020 in genital HSV-1 infections and 0.001 in oral HSV-2 infections. (3) The recurrences are more when HSV-1 is oral and HSV-2 is genital. (4) Acute HSV infections occurs at two peaks, one at the age of 6 months to 5 years and other at 20 years of age. (2) The virus causes chronic latent infection after inoculation along the sensory nerves such as trigeminal ganglion. Extraneuronal latency within the epithelium may result in recurrent lesions. The incubation period range is few days to three weeks. Severity of the lesion is related to the virulence of HSV and the host’s immunity. Virions remain latent in asymptomatic HSV infection with minimal epithelial destruction and infect adjacent epithelial cells with inflammatory response in symptomatic infections. (1) The predisposing factors include stress, fever, extremes in temperature, ultraviolet radiation, immunosuppression or trauma. Asymptomatic shedding of HSV in saliva may cause transmission of virus. (5) Virus infection causes acantholysis of intermediate and basal cells leading to vesicle formation. (6) After onset of symptoms, peak viral load occurs at 48 hrs, with no virus detected beyond 96 hrs. HSV type 1 may cause asymptomatic infection or acute herpetic gingivostomatitis (AHSG) as primary infection whereas recurrent infection results in herpetic labialis. (7) AHGS and herpetic labial is are self-limiting lesions. Acyclovir is conventional pharmacotherapy advised for acute painful and severe recurrent infections. Valacyclovir is altered form of acyclovir with good gastrointestinal absorption and better oral bioavailability. (2) CASE REPORT 1 A 24 years old female patient reported with lesions in the mouth with inability to brush, chew and take liquid diet. Patient gave history of fever 4 days back followed by lesion in mouth and throat. On examination submandibular lymph nodes were palpable, mobile and tender. Gingiva was erythematous with multiple shallow ulcers on hard palate (Figure-1). Diagnosis of AHGS was given. Valacyclovir 1000 mg twice /day was prescribed for 3 days along with acetamenophen-500mg T.D.S. with local anaesthetic agents, Benzydamine mouth rinse three times /day and soft diet. After 3 days, relief in pain and improvement of lesion was observed (Figure-2) and same medication was given for two days which resulted in complete resolution of the lesion. Figure: 1