Gingivostomatitis is the most common manifestation of primary infection with herpes simplex virus (HSV).
Since HSV has an affinity for cells of ectodermal origin, infection of the oral mucosa with HSV results in intraepithelial vesicles. These vesicles soon burst and cause erosion or shallow ulcer because the submucosal connective tissue it rarely involved in replication of the virus.
The present paper reports the clinical and laboratory findings and interferon therapy in a case of primary herpetic gingivostomatitis having unusual deep ulcers developed on the lip.
A 7-year-old boy came to our clinic on September 24, 1983 with chief complaint of the burnlike pains on the lower lip. About 3 days before the visit to our clinic, he had moderate general malaise and emergence of lip pain. On oral examination, deep ulcers were observed only in the lower lip mucosa. He complained of pain even by feather touch in this region. The regional submandibular lymph nodes were enlarged and painful to the touch. He had body temperature of 36.5°C. Laboratory data included red blood cells 516×104/mm3, white blood cells 5, 500/mm3, hemoglobin 13.7g/dl, hematocrit 41.8%, differential counts of leukocytes, neutrophil 62%, eosinophil 2%, basophil 0%, lymphocyte 32%, monocyte 4%, CRP positive (2+). These hematologic data seemed generally to indicate viral infection. Since HSV-1 was isolated by tissue culture work from the swabs of mucosal lesions, this patient was diagnosed as herpetic gingivostomatitis. Seven days later, numerous ulcerative lesions appeared in the oral mucosa including lower lip, tongue and gingiva, and the body temperature elevated up to 39°C. While the inflammatory reaction subsided by administration of antibiotics and anti-inflammatory drug, the mucosal lesions were treated with the gelfoam containing human interferon-ß. 2 months later, the lesions healed with linear scars at the sites of mucosal lesions. When serum of this patient was assayed for antibody level against HSV-1 by complement fixation test at various time intervals during the therapeutic period, this antibody titer in recovery period showed a four fold increase in comparison to that at onset. From these findings, this infectious disease was precisely diagnosed as primary herpetic gingiovastomatitis.
