Lichen planus and oral leukoplakia, white lesions of the oral cavity were examined using immunohistochemical methods. The monoclonal antibodies and enzymes disclosed a dysregulation of cell growth not previously recognized in these possibly premalignant lesions. In the specific entity of erosive lichen planus we observed an abnormal expression for the p53, and the stress proteins in the oral mucosa. In the characteristic inflammatory infiltrate we noted an increase in Bcl-2 expression. Nucleosome formation was also found to be increased in the basal segment of the oral mucosa. Oral leukoplakia exhibiting dysplasia also showed high levels of p53 expression with localized areas of nucleosome formation, and Bcl-2 staining. Taken together these results indicated a profound dysregulation of cell growth and death. Using tissues sections from a hamster buccal pouch oral mucosa treated with the carcinogen 7,12 dimethylbenz(a)anthracene (DMBA) a similar immunohistochemical study was performed using the identical monoclonal antibodies and enzymes. Early in the process of oral carcinogenesis we saw the expression of p53. and the stress proteins (70,25kD). Nucleosome formation was seen but was gradually replaced when carcinoma-in-situ was histopathologically evident, Bcl-2 was then noted in localized and expanding areas of the mucosa. In combination with markers for cell proliferation (PCNA, cell cycle) these studies indicated that oral carcinogeneses involved a suppression of programmed cell death and the normal expression of proteins such as p53 and stress proteins.
