Abstract

Background:Reactive lesions of the oral cavity are nonneoplastic proliferations with very similar appearance to benign neoplastic lesions and are associated with chronic local irritation or trauma. Although these lesions are uncommonly associated with carcinogen exposure, at times, they present histopathologically with dysplastic epithelium, thus making it difficult to differentiate it from true potentially malignant disorders. Hence, the present study was conducted to evaluate the expression of Bcl-2 protein, an antiapoptotic marker, in reactive lesions with and without atypical epithelium and in true epithelial dysplasia, which clinically presents as premalignant disorders.Materials and Methods:The samples included 15 cases each of normal oral mucosa (NOM), reactive lesions with and without dysplasia and oral epithelial dysplasia (OED) associated with carcinogen exposure. All the samples were subjected to immunohistochemical staining using Bcl-2 antibody. The total number of cells in the basal and parabasal layers in each field and total number of cells expressing Bcl-2 among them and the staining intensity were assessed.Statistical Analysis:Kruskal–Wallis ANOVA test was used to compare the number of positive cells among the four groups. The comparison of average percentage of positive cells between the study groups was done using Mann–Whitney U-test.Results:The immunohistochemical staining for Bcl-2 protein was identified in few cells in the basal layers of NOM, reactive lesions without atypical epithelium and in the basal and parabasal layers in reactive lesions with atypical epithelium and OED, as a granular cytoplasmic staining and as an accentuation around the nuclear membrane. There was a gradual increase in the expression and intensity of staining from Group I to IV.Interpretation and Conclusion:The altered or increased expression of Bcl-2 oncoprotein in reactive lesions with atypical epithelium and in OED with carcinogen exposure may lead to prolonged cell survival and can be considered as an early molecular event in carcinogenesis, helping us in understanding the nature of dysplasia in reactive lesions, which was not considered during the histopathology reporting.

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