Comparative study of Bcl-2 protein expression in the epithelial cells of Keratocystic Odontogenic Tumour and Ameloblastoma

Background: Keratocystic odontogenic tumour and ameloblastoma are classified under tumours by WHO. tumour development and progression involves tumour suppressor genes and down regulation of onco-genes. Apoptosis inhibition is an important event in tumour formation which increases the life span of these cells. Aims and Objectives: To investigate the involvement of apoptosis inhibition in these lesions, expression of Bcl-2 was examined in 10 cases of KCOT (keratocystic odontogenic tumour) and ameloblastoma each. Our study revealed over-expression of Bcl-2 in all the cases in both tumours. The expression was analysed both qualitatively and quantitatively. Materials and Methods: 10 KCOT cases (sporadic parakeratinized KCOT n-9 and BCCNS KCOT n-1) and 10 Ameloblastoma cases (SMA n-9 and unicystic ameloblastoma n- 1) were selected. Immunohistochemical staining of Bcl-2 was carried out. • BCCNS(Basal cell carcinoma nevus syndrome) • SMA(Solid multicystic Ameloblastoma) • UA(Unicystic Ameloblastoma) Statistical Analysis: Differences in the mean scores for immunostain among the two types of lesions were analysed by students t test to compare the similarity or dissimilarity in the cell count of mean Bcl-2 expression between ameloblastoma and KCOT and their various layers. Results: : The intensity varied among the layers from intense to weak in basal / peripheral ameloblast- like cells and parabasal layers respectively and negative staining was seen only in superficial layer of KCOT but not in Ameloblastoma-central stellate reticulum-like cells in qualitative assessment. Quantitatively the basal layer/ peripheral ameloblast- like cells of both tumours had similar over expression while parabasal and central/superficial cells showed considerable differences. Our study indicates similar over-expression of bcl-2 in both the odontogenic lesions specifically basal layer / peripheral ameloblast- like cells which may represent tumorigenesis by escaping apoptosis. However does antiapoptotic activity and proliferative index warrant reclassification to tumour needs to be addressed.