B - Catenin expression in odontogenic keratocyst

Abstract

The odontogenic keratocyst (OKC) is a unique odontogenic cyst with aggressive nature and potential of recurrences. In the last classification of the odontogenic tumors by the World Health Organization (WHO) their nomenclature has been proposed to be changed to keratocystic odontogenic tumors. Since recent reports could prove the involvement of wingless (Wnt)-signaling pathway and -catenin in the pathogenesis of many odontogenic and neoplastic lesions, we investigated the expression of -catenin in the OKC and compared the result with that in the ameloblastoma and dentigerous cyst (DC). Materials and methods: In this analytic-descriptive comparative study, 57 paraffin-embedded blocks of OKC, DC and ameloblastoma (19 specimens each one) were evaluated. All the samples were assessed by immunohistochemistry method for -catenin expression (DAKO monoclonal antibody, Denmark). Cases with stained cells >30% with regard to expression of -catenin were assigned as positive for -catenin expression. The data were analyzed by descriptive (frequency-percentage) statistics, Chi square or Fishers exact tests, One-way ANOVA and Tukey post-hoc test. Results :The expression rates of membranous, Cytoplasmic and nuclear -catenin were 68.4%, 89.5% and 5.3% in the OKC group; 78.9%, 100% and 26.3 in the ameloblastoma group; and 42.1%, 84.2% and 5.3% in the DC group, respectively. The expression rate of membranous -catenin was significantly lower in the DC group comparing with that in the OKC and ameloblastoma groups (p=0.05). The other expression rates were comparable between the three groups (p>0.05). Conclusion:Expression of membranous -catenin may help in differentiating between OKC and ameloblastoma from DC; however, its intracellular accumulation could not be used to define the neoplastic nature of OKC against DC. Nevertheless, considering the intracellular accumulation of -catenin in majority of cases in all three conditions indicates a role in development of odontogenic epithelium in these entities through inappropriate regulation of cell cycle.