CALCIFYING ODONTOGENIC CYST: CLINICAL, HISTOPATHOLOGIC, AND IMMUNOHISTOCHEMICAL ANALYSIS OF β-CATENIN

Abstract

Objective To evaluate clinical and histopathologic data of COC sample and analysis of the immunohistochemical expression of β-catenin. Study Design Descriptive probabilistic correlation study of clinical, histomorphologic, and immunostaining characteristics for β-catenin. Results Clinically, all cases of COC were intrabony with equal distribution in maxilla and mandible. Histologically, cystic cases predominated, some cases associated with odontoma, and a solid case. All lesions had a cystic structure covered by odontogenic epithelium of variable thickness with ghost cells and calcifications, as well as subepithelial dentinoid material. Basal and suprabasal cells of the epithelial lining showed predominantly weak immunostaining for β-catenin in most cases and ghost cells tended to exhibit strong immunopositivity. Conclusions The results suggest that in COC occurs in a regulatory mechanism of proliferation and differentiation mediated by β-catenin. Although previously classified as a cystic odontogenic neoplasm, the cases analyzed in this study showed a clinical, histologic, and immunohistochemical profile with no neoplastic characteristics, supporting the classification as an odontogenic cyst. To evaluate clinical and histopathologic data of COC sample and analysis of the immunohistochemical expression of β-catenin. Descriptive probabilistic correlation study of clinical, histomorphologic, and immunostaining characteristics for β-catenin. Clinically, all cases of COC were intrabony with equal distribution in maxilla and mandible. Histologically, cystic cases predominated, some cases associated with odontoma, and a solid case. All lesions had a cystic structure covered by odontogenic epithelium of variable thickness with ghost cells and calcifications, as well as subepithelial dentinoid material. Basal and suprabasal cells of the epithelial lining showed predominantly weak immunostaining for β-catenin in most cases and ghost cells tended to exhibit strong immunopositivity. The results suggest that in COC occurs in a regulatory mechanism of proliferation and differentiation mediated by β-catenin. Although previously classified as a cystic odontogenic neoplasm, the cases analyzed in this study showed a clinical, histologic, and immunohistochemical profile with no neoplastic characteristics, supporting the classification as an odontogenic cyst.