Comparison of b-Catenin Protein Expression in Calcifying Odontogenic Cyst and Dentinogenic Ghost Cell Tumour

Abstract

Introduction: Calcifying Cystic Odontogenic Tumour (CCOT)/ Calcifying Odontogenic Cyst (COC) display a varying tissue morphology, while exhibiting different biological progression also at the same time. Attempts at classifying COC have largely been unsuccessful due to the present lack of knowledge about the development of these tumours and their underlying molecular changes. Wingless-beta catenin (Wnt–β catenin) signalling pathway has been found to be a cornerstone in the ectodermal development and tumour initiation-progression to malignant tumours, but its specific role in the pathogenesis of odontogenic ghost cell lesions is unknown. Aim: To elucidate the participation and comparison of β-catenin protein expression in pathogenesis of benign odontogenic ghost cell lesions, CCOT and Dentinogenic Ghost Cell Tumour (DGCT). Materials and Methods: A cross-sectional Immunohistochemical (IHC) study was performed in the Department of Oral and Maxillofacial Pathology, AECS Maaruti College of Dental Sciences and Research Centre, Bengaluru, Karnataka, India, from December 2019 to June 2021. Research was conducted on tissue sections of centrally located 16 cases of CCOT categorised as group 1 and four cases of DGCT categorised as group 2 using β-catenin tumour marker. The study samples were retrieved from the archives. IHC stained slides were subjected for histopathological analysis, where labelling index of tumour cells were assessed in three high power fields. Resultant β-catenin expression was compared between Benign Odontogenic Ghost Cell Lesions (BOGCL). Results were subjected to statistical analysis, Statistical Package for Social Sciences for Windows 17.0 (SPSS, Philadelphia, IL) software to analyse the data. Results: β-catenin positivity was assessed in tumour cells of both the groups, 16 CCOT (group 1) and 4 DGCT (group 2). In each case, number of cells in three high power field i.e., under 40X magnification were evaluated. Both the groups expressed membranous, cytoplasmic and nuclear positivity in the basaloid tumour cells. Whereas, ghost cells showed no reactivity to the biomarker, β-catenin. On comparison using Mann Whitney U and Wilcoxon W test, there was no statistically significant difference in β-catenin expression between CCOT and DGCT. Conclusion: β-catenin plays an important role in the tumourigenesis of benign odontogenic ghost cell lesions. Immunohistochemically CCOT and DGCT showed no significant difference in the β-catenin expression. Hence, the results suggest that CCOT and DGCT may show variation in clinical behaviour but share similar histogenesis.