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.

Localization of beta catenin across the domain of odontogenic lesions: A systematic review

“…The data pool contained 56 articles after removal of the duplicates. These were further screened to 34 after scrutinising the title and abstract and eligibility evaluation was assessed by full text reading 1–11,13–35 . The final selection included 34 articles for qualitative analysis (Figure 2).…”

“…Wnt/β catenin/ TCF behaviour pathway comprises of the major pathway in odontogenesis where activated Wnt dissociates β catenin from the degradation complex during embryogenesis or homeostasis renewal, blocking its phosphorylation 13 . Subsequently the activated β catenin exhibits nuclear translocation stimulating cellular proliferation via transcription factors 13 . The development and progression of certain tumours can also stem from numerous interactions between stroma and epithelial cells 5 .…”

“…The bulk of the nuclear positivity was exhibited by odontoma and CCOT cases. Recent studies have reported that the ghost cell lesions have a propensity to manifest a hyperactivation of β catenin and oncogenic transformation of Wnt target genes causing uncontrolled cell multiplication 8,13 . Additionally, reports suggest that a balance exists between the activator Wnt1 and the inactivator Wnt5a in CCOT which plays a part in ghost cell development 7 .…”

“…activated β catenin exhibits nuclear translocation stimulating cellular proliferation via transcription factors. 13 The development and progression of certain tumours can also stem from numerous interactions between stroma and epithelial cells. 5 Being an indispensable part of the junctional complex, aberrant expression of β catenin and cadherin results in reduced cell-cell adhesion, impairs tissue morphogenesis and thus causes malignant cell invasion.…”

“…Based on the QUADAS-2 tool, 18 studies achieved a low risk rate on all domains, 2,[8][9][10][11]13,[15][16][17]19,20,23,[26][27][28][29]31,33 4 studies were evaluated as high risk 3,4,7,34 and 5 with unclear risk 1,6,30,32,35 in patient selection domain. Within Index test domain, 4 had high risk 4,14,21,25 while 1 was with unclear risk.…”