No abstract

Background and Objectives:The behavior of odontogenic lesions varies with some tumors behaving like a cyst and some cysts behaving like tumors. p63, a member of the p53 family of tumor suppressor genes has recently come into light in view of its role as an oncogene. The aim of the present study was to investigate the expression of p63 protein in OKC, Solid ameloblastoma, Unicystic Ameloblastoma and Follicular tissue.Materials and Methods:p63 expression was compared in 12 cases of OKC, 12 Solid Ameloblastoma, 14 cases of Unicystic ameloblastoma and 10 cases of Follicular tissue using immunohistochemical technique. All 48 cases were subjected to heat-induced antigen retrieval method using citrate buffer in a pressure cooker. Then the sections were stained with anti-p63 polyclonal antibody and visualized using super sensitive polymer HRP detection system. In each case, number of cells showing p63 positivity were assessed in two compartments - basal and suprabasal and compared.Results:Statistical analysis showed that p63 expression in the suprabasal compartment in Odontogenic keratocysts was equivalent to that of central neoplastic cells of Solid Ameloblastoma and Unicystic Ameloblastoma type 3. Statistically significant difference in the expression of p63 was observed between OKC and Unicystic Ameloblastoma Type 1 and Solid Ameloblastoma and Unicystic Ameloblastoma Type 1.Conclusion:We conclude that the higher expression of p63 in these odontogenic lesions correlates well with their aggressive behavior and thereby suggesting alterations in treatment modalities.

Background and Objectives:To determine the immunohistochemical (IHC) localization of basement membrane component laminin in histological grades of oral squamous cell carcinoma (OSCC). The purpose of this study was to demonstrate the loss of continuity of the basement membrane in OSCC using an antibody directed against laminin using advanced polymer staining system.Materials and Methods:A total of 30 cases of OSCC: 10 cases of well differentiated squamous cell carcinom (WDSCC), 10 cases of moderately differentiated squamous cell carcinoma (MDSCC), and 10 cases of poorly differentiated squamous cell carcinoma (PDSCC) were subjected to heat-induced antigen retrieval method using ethylene-di-amine-tetraacetic acid buffer in a microwave oven. Then the sections were stained with anti-laminin polyclonal antibody and visualized using super sensitive polymer horseradish peroxidase detection system. In each case, the integrity of the basement membrane laminin was assessed by using statistical analysis.Results:Statistical analysis showed a decreased distribution of laminin from WDSCC to MDSCC to PDSCC (P value 0.0573). The intracytoplasmic staining of laminin gradually increased from WDSCC to MDSCC to PDSCC (P value 0.0198).Interpretation and Conclusion:WDSCC cases showed more laminin expression in basement membrane around the tumor islands and less loss of continuity compared to MDSCC and PDSCC cases suggesting a greater enzymatic degradation of basement membrane components in MDSCC and PDSCC than WDSCC. The loss of structural basement membrane laminin and the presence of laminin in the tumor cells of PDSCC cases suggest that laminin helps in tumor invasion. The expression of laminin in the basement membrane may be a useful parameter to evaluate tumor histologic differentiation and aggressiveness.

Background and Objectives:This study aims at the observation of the immunohistochemical expression of laminin in adenoid cystic carcinoma (ACC) of salivary gland origin and to analyze the distribution of laminin in various components of the tumor and correlate the expression of laminin with the growth and differentiation of the tumor.Materials and Methods:Thirty cases of ACC were subjected to immunohistochemical study using polyclonal antihuman laminin primary antibody, distribution of laminin in each case of ACC was observed in the following areas: Intracellularly, inner borders of the pseudocystic spaces, within the lumen of the pseudocysts, around the tumor islands and in the intervening stroma.Results:Laminin positivity was observed in the inner aspect of the pseudocystic spaces in 15 cases, within the lumen of pseudocystic spaces in 22 cases, in the intervening stroma in 20 cases, bordering the tumor islands in 16 cases and intracellularly in 4 cases.Interpretation and Conclusion:Based on these observations, it can be assumed that laminin plays a major role in proliferation of the tumor cells and in pseudocyst formation. Thus, laminin might play a significant role in the growth and differentiation of ACC and also help in assessing the prognosis of the tumor.

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.