Aberrant Immunohistochemical Expression of P53 in Ameloblastoma, Ameloblastic Carcinoma, Dentigerous Cyst and Odontogenic Keratocyst: A comparative Study

Document Type : Original Article

Authors

1 Lecturer of Oral Pathology, Faculty of Oral and Dental Medicine, Future University in Egypt, Cairo

2 Associate Professor of Oral and Maxillofacial Surgery, Faculty of Oral and Dental Medicine, Future University in Egypt, Cairo

3 Lecturer of Oral and Maxillofacial Surgery, Faculty of Oral and Dental Medicine, Future University in Egypt, Cairo

4 Associate Professor of Oral Pathology, Faculty of Oral and Dental Medicine, Future University in Egypt, Cairo

Abstract

Background: odontogenic lesions comprise a diverse group exhibiting a wide range of clinical and biological behaviors, demanding a meticulous understanding for accurate diagnosis and management. In response to DNA damage, the p53 tumor suppressor protein functions as a key regulator, inducing either cell cycle arrest or apoptosis. Mutations in the p53 gene are frequently observed in human cancers; however, the role of p53 expression in odontogenic lesions remains unclear.
Material and methods: A retrospective design was employed to evaluate and compare p53 protein expression patterns, detected by immunohistochemistry, in ameloblastoma, ameloblastic carcinoma, dentigerous cyst, and odontogenic keratocyst. Formalin-fixed and paraffin-embedded archival tissue specimens from 42 patients were analyzed for p53 expression. Immunopositivity mean area fraction was determined following the removal of connective tissue. Statistical analysis to compare mean area fraction between groups was performed. Clinical records were reviewed to collect demographic data (age, gender and lesion site) for all cases included in the study.
Results: immunohistochemical p53 expression was demonstrated as cytoplasmic brown granular staining in the epithelial cells of ameloblastomas, dentigerous cyst and odontogenic keratocyst groups. Conversely, the ameloblastic carcinoma group exhibited significantly less mean values of P53 immunopositivity than the other cases. There was no significant difference between ameloblastoma, dentigerous cyst and odontogenic keratocyst groups. Meanwhile, our findings revealed an overall male predominance and prevalence to the mandible.
Conclusions: aberrant expression of p53 protein could be implicated in the pathogenesis of odontogenic lesions. Further research is needed to elucidate the precise mechanisms underlying p53-mediated progression for these lesions.

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