Cyclooxygenase-2 protein expression modulates cell proliferation and apoptosis in solid ameloblastoma and odontogenic keratocyst. An immunohistochemical study

Abstract

Background: Cyclooxygenase-2 protein is a critically important mediator in inflammation that influences proliferation, apoptosis, angiogenesis, and metastasis. Previous works showed a relationship between cyclooxygenase-2 and tumourigenesis in humans and animal models. In epithelial odontogenic tumours and cysts, increased cell proliferation and survival have been linked to its pathogenesis and tumour development. The aim of the present study was to analyze the immunohistochemical expression of cyclooxygenase-2 in solid ameloblastoma and odontogenic keratocyst and its association with proteins related to cell proliferation and apoptosis.

Methods: This study was conducted on 40 cases from the Pathological Anatomy Service, University of Chile. The cases were diagnosed as solid ameloblastoma (n=21) and odontogenic keratocyst (n=19) according to WHO 2017. Slides prepared from paraffin-embedded sections were immunohistochemically stained for cyclooxygenase-2, cyclin D1, Ki-67, p63, and Bcl- 2. Statistical evaluation was performed by the Shapiro-Wilk test, ANOVA Mann-Whitney test, and Spearman's correlation coefficient (P < 0.05).

Results: There were significant differences in the immunoexpression of cyclin D1, Ki-67, and Bcl-2 between solid ameloblastoma and odontogenic keratocyst. Likewise, there was a significant difference in the immunoexpression of p63 between follicular and plexiform histological types/subtypes of solid ameloblastoma. Lastly, there were statistical associations between cyclooxygenase-2 and Ki-67 for solid ameloblastoma and between cyclooxygenase-2 and p63 for odontogenic keratocyst.

Conclusion: A high level of cyclooxygenase-2 is related to increased cell survival and proliferative activity in solid ameloblastoma and odontogenic keratocyst. This event might contribute to tumoural progression and local invasiveness in these lesions.