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 analyse 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.

Immunohistochemical Analysis of Dentigerous Cysts & Odontogenic Keratocysts Associated with Impacted Third Molars: A Systematic Review

“…Cell adhesion, proliferation, and apoptosis markers such as Bcl-2, PCNA, p53, and Ki-67 play pivotal roles in the pathogenesis of odontogenic lesions, including dentigerous cysts (DC), radicular cysts (RC), and odontogenic keratocysts (OKC) [27,29,32,50]. The expression of these markers provides critical insights into the biological behaviors of these lesions and their implications for diagnosis, prognosis, and therapy.…”

“…Elevated expressions of Bcl-2 and Ki-67 are associated with the aggressiveness and likelihood of recurrence in these lesions [27,29]. Similarly, increased p53 expression is linked to greater cell proliferation and aggressiveness [32,50]. The variation in the expression of these biomarkers across different odontogenic lesions offers essential diagnostic and prognostic information, aiding in their differentiation and management.…”

“…In essence, the analysis of cell adhesion, proliferation, and apoptosis markers not only enriches our understanding of the pathogenesis of these conditions but also identifies key diagnostic and therapeutic targets. These insights are invaluable for the development of tailored treatment strategies and underscore the importance of ongoing research to find innovative management approaches for odontogenic lesions, with the goal of improving patient outcomes by addressing the molecular basis of these conditions [27,29,32,50] (Table 3).…”