Document Type

Article

Publication Date

4-2023

Abstract

Background: Odontogenic neoplasms and cysts have diverse biological behaviors, ranging from indolence to aggression along a spectrum. The proliferating cell nuclear antigen (PCNA) is an antigen involved in DNA synthesis and proliferation. Focal adhesion kinase (FAK) is a cytoplasmic molecule associated with cellular signaling, growth, and invasion. PCNA and FAK markers have been shown to be involved in neoplastic proliferation, invasion, and migration. Hence, an immunohistochemical assay of PCNA and FAK can be used as a predictive tool for the level of aggressive behavior of odontogenic lesions. Methods: The current study was conducted to evaluate the expressions of PCNA and FAK. A double immunohistochemical technique for conventional ameloblastoma (AB), unicystic AB, calcifying epithelial odontogenic tumor (CEOT), and glandular odontogenic cyst (GOC) was used to evaluate the role of both markers in assessments of the aggressiveness of selected odontogenic lesions. All formalin-fixed paraffin-embedded blocks (n = 10) for each studied group were double PCNA and FAK immunostained and then assessed using a transmission light microscope and an image-analyzer computer system. Statistical analysis was performed with a one-way analysis of variance (ANOVA) test followed by Tukey’s post hoc test. Results: All study groups showed nuclear immunoreactivity of PCNA and cytoplasmic immunoreactivity for FAK. The greatest mean nuclear count of PCNA and the greatest mean area percent for FAK were both recorded in the aggressive lesions; i.e., the CEOT group and conventional AB group. The non-aggressive unicystic AB group had a lower mean nuclear count for PCNA and showed the lowest mean area percent for FAK. Conclusions: In conclusion, PCNA and FAK immunoexpression profiles may have a strong correlation with the aggressive nature of AB, CEOT, and GOC. Hence, PCNA and FAK markers could aid in their routine examination, treatment planning, and prognosis.

Download

Share

COinS