Does YAP influence cell proliferation and apoptosis in benign epithelial odontogenic lesions?

Author:

Gonçalo Rani Iani Costa1ORCID,Sousa Julliany Taverny1ORCID,Costa Carla Samily de Oliveira1,Mafra Rodrigo Porpino1ORCID,Santos Janaina Lessa de Moraes dos1,da Silva Leorik Pereira2ORCID,Queiroz Lélia Maria Guedes1

Affiliation:

1. Department of Oral Pathology Federal University of Rio Grande do Norte Natal Brazil

2. Oral Histopathology Service Federal University of Campina Grande Patos PB Brazil

Abstract

AbstractObjectiveTo analyze the immunohistochemical expression of YAP and its correlation with markers involved in cell proliferation and apoptosis in benign epithelial odontogenic lesions.Study DesignThe sample consisted of 95 cases of odontogenic lesions (25 dentigerous cysts, 30 non‐syndromic odontogenic keratocysts, 30 conventional ameloblastomas, and 10 unicystic ameloblastomas) and 10 dental follicles used as normal odontogenic tissue. The histological sections were submitted to immunohistochemistry with YAP, cyclin D1, Ki‐67, and Bcl‐2 antibodies. Immunoexpression was analyzed qualitatively and quantitatively using an adapted method. The collected data were analyzed descriptively and statistically (p ≤ 0.05).ResultsThe highest YAP expression was observed in odontogenic keratocysts, followed by unicystic ameloblastomas and conventional ameloblastomas, which exhibited moderate immunoreactivity predominantly in peripheral cells. Furthermore, significant differences in YAP immunoexpression were observed between the groups analyzed, with significant positive correlations between YAP and cyclin D1 in dentigerous cysts and unicystic ameloblastomas and between YAP and Ki‐67 in unicystic ameloblastomas (p < 0.05). However, there were no statistically significant correlations between YAP and Bcl‐2 immunoexpression in the groups studied.ConclusionYAP may influence epithelial cell proliferation in odontogenic cysts and tumors, suggesting its possible participation in the progression of the odontogenic lesions studied.

Publisher

Wiley

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