Bone destruction in chronic otitis media is not mediated by the RANKL pathway or estrogen receptor-alpha

Author:

Heo Kyung Wook1,Noh MinHye2,Hur Dae Young2,Hong Tae Ui1,Park Sung Yool1,Kim Woo Jin1ORCID

Affiliation:

1. Department of Otorhinolaryngology-Head & Neck Surgery, Busan Paik Hospital, Busan, South Korea

2. Anatomy and Research Center for Tumor Immunology Inje University College of Medicine, Busan Paik Hospital, Busan, South Korea

Abstract

Background Chronic otitis media with or without cholesteatoma progresses with various degrees of bone resorption and remodeling. Estrogen mediates osteoprotective effects through the receptor activator of NF-κB ligand (RANKL) pathway, which is mainly mediated by estrogen receptor-alpha (ER-α). Objectives The present study investigated the expression patterns of receptor activator of NF-κB (RANK), osteoprotegerin (OPG), RANKL, and ER-α in pathological tissue from patients with chronic otitis media to determine the roles of those factors in osteolytic mechanisms underlying the pathogenesis of chronic otitis media. Methods Normal and pathological specimens from 18 patients with chronic otitis media were examined. Results There were no significant differences in RANK, OPG, RANKL, or ER-α mRNA expression between normal and pathological specimens of epithelial tissue. Conclusions Our findings suggested that RANK, OPG, RANKL, and ER-α are not associated with the bone destruction in chronic otitis media; other cytokines may directly activate the osteoclasts in chronic otitis media.

Funder

2021 Inje University Busan Paik Hospital research grant

Publisher

SAGE Publications

Subject

Multidisciplinary

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