慢性中耳炎中的骨质破坏并非由 RANKL 途径或雌激素受体-α介导。
Bone destruction in chronic otitis media is not mediated by the RANKL pathway or estrogen receptor-alpha.
机构信息
Department of Otorhinolaryngology-Head & Neck Surgery, Busan Paik Hospital, Busan, South Korea.
Anatomy and Research Center for Tumor Immunology Inje University College of Medicine, Busan Paik Hospital, Busan, South Korea.
出版信息
Sci Prog. 2023 Jul-Sep;106(3):368504231199204. doi: 10.1177/00368504231199204.
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.
背景
伴有或不伴有胆脂瘤的慢性中耳炎会出现不同程度的骨质吸收和重塑。雌激素通过核因子 κB 受体激活配体（RANKL）途径发挥骨保护作用，该途径主要由雌激素受体-α（ER-α）介导。
目的
本研究旨在探讨核因子 κB 受体激活剂（RANK）、骨保护素（OPG）、RANKL 和 ER-α在慢性中耳炎患者病理组织中的表达模式，以确定这些因子在慢性中耳炎发病机制中的溶骨性机制中的作用。
方法
检查了 18 例慢性中耳炎患者的正常和病理标本。
结果
上皮组织的正常和病理标本中 RANK、OPG、RANKL 或 ER-αmRNA 的表达无显著差异。
结论
我们的研究结果表明，RANK、OPG、RANKL 和 ER-α与慢性中耳炎的骨质破坏无关；其他细胞因子可能直接激活慢性中耳炎中的破骨细胞。
Zotero 插件