Cellular and Molecular Research Center, Iran University of Medical Sciences (IUMS), Tehran, Iran; Department of Tissue Engineering & Regenerative Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences (IUMS), Tehran, Iran.
Department of Veterinary Pre-Clinical Sciences, School of Veterinary Medicine, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH, UK.
Ageing Res Rev. 2017 Nov;40:20-30. doi: 10.1016/j.arr.2017.07.004. Epub 2017 Jul 31.
Osteoarthritis (OA), is a major cause of severe joint pain, physical disability and quality of life impairment in the aging population across the developed and developing world. Increased catabolism in the extracellular matrix (ECM) of the articular cartilage is a key factor in the development and progression of OA. The molecular mechanisms leading to an impaired matrix turnover have not been fully clarified, however cellular senescence, increased expression of inflammatory mediators as well as oxidative stress in association with an inherently limited regenerative potential of the tissue, are all important contributors to OA development. All these factors are linked to and tend to be maximized by aging. Nonetheless the role of aging in compromising joint stability and function in OA has not been completely clarified yet. This review will systematically analyze cellular and structural changes taking place in the articular cartilage and bone in the pathogenesis of OA which are linked to aging. A particular emphasis will be placed on age-related changes in the phenotype of the articular chondrocytes.
骨关节炎（OA）是发达国家和发展中国家老龄化人群中严重关节疼痛、身体残疾和生活质量下降的主要原因。关节软骨细胞外基质（ECM）的分解代谢增加是 OA 发展和进展的关键因素。导致基质周转率受损的分子机制尚未完全阐明，但是细胞衰老、炎症介质表达增加以及与组织固有再生潜力相关的氧化应激，都是 OA 发展的重要因素。所有这些因素都与衰老有关，并趋于最大化。尽管如此，衰老在 OA 中损害关节稳定性和功能的作用尚未完全阐明。这篇综述将系统地分析与衰老相关的 OA 发病机制中关节软骨和骨发生的细胞和结构变化。特别强调关节软骨细胞表型的年龄相关性变化。
