Aging and osteoarthritis: Central role of the extracellular matrix

• Published in: Ageing research reviews Vol. 40; pp. 20 - 30
• Main Authors: Rahmati, Maryam, Nalesso, Giovanna, Mobasheri, Ali, Mozafari, Masoud
• Format: Journal Article
• Language: English
• Published: England 01-11-2017
• Subjects: Aging - drug effects; Aging - metabolism; Aging - pathology; Animals; Bone Density Conservation Agents - pharmacology; Bone Density Conservation Agents - therapeutic use; Cartilage, Articular - drug effects; Cartilage, Articular - metabolism; Cellular Senescence - drug effects; Cellular Senescence - physiology; Chondrocytes - drug effects; Chondrocytes - metabolism; Chondrocytes - pathology; Disease Progression; Extracellular Matrix - drug effects; Extracellular Matrix - metabolism; Extracellular Matrix - pathology; Humans; Osteoarthritis - drug therapy; Osteoarthritis - metabolism; Osteoarthritis - pathology; Oxidative Stress - drug effects; Oxidative Stress - physiology; Quality of Life; Aging; Extracellular matrix; Inflammatory mediators; Articular cartilage; Chondrocyte; Osteoarthritis
• ISSN: 1568-1637; 1872-9649
• DOI: 10.1016/j.arr.2017.07.004

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.