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Aging and Osteoarthritis: Central Role of the Extracellular Matrix Publisher Pubmed



Rahmati M1, 2 ; Nalesso G3 ; Mobasheri A4, 5, 6 ; Mozafari M1, 2, 7
Authors
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Authors Affiliations
  1. 1. Cellular and Molecular Research Center, Iran University of Medical Sciences (IUMS), Tehran, Iran
  2. 2. Department of Tissue Engineering & Regenerative Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences (IUMS), Tehran, Iran
  3. 3. Department of Veterinary Pre-Clinical Sciences, School of Veterinary Medicine, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH, United Kingdom
  4. 4. The D-BOARD European Consortium for Biomarker Discovery, The APPROACH Innovative Medicines Initiative (IMI) Consortium, School of Veterinary Medicine, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH, United Kingdom
  5. 5. Arthritis Research UK Centre for Sport, Exercise and Osteoarthritis, Arthritis Research UK Pain Centre, Medical Research Council and Arthritis Research UK Centre for Musculoskeletal Ageing Research, University of Nottingham, Queen's Medical Centre, Nottingham, NG7 2UH, United Kingdom
  6. 6. Center of Excellence in Genomic Medicine Research (CEGMR), King Fahd Medical Research Center (KFMRC) and Sheik Salem Bin Mahfouz Scientific Chair for Treatment of Osteoarthritis with Stem Cells, King AbdulAziz University, Jeddah, 21589, Saudi Arabia
  7. 7. Bioengineering Research Group, Nanotechnology and Advanced Materials Department, Materials and Energy Research Center (MERC), P.O. Box 14155-4777, Tehran, Iran

Source: Ageing Research Reviews Published:2017


Abstract

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. © 2017 Elsevier B.V.