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The articular cartilage is exquisitely sensitive to mechanical load. Its structure is largely defined by the mechanical environment and destruction in osteoarthritis is the pathophysiological consequence of abnormal mechanics. It is often overlooked that disuse of joints causes profound loss of volume in the articular cartilage, a clinical observation first described in polio patients and stroke victims. Through the 1980s, the results of studies exploiting experimental joint immobilisation supported this. Importantly, this substantial body of work was also the first to describe metabolic changes that resulted in decreased synthesis of matrix molecules, especially sulfated proteoglycans. The molecular mechanisms that underlie disuse atrophy are poorly understood despite the identification of multiple mechanosensing mechanisms in cartilage. Moreover, there has been a tendency to equate cartilage loss with osteoarthritic degeneration. Here, we review the historic literature and clarify the structural, metabolic and clinical features that clearly distinguish cartilage loss due to disuse atrophy and those due to osteoarthritis. We speculate on the molecular sensing pathways in cartilage that may be responsible for cartilage mechanoadaptation.The mechanosensitivity of musculoskeletal tissues is extremely well documented but for the most part this has focused on muscle and bone rather than articular cartilage (Ziaaldini et al., 2017; Galea et al., 2017; Uda et al., 2017). Part of the reason for this lies in the fact that the cartilage is not easily visualised; its thickness is inferred from the gap between the ends of the bone (the joint space) on a plain radiograph. Cartilage has only relatively recently been directly visualised by MRI. This article is protected by copyright. All rights reserved.

Original publication




Journal article


The Journal of physiology

Publication Date



Arthritis Research UK Centre for OA Pathogenesis, Kennedy Institute of Rheumatology, University of Oxford.