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© Springer International Publishing Switzerland 2017. Mechanical stress is an obligatory aetiological factor in the development of OA so understanding how tissues of the joint respond to mechanical injury is likely to inform our understanding of pathogenesis. Much is known about how vascular tissues respond to damage, a process that involves activation of platelets on the exposed endothelium and recruitment of leukocytes to the site of injury. The articular cartilage is avascular yet responds rapidly and strongly to a range of mechanical stresses including cutting, avulsion, impact loading and shearing. It does so by activating a number of mechanosensitive pathways mediated by release of molecules trapped within the pericellular matrix as well as by triggering mechanoreceptors at the cell surface. In this way injury drives a number of intracellular signalling pathways, leading to a broad range of cellular responses. These pathways appear to be relevant to the in vivo response to mechanical disruption and affect the course of experimental OA.

Original publication





Book title

Cartilage: Volume 2: Pathophysiology

Publication Date



27 - 40