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It is widely accepted that cartilage injury leads to osteoarthritis (OA), although the mechanisms by which this occurs are still poorly understood. Research in this area has been somewhat neglected in recent years, but it was a highly fashionable academic pursuit in the 18th, 19th and early 20th centuries and many seminal observations were made during this time. These included the findings that acute cartilage injury induces an active chondrocytic response, involving both degradative as well as synthetic processes that resemble OA. There was also evidence of a repair response, determined to be both from the substance of the tissue and from the underlying bone marrow.In patients, injury to cartilage is defined as either direct, e.g. following intra-articular fracture, or indirect by repetitive wear on the tissue, with age or following joint destabilisation. Although both are associated with the risk of developing OA, this risk is variable and there are emerging data to suggest that some focal cartilage lesions not only do not progress, but may actually heal spontaneously. Recent in vitro studies have begun to unravel the molecular basis for these responses, and these are identifying potentially important pathways which may be involved in driving OA, as well as those that stimulate cartilage repair. © 2010 Woodhead Publishing Limited All rights reserved.

Original publication

DOI

10.1533/9781845697792.1.137

Type

Chapter

Book title

Regenerative Medicine and Biomaterials for the Repair of Connective Tissues

Publication Date

01/01/2010

Pages

137 - 154