Abstract
Summary: Failure to appreciate how pain arises in tendinopathies may be limiting medical progress. It is assumed that tendon overuse causes inflammation, and thus pain. We critically review the inflammatory model of pain in tendinopathy and find that it does not withstand scrutiny. The generally proposed alternative model is that of mechanical discontinuity of collagen fibers, but this as well is inconsistent with numerous surgical observations. We review data suggesting that pain of tendinopathy may be largely due to yet unidentified biochemical factors activating peritendinous nociceptors when they are exposed to the environs as a result of tendon overuse injury. The noxious agent could include matrix substances and minor collagens. Glutamate can mediate pain, and this is present in higher concentrations in subjects with Achilles tendinopathy than in controls. Chondroitin sulphate is another candidate. Examining alternative models of pain, particularly a mixed biochemical-mechanical model, may allow significant progress in management of these troublesome conditions.
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