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Traditional dogma would have it that pain in tendinopathy arises through one of two mechanisms. Firstly, it may result from inflammation in “tendinitis”. Secondly, it may be due to separation of collagen fibres in more severe forms of tendinopathy. The latter situation parallels the mechanism of pain with collagen separation after an acute grade I or II ligament injury (fig 1).
Despite the wide acceptance of these two classical models of pain production, a number of studies provide data inconsistent with either theory. Consider first the inflammation mechanism. Histopathological examination of surgical specimens from patients with chronic tendon pain are devoid of inflammatory cells.1 This applies to tissue from the Achilles, patellar, lateral elbow, medial elbow, and rotator cuff tendons. Furthermore, prostaglandin E2 (a marker of the inflammatory process) is no more abundant in patients with Achilles tendon pain than in normal controls.2
Unfortunately, the collagen separation theory does not hold up under scrutiny either. The following five observations about pain and collagen in the patellar tendon are inexplicable. (a) Patients who have patellar tendon allograft anterior cruciate ligament reconstruction have minimal donor site knee pain, yet …
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