The pathogenesis of tendinopathy. A molecular perspective

Abstract

The tendon matrix is ideally constructed to perform its major function, the transfer of force from muscle to bone. It is not a static tissue, and the matrix will adapt according to the level, direction and frequency of the applied load, a process of remodelling mediated by the tendon fibroblasts. The tendon matrix is constantly remodelled throughout life, although higher rates of turnover are found at sites exposed to high levels of strain, compression or shear forces, such as the Achilles and the supraspinatus. Matrix changes in tendon pathology could be attributed to intrinsic factors, such as changes in cell activity with age, or extrinsic factors, such as 'overuse', repetitive strain and microtrauma. In degenerate tendon there is an increased rate of matrix remodelling, leading to a qualitatively different and mechanically less stable tendon, which is susceptible to damage. Thus tendon degeneration may result from a failure to regulate specific MMP activities in response to repeated injury or mechanical strain. Whether tendon repair can be improved merits further investigation of the factors controlling matrix remodelling in tendon. These factors include mechanical strain, growth factors, cytokines and neuropeptides, all of which have been implicated in the control of tendon homeostasis, adaptation and repair.