The pathogenesis of tendinopathy. A molecular perspective

Extract

There are many publications that discuss the aetiology, diagnosis and treatment of the various forms of tendinopathy, but few are based on conclusive scientific evidence. The pathogenesis of tendinopathy is difficult to study because tendon biopsies are rarely obtained before a tendon has ruptured. There are interesting comparisons with animal tendinopathy, particularly in the equine athlete, although many animal models do not accurately reflect the human condition—the tendon lesions usually heal. However, the application of biochemical and molecular techniques to the study of both animal and human tendinopathy has led to a greater understanding of these common and disabling conditions. This article summarizes current knowledge of the pathogenesis of tendinopathy, with particular emphasis on the molecular pathology of the tendon matrix.

Classification and terminology

Tendons may be affected by a variety of different pathological conditions. Many systemic diseases are associated with general defects in matrix metabolism and structure that compromise tendon strength and elasticity, or result in inflammation of the tendon or its insertion [1–3] (Table 1). These conditions are not the subject of this review, although they must be considered as part of the differential diagnosis.