Abstract

Tendon pain remains an enigma. Many clinical features are consistent with tissue disruption—the pain is localised, persistent and specifically associated with tendon loading, whereas others are not—investigations do not always match symptoms and painless tendons can be catastrophically degenerated. As such, the question ‘what causes a tendon to be painful?’ remains unanswered. Without a proper understanding of the mechanism behind tendon pain, it is no surprise that treatments are often ineffective. Tendon pain certainly serves to protect the area—this is a defining characteristic of pain—and there is often a plausible nociceptive contributor. However, the problem of tendon pain is that the relation between pain and evidence of tissue disruption is variable. The investigation into mechanisms for tendon pain should extend beyond local tissue changes and include peripheral and central mechanisms of nociception modulation. This review integrates recent discoveries in diverse fields such as histology, physiology and neuroscience with clinical insight to present a current state of the art in tendon pain. New hypotheses for this condition are proposed, which focus on the potential role of tenocytes, mechanosensitive and chemosensitive receptors, the role of ion channels in nociception and pain and central mechanisms associated with load and threat monitoring. Verf.-Referat