Tendon pain is still a mystery. 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 disastrously degenerated. As such, the question ‘what causes a tendon to be painful?’ has yet to be answered. Without an adequate understanding of the mechanism underlying tendon pain, it is not suprising that treatments are often ineffective. Tendon pain doubtlessly 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 reach beyond local tissue changes and include peripheral and central mechanisms of nociception modulation.
In this review the authors’ integrate 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. They suggest new hypotheses for this condition 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.