Overuse tendinopathies are a common cause of pain and disability in athletes. According to histological findings, it is a “failed healing response” to overuse tendon injury. In obesity, macrophages and mast cells migrate to adipose tissue, and the resulting decreased availability of immune circulating cells should be responsible for less effective immune responses to acute tendon injury. In diabetic patients, free glucose molecules attach to collagen, alter collagen solubility, increase resistance to enzymatic degradation, and impair cross linking, contributing to the subsequent development of chronic tendinopathy secondary to a failed healing response to a tendon insult. Prolonged systemic, low-grade inflammation and impaired insulin sensitivity act as a risk factor for a “failed healing response” after an acute tendon insult, and predispose to the development of chronic overuse tendinopathies. Further studies may reveal novel therapeutic treatment approaches.

Overuse tendon injuries present with pain and swelling of the affected tendon with associated decrease in exercise tolerance and function of the limb. After early inflammatory and degenerative hypotheses, the term "tendinopathy" is now deemed a more appropriate reflection of the mixed histopathological picture seen in operative biopsies from affected patients. The condition presents histopathological evidence of "failed healing response," but its etiology remains unclear. The incidence of tendinopathy is increased in individuals with obesity and decreased insulin sensitivity (as seen in type 1 and type 2 diabetes mellitus). These groups of patients also exhibit an increased risk of developing a state of chronic low-grade, systemic inflammation. This paper considers the theoretical bases to discuss whether these conditions may predispose to the development of tendinopathy and the implication that such a relationship may have on its management.

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