Continuing progress in research in molecular biology and biomechanics has provided considerable new information and has given rise to new hypotheses in chronic tendinopathy. Overloading is still, however, crucial in the development of tendinopathy. Most of the histologic findings in tendinopathy represent chronic degeneration, regeneration, and microtears of the tendinous tissue. The prevailing opinion is that no histological evidence of acute inflammation has been documented, but in newer studies using immunohistochemistry and flow cytometry inflammatory cells have been detected. The existing data indicate that the initiators of the tendinopathic pathway include many proinflammatory agents (e.g. cytokines, prostaglandins, different growth factors, and neuropetides). Because of the complex interaction between the classic proinflammatory agents and the neuropeptides, it seems impossible and somewhat irrelevant to distinguish sharply between chemical and neurogenic inflammation. Furthermore, glucocorticoids are, at the moment, the most effective treatment in tendinopathy with regard to reduction of pain, tendon thickness, and neovascularization. This review indicates - despite a great deal of uncertainty regarding the concepts - that an inflammatory process may be related not only to the development of tendinopathy but also chronic tendinopathy. More attention should be directed towards the "tendinitis myth" in the future.