Abstract
Our understanding of the pathogenesis of "tendinopathy" is based on fragmented evidences like pieces of a jigsaw puzzle. We propose a "failed healing theory" to knit these fragments together, which can explain previous observations. We also propose that albeit "overuse injury" and other insidious "micro trauma" may well be primary triggers of the process, "tendinopathy" is not an "overuse injury" per se. The typical clinical, histological and biochemical presentation relates to a localized chronic pain condition which may lead to tendon rupture, the latter attributed to mechanical weakness. Characterization of pathological "tendinotic" tissues revealed coexistence of collagenolytic injuries and an active healing process, focal hypervascularity and tissue metaplasia. These observations suggest a failed healing process as response to a triggering injury. The pathogenesis of tendinopathy can be described as a three stage process: injury, failed healing and clinical presentation. It is likely that some of these "initial injuries" heal well and we speculate that predisposing intrinsic or extrinsic factors may be involved. The injury stage involves a progressive collagenolytic tendon injury. The failed healing stage mainly refers to prolonged activation and failed resolution of the normal healing process. Finally, the matrix disturbances, increased focal vascularity and abnormal cytokine profiles contribute to the clinical presentations of chronic tendon pain or rupture. With this integrative pathogenesis theory, we can relate the known manifestations of tendinopathy and point to the "missing links". This model may guide future research on tendinopathy, until we could ultimately decipher the complete pathogenesis process and provide better treatments.
Highlights
In the past decades, our concepts on chronic tendon pain have evolved from “tendinitis” which focused on clinical inflammatory signs, into “tendinosis” which stressed the pathologic features of the free tendon as observed by histology and biochemistry, and “tendinopathy” which declared nothing further about its nature, just introducing a new label for chronic tendon and insertion problems in general [1]
Stem cell therapy was tried in horse models [95]. These studies may suggest the involvement of disturbances in cytokines, neovascularization, innervations or cell differentiation in the pathogenesis of tendinopathy
We propose that the pathogenesis of tendinopathy can be perceived as a 3-stages process: injury, failed healing and clinical presentation
Summary
Our concepts on chronic tendon pain have evolved from “tendinitis” which focused on clinical inflammatory signs, into “tendinosis” which stressed the pathologic features of the free tendon as observed by histology and biochemistry, and “tendinopathy” which declared nothing further about its nature, just introducing a new label for chronic tendon and insertion problems in general [1]. These pathological tissues may aggravate the nociceptive responses by various pathways which are no longer responsive to conventional treatment such as inhibition of prostaglandin synthesis; otherwise the insidious mechanical deterioration without pain may render increased risk of ruptures Based on these points, we propose that the pathogenesis of tendinopathy can be perceived as a 3-stages process: injury, failed healing and clinical presentation. The recent discovery of tendon-derived stem cells and characterization of pathological tissues of tendinopathy have provided evidences to support the ideas of erroneous cell differentiation that contribute to failed tendon healing According to this theory of pathogenesis, we shall have a theoretical framework to develop a more representative animal model of tendinopathy for further study and verification. The interactions between healing tendons and the peritendinous tissues are seldom investigated and it is difficult to evaluate the potential involvement of peritendinous tissues in the development of tendinopathy
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