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The three stages of tendinopathy

PainSci » bibliography » Fu et al 2010
updated
Tags: etiology, IT band pain, plantar fasciitis, biology, knee, tendinitis, foot, pro, leg, limbs, pain problems, overuse injury, injury, running, exercise, self-treatment, treatment

One article on PainSci cites Fu 2010: The Complete Guide to Patellofemoral Pain Syndrome

PainSci notes on Fu 2010:

Researchers first proposed a theory — “failed healing theory” — as a cause of tendinopathy. Then they describe a three stage process of “injury, failed healing and clinical presentation.”

With this hypothesis, they conclude: “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.”

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

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.

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