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首页> 外文期刊>BMC sports science, medicine & rehabilitation >Deciphering the pathogenesis of tendinopathy: a three-stages process
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Deciphering the pathogenesis of tendinopathy: a three-stages process

机译：解读肌腱病的发病机理：一个三个阶段的过程

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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.
机译：我们对“腱病”发病机理的理解是基于零碎的证据，例如拼图碎片。我们提出了一种“失败的愈合理论”，将这些碎片编织在一起，这可以解释以前的观察结果。我们还提出，尽管“过度使用伤害”和其他隐患的“微创伤”很可能是该过程的主要诱因，但“腱病”本身并不是“过度使用伤害”。典型的临床，组织学和生化表现涉及局部慢性疼痛状况，可能导致肌腱断裂，后者是机械性肌无力引起的。病理性“腱鞘”组织的表征显示胶原蛋白溶解性损伤与活跃的愈合过程，局灶性高血管形成和组织化生共存。这些观察表明，失败的愈合过程是对触发性损伤的反应。肌腱病的发病机理可描述为三个阶段：损伤，愈合失败和临床表现。这些“最初的伤害”中的一些可能会he愈，我们推测可能涉及易患的内在或外在因素。损伤阶段涉及进行性胶原分解肌腱损伤。失败的愈合阶段主要是指正常激活过程的激活时间延长和解决失败。最后，基质紊乱，局灶性血管扩张和异常的细胞因子谱有助于慢性肌腱疼痛或破裂的临床表现。通过这种综合的发病机理理论，我们可以将肌腱病的已知表现联系起来，并指出“缺失的环节”。该模型可以指导肌腱病的未来研究，直到我们最终能够破译完整的发病机理并提供更好的治疗方法为止。

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