Deciphering the pathogenesis of tendinopathy: a three-stages process.
Deciphering the pathogenesis of tendinopathy: a three-stages process.
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DOI：
10.1186/1758-2555-2-30
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发表时间：
2010-12-13
期刊：
影响因子：
--
通讯作者：
Chan KM
中科院分区：
文献类型：
--
作者：
Fu SC;Rolf C;Cheuk YC;Lui PP;Chan KM
我们对"肌腱病"发病机制的理解是基于支离破碎的证据，就像拼图游戏一样。我们提出了一个“失败的愈合理论”来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“过度使用损伤”和其他潜在的“微创伤”可能是该过程的主要触发因素，但“肌腱病”本身并不是“过度使用损伤”。典型的临床、组织学和生化表现与局部慢性疼痛有关，可能导致肌腱断裂，后者归因于机械性无力。病理性"肌腱病"组织的表征显示胶原溶解损伤和主动愈合过程、局灶性血管增生和组织化生共存。这些观察结果表明，作为对触发损伤的响应，愈合过程失败。肌腱病的发病机制可以描述为三个阶段的过程：损伤，愈合失败和临床表现。很可能这些“初始损伤”中的一些愈合良好，我们推测可能涉及诱发性内在或外在因素。损伤阶段涉及进行性胶原溶解性肌腱损伤。愈合失败阶段主要是指正常愈合过程的激活延长和消退失败。最后，基质紊乱，增加局灶性血管和异常细胞因子谱有助于慢性肌腱疼痛或断裂的临床表现。有了这个综合发病机制理论，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”。这个模型可以指导未来对肌腱病的研究，直到我们最终能够破译完整的发病过程并提供更好的治疗方法。
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.