BACKGROUND This article systematically reviews the current evidence regarding inflammation in Tendinopathy with the aim to increase understanding of a potential common pathophysiology. METHODS Following the PRISMA statements, the terms: (tendinopathy OR (tendons AND rupture)) AND (inflammation OR (inflammation AND cells) OR immune system OR inflammation mediators OR bacteria) were used. One thousand four hundred thirty-one articles were identified which was screened down to 53. RESULTS 39/53 studies mentioned inflammatory cells but had contradicting conclusions. Macrophages were the most common cell type and inflammatory markers were detectable in all the articles which measure them. CONCLUSIONS The included studies show different conclusions, but this heterogeneity is not unexpected since the clinical criteria of 'tendinopathy' encompass a huge clinical spectrum. Different 'tendinopathy' conditions may have different pathophysiology, and even the same clinical condition may be at different disease stages during sampling, which can alter the histological and biochemical picture. Control specimen sampling was suboptimal since the healthy areas of the pathological-tendon may actually be sub-clinically diseased, as could the contralateral tendon in the same subject. Detection of inflammatory cells is most sensitive using immunohistochemistry targeting the cluster of differentiation markers, especially when compared to the conventional haematoxylin and eosin staining methods. The identified inflammatory cell types favour a chronic inflammatory process; which suggests a persistent stimulus. This means NSAID and glucocorticoids may be useful since they suppress inflammation, but it is noted that they may hinder tendon healing and cause long term problems. This systematic review demonstrates a diversity of data and conclusions in regard to inflammation as part of the pathogenesis of Tendinopathy, ranging from ongoing or chronic inflammation to non-inflammatory degeneration and chronic infection. Whilst various inflammatory markers are present in two thirds of the reviewed articles, the heterogenicity of data and lack of comparable studies means we cannot conclude a common pathophysiology from this systematic review.

中文翻译：

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对人类肌腱炎炎性细胞和标志物的系统评价。

背景技术本文系统地回顾了有关腱鞘炎中炎症的当前证据，目的是增进对潜在的常见病理生理学的了解。方法在PRISMA声明之后，使用以下术语：（肌腱病变或（肌腱和破裂））和（炎症或（炎症和细胞）或免疫系统或炎症介质或细菌）。鉴定了131篇文章，筛选到53篇。结果39/53研究提到了炎症细胞，但结论相矛盾。巨噬细胞是最常见的细胞类型，在所有测量它们的文章中均检测到炎症标记。结论所包括的研究显示了不同的结论，但是这种异质性并不意外，因为“ tendinopathy”的临床标准 涵盖了巨大的临床范围。不同的“腱病”病状可能具有不同的病理生理学，甚至相同的临床病状在采样期间可能处于不同的疾病阶段，这可能会改变组织学和生化特征。由于病理肌腱的健康区域实际上可能是亚临床疾病，而对侧肌腱也可能在同一受试者中，因此对照标本取样不是最佳的。使用针对分化标志物簇的免疫组织化学方法对炎症细胞的检测最为敏感，特别是与常规苏木精和曙红染色方法相比。确定的炎症细胞类型有利于慢性炎症过程。这表明持续的刺激。这意味着NSAID和糖皮质激素可能会有用，因为它们可以抑制炎症，但是要注意，它们可能会阻碍腱的愈合并引起长期问题。这篇系统的综述证明了有关作为腱病发病机理一部分的炎症的数据和结论的多样性，从正在进行的或慢性的炎症到非炎性的变性和慢性感染。虽然三分之二的文章中存在各种炎症标记物，但数据的异质性和缺乏可比性研究意味着我们无法从该系统评价中得出共同的病理生理学。这篇系统的综述证明了有关作为腱病发病机理一部分的炎症的数据和结论的多样性，从正在进行的或慢性的炎症到非炎性的变性和慢性感染。虽然三分之二的文章中存在各种炎症标记物，但数据的异质性和缺乏可比性研究意味着我们无法从该系统评价中得出共同的病理生理学。这篇系统的综述证明了有关作为腱病发病机理一部分的炎症的数据和结论的多样性，从正在进行的或慢性的炎症到非炎性的变性和慢性感染。虽然三分之二的文章中存在各种炎症标记物，但数据的异质性和缺乏可比性研究意味着我们无法从该系统评价中得出共同的病理生理学。