Biological Aspect of Pathophysiology for Frozen Shoulder.

Biological Aspect of Pathophysiology for Frozen Shoulder.
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DOI:
10.1155/2018/7274517
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发表时间:
2018
影响因子:
--
通讯作者:
Lho YM
Lho YM
中科院分区:
生物学3区
文献类型:
--
作者:
Cho CH;Song KS;Kim BS;Kim DH;Lho YM

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众所周知,冻结肩包括几个阶段,反映了从包膜炎症和纤维化到纤维化自发消退的一系列过程。然而,潜在的病理生理过程仍然很难确定。出于这个原因,冻结肩的治疗仍然存在争议。确定肩周炎的病理生理过程是开发治疗肩周炎的新疗法的一个重要里程碑。本文就冻结肩的生物病理生理学研究进展作一综述。尽管有关冻结肩的病理生理学的文章提供了不一致和不确定的结果,但他们认为炎症和纤维化都是由细胞因子、生长因子、基质金属蛋白酶和免疫细胞介导的。免疫细胞释放的促炎细胞因子和生长因子控制成纤维细胞的活动,基质重塑受基质金属蛋白酶及其抑制物的调节。为了提高我们对疾病连续体的理解,需要在明确定义的阶段更好地描述这些过程的生物学特征。进一步的基础研究需要使用标准化的方案,以更狭隘地确定细胞因子、生长因子、基质金属蛋白酶和免疫细胞的作用。这些研究的结果将对肩周炎的发病机制提供必要的澄清,并有助于确定其治疗的新的治疗靶点。
It is fairly well understood that frozen shoulder involves several stages, which reflect the series of process from capsular inflammation and fibrosis to spontaneous resolution of this fibrosis. However, the underlying pathophysiologic process remains poorly determined. For this reason, management of frozen shoulder remains controversial. Determining the pathophysiological processes of frozen shoulder is a pivotal milestone in the development of novel treatment for patients with frozen shoulder. This article reviews what is known to date about the biological pathophysiology of frozen shoulder. Although articles for the pathophysiology of frozen shoulder provide inconsistent and inconclusive results, they have suggested both inflammation and fibrosis mediated by cytokines, growth factors, matrix metalloproteinases, and immune cells. Proinflammatory cytokines and growth factors released from immune cells control the action of fibroblast and matrix remodeling is regulated by the matrix metalloproteinases and their inhibitors. To improve our understanding of the disease continuum, better characterizing the biology of these processes at clearly defined stages will be needed. Further basic studies that use standardized protocols are required to more narrowly identify the role of cytokines, growth factors, matrix metalloproteinases, and immune cells. The results of these studies will provide needed clarity into the control mechanism of the pathogenesis of frozen shoulder and help identify new therapeutic targets for its treatment.
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