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冻结肩的病理生理学的生物学方面。

Biological Aspect of Pathophysiology for Frozen Shoulder.

机构信息

Pain Research Center, Department of Orthopedic Surgery, Dongsan Medical Center, School of Medicine, Keimyung University, Daegu, Republic of Korea.

Department of Rehabilitation Medicine, Dongsan Medical Center, School of Medicine, Keimyung University, Daegu, Republic of Korea.

出版信息

Biomed Res Int. 2018 May 24;2018:7274517. doi: 10.1155/2018/7274517. eCollection 2018.

DOI:10.1155/2018/7274517
PMID:29992159
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5994312/
Abstract

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.

摘要

人们已经较为充分地认识到,冻结肩涉及几个阶段,反映了从囊炎症和纤维化到这种纤维化自发性消退的一系列过程。然而,其潜在的病理生理过程仍未得到明确确定。由于这个原因,冻结肩的治疗仍存在争议。确定冻结肩的病理生理过程是为冻结肩患者开发新治疗方法的一个关键里程碑。本文综述了目前已知的有关冻结肩的生物学病理生理学的知识。尽管有关冻结肩病理生理学的文章提供了不一致和不确定的结果,但它们都表明了细胞因子、生长因子、基质金属蛋白酶和免疫细胞介导的炎症和纤维化。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作用,而基质金属蛋白酶及其抑制剂调节基质重塑。为了更好地了解疾病的连续性,需要在明确界定的阶段更好地描述这些过程的生物学特性。需要进一步使用标准化方案进行基础研究,以更明确地确定细胞因子、生长因子、基质金属蛋白酶和免疫细胞的作用。这些研究的结果将为冻结肩发病机制的控制机制提供所需的清晰度,并有助于确定其治疗的新治疗靶点。

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本文引用的文献

1
The pathophysiology associated with primary (idiopathic) frozen shoulder: A systematic review.与原发性(特发性)肩周炎相关的病理生理学:一项系统综述。
BMC Musculoskelet Disord. 2016 Aug 15;17(1):340. doi: 10.1186/s12891-016-1190-9.
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The roles of Tenascin C and Fibronectin 1 in adhesive capsulitis: a pilot gene expression study.肌腱蛋白C和纤连蛋白1在粘连性肩周炎中的作用:一项初步基因表达研究。
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Primary frozen shoulder: brief review of pathology and imaging abnormalities.原发性冻结肩:病理学与影像异常简述
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5
Matrix metalloproteinase, tissue inhibitor of metalloproteinase and transforming growth factor-beta 1 in frozen shoulder, and their changes as response to intensive stretching and supervised neglect exercise.冻结肩中基质金属蛋白酶、金属蛋白酶组织抑制剂及转化生长因子-β1 及其对强化拉伸和监督下的忽视训练的反应变化
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Intercellular adhesion molecule-1 (ICAM-1, CD54) is increased in adhesive capsulitis.细胞间黏附分子-1(ICAM-1,CD54)在粘连性关节囊炎中增加。
J Bone Joint Surg Am. 2013 Feb 20;95(4):e181-8. doi: 10.2106/JBJS.K.00525.
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An MRI study of symptomatic adhesive capsulitis.MRI 研究对症状性粘连性肩关节囊炎的研究。
PLoS One. 2012;7(10):e47277. doi: 10.1371/journal.pone.0047277. Epub 2012 Oct 17.
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Inflammatory cytokines are overexpressed in the subacromial bursa of frozen shoulder.在冻结肩的肩峰下滑囊中有炎症细胞因子过度表达。
J Shoulder Elbow Surg. 2013 May;22(5):666-72. doi: 10.1016/j.jse.2012.06.014. Epub 2012 Sep 21.
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Frozen shoulder.肩周炎
J Bone Joint Surg Br. 2012 Jan;94(1):1-9. doi: 10.1302/0301-620X.94B1.27093.
10
Enhanced expression of neuronal proteins in idiopathic frozen shoulder.特发性冻结肩患者神经元蛋白表达增强。
J Shoulder Elbow Surg. 2012 Oct;21(10):1391-7. doi: 10.1016/j.jse.2011.08.046. Epub 2011 Oct 17.