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作 者:李博源 邱庭辉 潘海乐[1] Li Boyuan;Qiu Tinghui;Pan Haile(Department of Orthopedics, Second Affiliated Hospital of Harbin Medical University, Harbin 150000, China)
机构地区:[1]哈尔滨医科大学附属第二医院骨四科
出 处:《中国组织化学与细胞化学杂志》2019年第2期179-184,共6页Chinese Journal of Histochemistry and Cytochemistry
基 金:哈尔滨科技局创新人才研究专项课题(2011RFLYS026)
摘 要:肩周炎(FS)是一种常见疾病,分为急性期、慢性期和恢复期3个阶段,其特点是肩部疼痛和各个方向的运动受限。由于长期肩关节活动受限,一些患者生活质量明显下降。目前,关于肩周炎活动受限的分子生物学的文献很少,并且对关节周围炎引起的肩关节运动受限的分子生物学机制仍不清楚。有研究表明,肩周炎患者较正常人滑膜组织内某些炎症介质和纤维化相关细胞因子有所改变,这些细胞因子可能通过引起肩关节结构变化导致肩关节运动受限,从而参与肩周炎的发生。Frozen shoulder (FS) is a common disease that is divided into three phases: acute phase, chronic phase, and recovery phase, which are characterized by shoulder pain and limited movement in all directions. Due to long-term limited activity of shoulder joint, the life quality of some patients has decreased significantly. At present, there is little literature on the molecular biology research of shoulder joint movement limitation caused by inflammation around the joint, the molecular biological mechanism of which still remains unclear. Some studies have shown that some inflammatory mediators and fibrosis-associated cytokines are altered in patients with frozen shoulder than those in normal human synovial tissue. These cytokines may result in limited movement of the shoulder joint via causing changes in the structure of the shoulder joint and thus participate in the pathogenesis of frozen shoulder.
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