Cui Jiaming, Lu Wei, He Yong, Jiang Luoyong, Li Kuokuo, Zhu Weimin, Wang Daping
Guangzhou Medical University, Guangzhou 510182, P. R. China.
Department of Sports Medicine, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, P. R. China.
J Res Med Sci. 2017 May 30;22:61. doi: 10.4103/jrms.JRMS_1005_16. eCollection 2017.
Frozen shoulder is a chronic condition characterized by pain in the shoulder and restriction of movements in all directions. Some patients are left with long-term limitation of shoulder joint activity with various severities, which results in reduced quality of life. Currently, there is a paucity of literature on the molecular biology of frozen shoulder, and the molecular biological mechanism for periarthritis-induced limitation of shoulder joint movements remains unclear. Research in this field is focused on inflammation and cytokines associated with fibrosis. Repeated investigations confirmed alterations of specified inflammatory mediators and fibrosis-associated cytokines, which might be involved in the pathogenesis of frozen shoulder by causing structural changes of the shoulder joint and eventually the limitation of shoulder movements. The aim of this article is to review studies on molecular biology of frozen shoulder and provide a reference for subsequent research, treatment, and development of new drugs.
肩周炎是一种慢性疾病,其特征为肩部疼痛和各个方向的活动受限。一些患者会长期存在不同程度的肩关节活动受限,这导致生活质量下降。目前,关于肩周炎分子生物学的文献较少,肩周炎所致肩关节活动受限的分子生物学机制仍不清楚。该领域的研究集中在与纤维化相关的炎症和细胞因子上。反复研究证实了特定炎症介质和纤维化相关细胞因子的改变,这些改变可能通过引起肩关节结构变化并最终导致肩部活动受限而参与肩周炎的发病机制。本文旨在综述肩周炎分子生物学的研究,为后续研究、治疗及新药开发提供参考。