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BioMed Research International
Volume 2017 (2017), Article ID 3681645, 7 pages
Research Article

A Study of IL-1β, MMP-3, TGF-β1, and GDF5 Polymorphisms and Their Association with Primary Frozen Shoulder in a Chinese Han Population

Department of Orthopedics, Jinling Hospital, Southern Medical University, 305 Zhongshan East Road, Nanjing, Jiangsu 210002, China

Correspondence should be addressed to Nirong Bao; moc.anis@rnbrnb

Received 15 March 2017; Revised 22 April 2017; Accepted 8 May 2017; Published 6 June 2017

Academic Editor: Sae H. Kim

Copyright © 2017 Wenxiang Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Primary frozen shoulder (PFS) is a common condition of uncertain etiology that is characterized by shoulder pain and restriction of active and passive glenohumeral motions. The pathophysiology involves chronic inflammation and fibrosis of the joint capsule. Single nucleotide polymorphisms (SNPs) at IL-1β, MMP3, TGF-β1, and GDF5 have been associated with risk of a variety of inflammatory diseases; however, no studies have examined these SNPs with susceptibility to PFS. We investigated allele and genotype frequencies of rs1143627 at IL-1β, rs650108 at MMP-3, rs1800469 at TGF-β1, and rs143383 at GDF5 in 42 patients with PFS and 50 healthy controls in a Chinese Han population. Serum samples from both cohorts were evaluated to determine the expression levels of IL-1β. We found that the IL-1β rs1143627 CC genotype was associated with a decreased risk of PFS compared to the TT genotype () and that serum IL-1β was expressed at a significantly higher level in the PFS cohort compared to that found in the control group (). Our findings indicated no evidence of an association between rs650108, rs1800469, or rs143383 and PFS. IL-1β is associated with susceptibility to PFS and may have a role in its pathogenesis in a Chinese Han population.