| Literature DB >> 26014262 |
Satoshi Oki1, Hideyuki Shirasawa1, Masaki Yoda2, Noboru Matsumura1, Takahide Tohmonda2, Kazuki Yuasa3, Masaya Nakamura1, Morio Matsumoto1, Keisuke Horiuchi1,2.
Abstract
Frozen shoulder is a relatively common disorder that leads to severe pain and stiffness in the shoulder joint. Although this disorder is self-limiting in nature, the symptoms often persist for years, resulting in severe disability. Recent studies using human specimens and animal models have shown distinct changes in the gene expression patterns in frozen shoulder tissue, indicating that novel therapeutic intervention could be achieved by controlling the genes that are potentially involved in the development of frozen shoulder. To achieve this goal, it is imperative to develop a reliable animal joint contracture model in which gene expression can be manipulated by gene targeting and transgenic technologies. Here, we describe a novel shoulder contracture mouse model. We found that this model mimics the clinical presentation of human frozen shoulder and recapitulates the changes in the gene expression pattern and the histology of frozen shoulder and joint contracture in humans and other larger animal models. The model is highly reproducible, without any major complications. Therefore, the present model may serve as a useful tool for investigating frozen shoulder etiology and for identifying its potential target genes.Entities:
Keywords: functional analysis; gene expression analysis; mouse model; shoulder contracture
Mesh:
Year: 2015 PMID: 26014262 DOI: 10.1002/jor.22943
Source DB: PubMed Journal: J Orthop Res ISSN: 0736-0266 Impact factor: 3.494