Oki Satoshi, Shirasawa Hideyuki, Yoda Masaki, Matsumura Noboru, Tohmonda Takahide, Yuasa Kazuki, Nakamura Masaya, Matsumoto Morio, Horiuchi Keisuke
Department of Orthopedic Surgery, Keio University School of Medicine, city, Shinjuku-ku, Tokyo, 160-8582, Japan.
Department of Anti-Aging Orthopedic Research, Keio University School of Medicine, Tokyo, 160-8582, Japan.
J Orthop Res. 2015 Nov;33(11):1732-8. doi: 10.1002/jor.22943. Epub 2015 May 29.
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.
肩周炎是一种较为常见的疾病,会导致肩关节严重疼痛和僵硬。尽管这种疾病本质上是自限性的,但症状往往会持续数年,导致严重残疾。最近使用人体标本和动物模型进行的研究表明,肩周炎组织中的基因表达模式有明显变化,这表明通过控制可能参与肩周炎发病的基因,可以实现新的治疗干预。为了实现这一目标,开发一种可靠的动物关节挛缩模型至关重要,在该模型中可以通过基因靶向和转基因技术来操纵基因表达。在此,我们描述了一种新型的肩部挛缩小鼠模型。我们发现该模型模拟了人类肩周炎的临床表现,并概括了人类和其他大型动物模型中肩周炎和关节挛缩的基因表达模式及组织学变化。该模型具有高度可重复性,没有任何重大并发症。因此,目前的模型可作为研究肩周炎病因和识别其潜在靶基因的有用工具。