Characterization of a frozen shoulder model using immobilization in rats
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RESEARCH ARTICLE
Open Access
Characterization of a frozen shoulder model using immobilization in rats Du Hwan Kim2†, Kil-Ho Lee3†, Yun-Mee Lho4, Eunyoung Ha4, Ilseon Hwang5, Kwang-Soon Song1 and Chul-Hyun Cho1*
Abstract Background: The objective of this study was to investigate serial changes for histology of joint capsule and range of motion of the glenohumeral joint after immobilization in rats. We hypothesized that a rat shoulder contracture model using immobilization would be capable of producing effects on the glenohumeral joint similar to those seen in patients with frozen shoulder. Methods: Sixty-four Sprague-Dawley rats were randomly divided into one control group (n = 8) and seven immobilization groups (n = 8 per group) that were immobilized with molding plaster for 3 days, or for 1, 2, 3, 4, 5, or 6 weeks. At each time point, eight rats were euthanized for histologic evaluation of the axillary recess and for measurement of the abduction angle. Results: Infiltration of inflammatory cells was found in the synovial tissue until 2 weeks after immobilization. However, inflammatory cells were diminished and fibrosis was dominantly observed in the synovium and subsynovial tissue 3 weeks after immobilization. From 1 week after immobilization, the abduction angle of all immobilization groups at each time point was significantly lower than that of the control group. Conclusions: Our study demonstrated that a rat frozen shoulder model using immobilization generates the pathophysiologic process of inflammation leading to fibrosis on the glenohumeral joint similar to that seen in patients with frozen shoulder. This model was attained within 3 weeks after immobilization. It may serve as a useful tool to investigate pathogenesis at the molecular level and identify potential target genes that are involved in the development of frozen shoulder. Keywords: Frozen shoulder, Animal model, Rat, Immobilization
Background Frozen shoulder is a common shoulder disorder characterized by pain and gradual loss of active and passive glenohumeral motion that occurs in 2–5% of the general population [1–4]. However, the etiology and pathophysiologic mechanisms that lead to the development of frozen shoulder are poorly understood, and there is no consensus regarding optimal treatment [2, 4–7]. The primary pathologic site of frozen shoulder is the glenohumeral capsular tissue that particularly localized to the rotator interval and axillary recess [1, 6, 8]. Most * Correspondence: [email protected] † Equal contributors 1 Pain Research Center, Department of Orthopedic Surgery, Dongsan Medical Center, School of Medicine, Keimyung University, 56 Dalseong-ro, Jung-gu, Daegu 41931, South Korea Full list of author information is available at the end of the article
likely, a sequential pathologic process from synovial inflammation to capsular fibrosis is the main source of pain and limited motion in frozen shoulder [2, 3, 5, 9–12]. Rodeo et al. [3] reported that a hypervascular synovial hyperplasia was present in the early stages, and resu
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