Development of arthrogenic joint contracture as a result of pathological changes in remobilized rat knees.
This study aimed to elucidate how rats recover from immobilization-induced knee joint contracture. Rats' right knees were immobilized by an external fixator at a flexion of 140° for 3 weeks. After removal of the fixator, the joints were allowed to move freely (remobilization) for 0, 1, 3, 7, or 14 days (n = 5 each). To distinguish myogenic and arthrogenic contractures, the passive extension range of motion was measured before and after myotomy of the knee flexors. Knee joints were histologically analyzed and the expression of genes encoding inflammatory or fibrosis-related mediators, interleukin-1β (1L-1β), fibrosis-related transforming growth factor-β1 (TGF-β1), and collagen type I (COL1A1) and III (COL3A1), were examined in the knee joint posterior capsules using real-time PCR. Both myogenic and arthrogenic contractures were established within 3 weeks of immobilization. During remobilization, the myogenic contracture decreased over time. In contrast, the arthrogenic contracture developed further during the remobilization period. On day 1 of remobilization, inflammatory changes characterized by edema, inflammatory cell infiltration, and upregulation of IL-1β gene started in the knee joint posterior capsule. In addition, collagen deposition accompanied by fibroblast proliferation, with upregulation of TGF-β1, COL1A1, and COL3A1 genes, appeared in the joint capsule between days 7 and 14. These results suggest the progression of arthrogenic contracture following remobilization, which is characterized by fibrosis development, is possibly triggered by inflammation in the joint capsule. It is therefore necessary to focus on developing new treatment strategies for immobilization-induced joint contracture. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1414-1423, 2017.
Major in Medical Engineering and Technology, Graduate School of Medical Technology and Health Welfare Sciences, Hiroshima International University, Kurose-Gakuendai 555-36, Higashi-Hiroshima, Hiroshima, Japan.
Akinori
A
Kaneguchi
Faculty of Rehabilitation, Department of Rehabilitation, Hiroshima International University, Kurose-Gakuendai 555-36, Higashi-Hiroshima, Hiroshima 739-2695, Japan.
Junya
J
Ozawa
Institute of Biomedical and Health Sciences, Hiroshima University, 1-2-3, Kasumi, Minami-Ku, Hiroshima, Japan.
Seiichi
S
Kawamata
Faculty of Rehabilitation, Department of Rehabilitation, Hiroshima International University, Kurose-Gakuendai 555-36, Higashi-Hiroshima, Hiroshima 739-2695, Japan.
Kaoru
K
Yamaoka
D000818:Animals; D003286:Contracture / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D005355:Fibrosis; D015870:Gene Expression; D007103:Immobilization / Q000009:adverse effects*; D053583:Interleukin-1beta / Q000378:metabolism; D017746:Joint Capsule / Q000473:pathology*; D007719:Knee Joint / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D016059:Range of Motion, Articular; D017208:Rats, Wistar
C000594089:IL1B protein, rat; D053583:Interleukin-1beta
fibrosis; immobilization; inflammation; joint contracture; remobilization