Rabbit Model of Extending Knee Joint Contracture: Progression of Joint Motion Restriction and Subsequent Joint Capsule Changes after Immobilization

Abstract

This study aimed to develop a rabbit model of knee contracture in extension and investigate the natural history of motion loss and time-dependent changes in the joint capsule after immobilization. We immobilized the unilateral knee joints of 32 rabbits by maintaining the knee joint in a plaster cast at full extension. Eight rabbits were euthanized at 2, 4, 6, and 8 weeks after casting, respectively, and the lower extremities were disarticulated at the hip joint. Eight control group rabbits that did not undergo immobilization were also examined. We assessed the progression of joint contracture by measuring the joint range of motion, evaluating the histologic alteration of the capsule, and assessing the mRNA levels of transforming growth factor β1 (TGF-β1) in the anterior and posterior joint capsules. After 2 weeks of joint immobilization, the knee joint range of motion was limited, the synovial membrane of the suprapatellar and posterior joint capsules was thickened, the collagen deposition was increased, and the mRNA levels of TGF-β1 were elevated in the anterior and posterior joint capsules. These changes progressed rapidly until 6 weeks of immobilization and may advance slowly after 6 weeks. Joint contracture developed at the early stage of immobilization and progressed over time. The changes in the anterior and posterior joint capsules after joint immobilization may contribute to the limitation in flexion. The elevated mRNA expression of TGF-β1 may be related to joint capsule fibrosis and may be one of the causes of joint contracture.

Thermal and non-thermal effects of capacitive–resistive electric transfer application on different structures of the knee: a cadaveric study

“…In addition, we observed a high current flow (0.104 A ± 0.06), which is known to be associated with a cell proliferation effect 30,31 . This application could be interesting in more chronic phases in which the main objective is to improve the viscoelasticity of tissues, especially the capsule and ligaments, since, as reported in the literature, these structures are directly related to limitation of ROM after prolonged immobilization or chronic pathologies 17,18,25 .…”

“…Arthrogenic components, particularly of the joint capsule, are reported to be important factors in the formation of joint contractures. Previous studies have suggested that joint capsule fibrosis and overexpression of type I collagen occur and progress within 1 week after immobilization, and an increase in myofibroblasts is associated with this fibrosis 17 , especially in the posterior knee capsule 18 .…”

Effect of Ultrashort Wave on Joint Dysfunction and Muscle Atrophy in a Rabbit Model of Extending Knee Joint Contracture: Enhanced Expression of MyoD

“…Like our previous study, ROM of the left knee joint was measured by the joint motion measuring instrument. 11,12 According to the method described by Trudel G, 13…”

Suppression of TGF-beta activity with remobilization attenuates immobilization-induced joint contracture in rats

“…It is widely accepted that in ammatory cytokines and pro brotic factors trigger the progression of brosis in the joint capsule and synovium [9][10][11]. Previous studies indicated that pro brotic growth factors are elevated during joint immobilization [12,13]. Of these, transforming growth factor-β (TGF-β), as a dominating pro brotic factor of arthro brosis, induces the plasticity and proliferation of broblasts with upregulated collagen in muscle contractures and other brotic tissues [11][12][13].…”

“…Previous studies indicated that pro brotic growth factors are elevated during joint immobilization [12,13]. Of these, transforming growth factor-β (TGF-β), as a dominating pro brotic factor of arthro brosis, induces the plasticity and proliferation of broblasts with upregulated collagen in muscle contractures and other brotic tissues [11][12][13]. Fibrous adhesion formation can be reduced by small proteoglycan, decorin, via the inhibition of TGF-β [14].…”