Background Concomitant with joint contracture, the inflammatory reactions have been shown in immobilized joint. Several investigators reported the effect of anti-inflammatory drugs on joint contracture formation followed by immobilization, however, the exact effect remains uncertain.
Objectives We aimed to investigate a favorable effect of selective cyclooxygenase (COX)-2 inhibitor celecoxib (CBX) treatment on immobilization-induced contracture in a rat model.
Methods Thirteen-week-old male Wistar rats (n=30) were used in this study. Rats were divided into three groups; control, immobilization (Im), and Im+CBX groups (n=10 each). In IM and Im + CBX groups, the right knee was immobilized by external fixation at 140° of flexion for 3 weeks. In Im+CBX group, CBX (50 mg/kg orally once a day) were treated during immobilization periods. Age-matched untreated animals were used as control group. At the end of intervention period, knee joint passive range of motion (ROM) were measured with14.6 Nmm extension moments before and after transection of knee flexor muscles (the former mainly indicates myogenic-, and the latter indicates arthrogenic contracture). In addition, the knee flexor semitendinosus muscles and knee joints were histologically analyzed to investigate the involvement of morphological alterations on joint contracture formation. For all data, one-way analysis of variance were used for statistically analysis, and the Tukey's post-hoc test were applied. P-value of <0.05 was considered statistically significant.
Results Before myotomy, knee extension ROMs significantly decreased in IM group (61%) and IM+CBX group (70%) than those in control group. In comparison between IM and IM+CBX groups, ROM limitations were alleviated in IM+CBX group compared with those in IM group (P <0.05). After myotomy, ROMs also decreased in IM group (83%) and IM + CBX group (86%) compared with those in control and there was no difference between IM and IM+CBX groups. The semitendinosus muscle lengths and the serial sarcomere numbers were both decreased by immobilization, but CBX treatment could partially inhibit these changes (P <0.05). Intra-articular hemorrhages, which is shown to accelerate immobilization- induced joint contracture, were observed in both IM and IM+CBX groups, and were not inhibited by CBX administration.
Conclusions Our results demonstrate the existence of COX-2-mediated pathway as a trigger for the formation of joint contracture, despite the immobilization-induced model. CBX treatment can partially prevent the progression of contracture acting on muscular components. Arthrogenic contracture may be regulated by infiltrated blood cells in joint cavity. These results suggest that anti-inflammatory therapies (ie., drugs or physical agents) may be useful for alleviation of immobilization-induced joint contracture.
Disclosure of Interest None declared