Department of Rehabilitation, Mori Orthopaedic Clinic, 1-3-16, Hikarimachi, Higashi-Ku Hiroshima, Hiroshima, Japan.
Department of Rehabilitation, Faculty of Rehabilitation, Hiroshima International University, Kurose-Gakuendai 555-36, Higashi, Hiroshima, 739-2695, Japan.
Inflammation. 2018 Aug;41(4):1409-1423. doi: 10.1007/s10753-018-0788-5.
Joint inflammation following remobilization is an important factor in the progression of arthrogenic contracture. We evaluated the effects of an anti-inflammatory treatment during the remobilization period of recovery after joint immobilization in rats. Three groups of rats had their right knee joints immobilized for 3 weeks using an external fixator at a flexion of 140° to generate flexion contracture. Next, the fixation device was removed, allowing immobilized knees to freely move again for 1 or 7 days. These rats were daily injected with either the steroidal anti-inflammatory drug dexamethasone or saline. Untreated knees were used as controls. At 1 day of remobilization, gene expression of pro-inflammatory cytokines, interleukin (IL)-1β, and IL-6 were both increased in the posterior joint capsule, while dexamethasone treatment inhibited increase of these markers. Passive extension range of motion (ROM) was measured before and after myotomy of the knee flexors. Restriction of ROM before myotomy mainly represents the myogenic, and ROM after myotomy shows the arthrogenic changes. Joint immobilization reduced ROM both before and after myotomy. Seven days of remobilization improved ROM before but not after myotomy. Arthrogenic contracture progression following remobilization was characterized by fibrotic reactions of hypercellularity, upregulation of collagen genes, and increased type I and III collagen proteins in the posterior joint capsule. Dexamethasone treatment during the remobilization period improved both myogenic and arthrogenic contractures. Furthermore, remobilization-induced fibrotic reactions in the joint capsule were mostly prevented using dexamethasone. Anti-inflammatory treatment during the recovery period may be a potential therapeutic treatment for joint contracture.
关节再活动后的炎症反应是导致关节源性挛缩进展的一个重要因素。我们评估了在关节固定解除后再活动阶段给予抗炎治疗对大鼠膝关节挛缩的影响。三组大鼠通过膝关节外固定器固定膝关节于 140°屈曲位 3 周以产生屈曲挛缩。随后去除固定装置，让固定的膝关节自由活动 1 天或 7 天。这些大鼠每天接受甾体类抗炎药地塞米松或生理盐水注射。未治疗的膝关节作为对照。在再活动 1 天，后关节囊中的促炎细胞因子白细胞介素（IL）-1β和 IL-6 的基因表达均增加，而地塞米松治疗抑制了这些标志物的增加。在膝关节屈肌切开术前和术后测量被动伸展活动度（ROM）。切开术前的 ROM 限制主要代表肌源性的，而切开术后的 ROM 则显示出关节源性的变化。关节固定既降低了切开术前又降低了切开术后的 ROM。7 天的再活动改善了切开术前但没有改善切开术后的 ROM。再活动后关节挛缩的进展表现为后关节囊的纤维反应、细胞过度增生、胶原基因上调以及 I 型和 III 型胶原蛋白增加。再活动阶段给予地塞米松治疗改善了肌源性和关节源性挛缩。此外，地塞米松治疗在很大程度上预防了再活动引起的关节囊纤维反应。在恢复期给予抗炎治疗可能是治疗关节挛缩的一种潜在治疗方法。
