Abstract
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 3weeks 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 7days. These rats were daily injected with either the steroidal anti-inflammatory drug dexamethasone or saline. Untreated knees were used as controls. At 1day 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.
Published Version
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