Most cited article - PubMed ID 31852201
Intra-articular injection of mitomycin C prevents progression of immobilization-induced arthrogenic contracture in the remobilized rat knee
Joint immobilization is frequently administered after fractures and ligament injuries and can cause joint contracture as a side effect. The structures responsible for immobilization-induced joint contracture can be roughly divided into muscular and articular. During remobilization, although myogenic contracture recovers spontaneously, arthrogenic contracture is irreversible or deteriorates further. Immediately after remobilization, an inflammatory response is observed, characterized by joint swelling, deposit formation in the joint space, edema, inflammatory cell infiltration, and the upregulation of genes encoding proinflammatory cytokines in the joint capsule. Subsequently, fibrosis in the joint capsule develops, in parallel with progressing arthrogenic contracture. The triggers of remobilization-induced joint inflammation are not fully understood, but two potential mechanisms are proposed: 1) micro-damage induced by mechanical stress in the joint capsule, and 2) nitric oxide (NO) production via NO synthase 2. Some interventions can modulate remobilization-induced inflammatory and subsequent fibrotic reactions. Anti-inflammatory treatments, such as steroidal anti-inflammatory drugs and low-level laser therapy, can attenuate joint capsule fibrosis and the progression of arthrogenic contracture in remobilized joints. Antiproliferative treatment using the cell-proliferation inhibitor mitomycin C can also attenuate joint capsule fibrosis by inhibiting fibroblast proliferation without suppressing inflammation. Conversely, aggressive exercise during the early remobilization phases is counterproductive, because it facilitates inflammatory and then fibrotic reactions in the joint. However, the adverse effects of aggressive exercise on remobilization-induced inflammation and fibrosis are offset by anti-inflammatory treatment. To prevent the progression of arthrogenic contracture during remobilization, therefore, care should be taken to control inflammatory and fibrotic reactions in the joints.
- MeSH
- Anti-Inflammatory Agents pharmacology MeSH
- Fibrosis MeSH
- Knee Joint MeSH
- Contracture * drug therapy MeSH
- Humans MeSH
- Range of Motion, Articular MeSH
- Inflammation pathology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Names of Substances
- Anti-Inflammatory Agents MeSH
Therapeutic approaches to treat joint contracture after anterior cruciate ligament (ACL) reconstruction have not been established. Arthrofibrosis accompanied by joint inflammation following ACL reconstruction is a major cause of arthrogenic contracture. In this study, we examined whether anti-inflammatory treatment using low-level laser therapy (LLLT) can prevent ACL reconstruction-induced arthrogenic contracture. Rats underwent ACL transection and reconstruction surgery in their right knees. Unoperated left knees were used as controls. After surgery, rats were reared with or without daily LLLT (wavelength: 830 nm; power output: 150 mW; power density: 5 W/cm2; for 120 s/day). We assessed the passive extension range of motion (ROM) after myotomy at one and two weeks post-surgery; the reduction in ROM represents the severity of arthrogenic contracture. ROM was markedly decreased by ACL reconstruction at both time points; however, LLLT partially attenuated the decrease in ROM. One week after ACL reconstruction, the gene expression of the proinflammatory cytokine interleukin-1beta in the joint capsule was significantly upregulated, and this upregulation was significantly attenuated by LLLT. Fibrotic changes in the joint capsule, including upregulation of collagen type I and III genes, shortening of the synovium, and thickening were caused by ACL reconstruction and seen at both time points. LLLT attenuated these fibrotic changes as well. Our results indicate that LLLT after ACL reconstruction could attenuate the formation of arthrogenic contracture through inhibition of inflammation and fibrosis in the joint capsule. Thus, LLLT may become a novel therapeutic approach for ACL reconstruction-induced joint contracture.
- MeSH
- Fibrosis MeSH
- Knee Joint surgery MeSH
- Contracture * etiology prevention & control MeSH
- Rats MeSH
- Low-Level Light Therapy * adverse effects MeSH
- Anterior Cruciate Ligament Injuries * complications surgery MeSH
- Anterior Cruciate Ligament Reconstruction * adverse effects MeSH
- Range of Motion, Articular MeSH
- Inflammation pathology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
The effects of exercise on mechanical hyperalgesia, joint contracture, and muscle injury resulting from immobilization are not completely understood. This study aimed to investigate the effects of cyclic stretching on these parameters in a rat model of chronic post-cast pain (CPCP). Seventeen 8-week-old Wistar rats were randomly assigned to (1) control group, (2) immobilization (CPCP) group, or (3) immobilization and stretching exercise (CPCP+STR) group. In the CPCP and CPCP+STR groups, both hindlimbs of each rat were immobilized in full plantar flexion with a plaster cast for a 4-week period. In the CPCP+STR group, cyclic stretching exercise was performed 6 days/week for 2 weeks, beginning immediately after cast removal prior to reloading. Although mechanical hyperalgesia in the plantar skin and calf muscle, ankle joint contracture, and gastrocnemius muscle injury were observed in both immobilized groups, these changes were significantly less severe in the CPCP+STR group than in the CPCP group. These results clearly demonstrate the beneficial effect of cyclic stretching exercises on widespread mechanical hyperalgesia, joint contracture, and muscle injury in a rat model of CPCP.
- MeSH
- Chronic Pain etiology pathology rehabilitation MeSH
- Hyperalgesia etiology pathology rehabilitation MeSH
- Immobilization MeSH
- Physical Conditioning, Animal methods MeSH
- Contracture etiology pathology rehabilitation MeSH
- Muscle, Skeletal physiology MeSH
- Rats MeSH
- Humans MeSH
- Disease Models, Animal MeSH
- Rats, Wistar MeSH
- Casts, Surgical MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Humans MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH