Passive Extension Range Of Motion Research Articles

Neural mechanosensitivity findings in patients with adhesive capsulitis

BACKGOURND: The pathophysiology of adhesive capsulitis may be associated with increased neural mechanosensitivity in upper limb neurodynamic test. OBJECTIVE: To investigate the findings of neurodynamic assessment in patients with more than four month history of adhesive capsulitis. METHODS: Thirty-five patients with more than four month history of adhesive capsulitis were participated in this study. A physiotherapist performed the Upper Limb Neurodynamic test 1 procedure on the participant’s upper limb. Elbow extension range of motion at the end of the Upper Limb Neurodynamic test 1 was compared with the participant’s elbow extension at the end of Upper Limb Neurodynamic test 1 performed on the opposite upper limb and to elbow extension on the symptomatic side performed with the arm by the side. RESULTS: The intensity of pain in Upper Limb Neurodynamic test 1 increased with lateral flexion of the neck to the unaffected side and eased with lateral flexion to the affected side in all participants. A marked restriction of the elbow passive extension range of motion in Upper Limb Neurodynamic test 1 on the affected side (–54.6±17.8°) compared to the unaffected side was found (–7.3±10.7°) (p < 0.001). CONCLUSIONS: Restriction of elbow passive extension range of motion at the end of the Upper Limb Neurodynamic 1 test reproduced patients’ familiar adhesive capsulitis associated pain and the pain changed with structural differentiation using cervical lateral flexion. Neurodynamic assessment may need to be considered to assess neural mechanosensitivity in patients with adhesive capsulitis.

Formation process of extension knee joint contracture following external immobilization in rats.

Current research lacks a model of knee extension contracture in rats. To elucidate the formation process of knee extension contracture. We developed a rat model using an aluminum external fixator. Sixty male Sprague-Dawley rats with mature bones were divided into the control group (n = 6) and groups that had the left knee immobilized with an aluminum external fixator for 1, 2, and 3 d, and 1, 2, 3, 4, 6, and 8 wk (n = 6 in each group). The passive extension range of motion, histology, and expression of fibrosis-related proteins were compared between the control group and the immobilization groups. Myogenic contracture progressed very quickly during the initial 2 wk of immobilization. After 2 wk, the contracture gradually changed from myogenic to arthrogenic. The arthrogenic contracture progressed slowly during the 1st week, rapidly progressed until the 3rd week, and then showed a steady progression until the 4rd week. Histological analyses confirmed that the anterior joint capsule of the extended fixed knee became increasingly thicker over time. Correspondingly, the level of transforming growth factor beta 1 (TGF-β1) and phosphorylated mothers against decapentaplegic homolog 2 (p-Smad2) in the anterior joint capsule also increased with the immobilization time. Over time, the cross-sectional area of muscle fibers gradually decreased, while the amount of intermuscular collagen and TGF-β1, p-Smad2, and p-Smad3 was increased. Unexpectedly, the amount of intermuscular collagen and TGF-β1, p-Smad2, and p-Smad3 was decreased during the late stage of immobilization (6-8 wk). The myogenic contracture was stabilized after 2 wk of immobilization, whereas the arthrogenic contracture was stabilized after 3 wk of immobilization and completely stable in 4 wk. This rat model may be a useful tool to study the etiology of joint contracture and establish therapeutic approaches.

Low-Level Laser Therapy Attenuates Arthrogenic Contracture Induced by Anterior Cruciate Ligament Reconstruction Surgery in Rats

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.

Development of a novel knee contracture mouse model by immobilization using external fixation

ABSTRACT Aims Several studies have used animal models to examine knee joint contracture; however, few reports detail the construction process of a knee joint contracture model in a mouse. The use of mouse models is beneficial, as genetically modified mice can be used to investigate the pathogenesis of joint contracture. Compared to others, mouse models are associated with a lower cost to evaluate therapeutic effects. Here, we describe a novel knee contracture mouse model by immobilization using external fixation. Methods The knee joints of mice were immobilized by external fixation using a splint and tape. The passive extension range of motion (ROM), histological and immunohistochemical changes, and expression levels of fibrosis-related genes at 2 and 4 weeks were compared between the immobilized (Im group) and non-immobilized (Non-Im group) groups. Results The extension ROM at 4 weeks was significantly lower in the Im group than in the Non-Im group (p < 0.01). At 2 and 4 weeks, the thickness and area of the joint capsule were significantly greater in the Im group than in the Non-Im group (p < 0.01 in all cases). At 2 weeks, the mRNA expression levels of the fibrosis-related genes, except for the transforming growth factor-β1, and the protein levels of cellular communication network factor 2 and vimentin in the joint capsule were significantly higher in the Im group (p < 0.01 in all cases). Conclusion This mouse model may serve as a useful tool to investigate the etiology of joint contracture and establish new treatment methods.

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

Joint contracture is a common complication of joint injury. This study aimed to assess the effect of inhibiting the transforming growth factor-β (TGF-β) signaling during joint immobilization and remobilization on immobilization-induced joint contracture in rats. The knees of rats were immobilized using Kirschner wires following trauma to the femoral condyles to generate joint contracture. After immobilization, levels of TGF-β and passive extension range of motion (ROM) were measured at different time points, joints were histologically analyzed by hematoxylin and eosin (H&E) and Masson trichrome staining, and the expression of inflammatory or fibrosis-related mediators, including interleukin-1β (IL-1β), phosphorylated Smad2/3 (p-Smad2/3), α-smooth muscle actin (α-SMA) and collagen types I (Col 1) and III (Col 3), were examined in joint capsules using immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR). Rats were also treated with LY2157299, a TGF-β receptor I kinase inhibitor, at different stages of immobilization and remobilization. TGF-β1 levels in the serum and the number of p-Smad2/3+ cells in the joint capsule were significantly elevated after immobilization. ROM decreased during the 6 weeks of immobilization and partly recovered after remobilization. After treatment with LY2157299 during immobilization, the restricted ROM moderately increased, but this effect was stronger when combined with active motion. Mechanistically, the expression of IL-1β, TGF-β, fibrosis-related factors, and the density of collagen significantly decreased after treatment with LY2157299. Inhibiting TGF-β signaling paired with active motion effectively attenuated the formation of immobilization-induced joint contracture in rats.

Immediate effects of neurodynamic nerve gliding versus static stretching on hamstring neuromechanical properties.

We investigated the immediate effects of neurodynamic nerve gliding (ND) on hamstring flexibility, viscoelasticity, and mechanosensitivity, compared with traditional static stretching (ST). Twenty-two physically active men aged 21.9 ± 1.9years were divided randomly into two equal intervention groups using ST or ND. An isokinetic dynamometer was used to measure the active knee joint position sense, perform passive knee extension, record the passive extension range of motion (ROM) and the passive-resistive torque of hamstrings. Stiffness was determined from the slope of the passive torque-angle relationship. A stress relaxation test (SRT) was performed to analyze the viscoelastic behavior of the hamstrings. The passive straight leg raise (SLR) test was used to evaluate hamstring flexibility. A significant interaction was observed for ROM and passive ultimate stiffness, reflected by an increase in these indicators after ND but not after SD. SLR increased significantly in both groups. After ST, a significantly faster initial stress relaxation was observed over the first 4s. than after ND. There was no significant change in the active knee joint position sense. ND provided a slightly greater increase in hamstring extensibility and passive stiffness, possibly by decreasing nerve tension and increasing strain in connective tissues than ST. The ST mostly affected the viscoelastic behavior of the hamstrings, but neither intervention had a significant impact on proprioception.

Intra-articular injection of mitomycin C prevents progression of immobilization-induced arthrogenic contracture in the remobilized rat knee.

This study tested whether cell cycle inhibitor mitomycin C (MMC) prevents arthrogenic contracture progression during remobilization by inhibiting fibroblast proliferation and fibrosis in the joint capsule. Rat knees were immobilized in a flexed position to generate flexion contracture. After three weeks, the fixation device was removed and rat knees were allowed to freely move for one week. Immediately after and three days after fixator removal, rats received intra-articular injections of MMC or saline. The passive extension range of motion (ROM) was measured before and after myotomy of the knee flexors to distinguish myogenic and arthrogenic contractures. In addition, both cellularity and fibrosis in the posterior joint capsule were assessed histologically. Joint immobilization significantly decreased ROMs both before and after myotomy compared with untreated controls. In saline-injected knees, remobilization increased ROM before myotomy, but further decreased that after myotomy compared with that of knees immediately after three weeks of immobilization. Histological analysis revealed that hypercellularity, mainly due to fibroblast proliferation, and fibrosis characterized by increases in collagen density and joint capsule thickness occurred after remobilization in saline-injected knees. Conversely, MMC injections were able to prevent the remobilization-enhanced reduction of ROM after myotomy by inhibiting both hypercellularity and joint capsule fibrosis. Our results suggest that joint capsule fibrosis accompanied by fibroblast proliferation is a potential cause of arthrogenic contracture progression during remobilization, and that inhibiting fibroblast proliferation may constitute an effective remedy.

Anti-inflammatory Drug Dexamethasone Treatment During the Remobilization Period Improves Range of Motion in a Rat Knee Model of Joint Contracture

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.

Development of arthrogenic joint contracture as a result of pathological changes in remobilized rat knees.

This study aimed to elucidate how rats recover from immobilization-induced knee joint contracture. Rats' right knees were immobilized by an external fixator at a flexion of 140° for 3 weeks. After removal of the fixator, the joints were allowed to move freely (remobilization) for 0, 1, 3, 7, or 14 days (n = 5 each). To distinguish myogenic and arthrogenic contractures, the passive extension range of motion was measured before and after myotomy of the knee flexors. Knee joints were histologically analyzed and the expression of genes encoding inflammatory or fibrosis-related mediators, interleukin-1β (1L-1β), fibrosis-related transforming growth factor-β1 (TGF-β1), and collagen type I (COL1A1) and III (COL3A1), were examined in the knee joint posterior capsules using real-time PCR. Both myogenic and arthrogenic contractures were established within 3 weeks of immobilization. During remobilization, the myogenic contracture decreased over time. In contrast, the arthrogenic contracture developed further during the remobilization period. On day 1 of remobilization, inflammatory changes characterized by edema, inflammatory cell infiltration, and upregulation of IL-1β gene started in the knee joint posterior capsule. In addition, collagen deposition accompanied by fibroblast proliferation, with upregulation of TGF-β1, COL1A1, and COL3A1 genes, appeared in the joint capsule between days 7 and 14. These results suggest the progression of arthrogenic contracture following remobilization, which is characterized by fibrosis development, is possibly triggered by inflammation in the joint capsule. It is therefore necessary to focus on developing new treatment strategies for immobilization-induced joint contracture. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1414-1423, 2017.

Nociception contributes to the formation of myogenic contracture in the early phase of adjuvant-induced arthritis in a rat knee

It is unknown how joint contracture is generated in inflamed joints. This study aimed to clarify the role of nociception on the formation of joint contracture secondary to arthritis. Monoarthritis was induced by intra-articular injections of complete Freund's adjuvant (CFA) into rat knees. On day 5 after CFA injection, the passive extension range of motion (ROM) of knee joints were measured, both before and after myotomy of knee flexors, to evaluate the extent of muscular contribution to CFA-induced joint contracture. The steroidal anti-inflammatory drug dexamethasone could prevent ROM restrictions completely, both before and after myotomy. On the other hand, the opioid analgesic drug morphine did not prevent the development of restricted ROM observed after myotomy, while it did before myotomy. This indicates that nociception contributes to joint contracture through alterations in muscular structure (myogenic factors). Next, we tested the hypothesis that nociception-induced reflexive flexor muscle contractions cause myogenic contracture in arthritic joints. To do this, chemical denervation was performed by Botulinum toxin type A (BTX-A) injections into knee flexor muscles, simultaneously with CFA injections into the knee. As expected, BTX-A could alleviate ROM restrictions observed before myotomy. These findings suggest that nociceptive-related muscle contractions play an essential role in the formation of joint contracture. Thus, our study indicates that analgesic management during an early stage of joint arthritis is an essential mean to prevent the formation of joint contracture. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1404-1413, 2017.

Toe flexors strength and passive extension range of motion of the first metatarsophalangeal joint in individuals with plantar fasciitis.

Cross-sectional study. To determine if a difference exists in toe flexors strength and passive extension range of motion of the first metatarsophalangeal joint between individuals with unilateral plantar fasciitis and control subjects. Weakness of the dynamic longitudinal arch supporters and shortening of the plantar fascia have been suggested as etiologic factors for plantar fasciitis. METHOD AND MEASURES: Twenty subjects with unilateral plantar fasciitis participated in the study. Subjects had had symptoms for an average (+/-SD) of 19.9 +/- 33.2 months prior to participating in the study. Twenty control subjects matched for sex and age were also tested. Each subject was measured bilaterally for passive extension range of motion of the first metatarsophalangeal joint and peak resistance force observed during an isometric test of toe flexors strength. Subjects with unilateral plantar fasciitis demonstrated weaker toe flexors (P<.05) than the control subjects. A significant main effect for feet also indicated that the toe flexors for the involved feet were significantly weaker than the uninvolved feet (P<.05) of subjects with unilateral plantar fasciitis. Passive extension range of motion of the first metatarsophalangeal joint was not significantly different between the involved and the uninvolved feet for subjects with plantar fasciitis. Results for our subjects indicate that the extensibility of soft tissues influencing extension of the first metatarsophalangeal joint was not related to the presence of plantar fasciitis. Additional research is needed to determine if toe flexors weakness is a cause or a result of plantar fasciitis and if strengthening regimes for the toe flexors are effective interventions for plantar fasciitis.