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Abstract Objective While joint immobilization is a useful repair method for intra-articular ligament injury and periarticular fracture, prolonged joint immobilization can cause multiple complications. A better understanding how joint immobilization and remobilization impact joint function and homeostasis will help clinicians develop novel strategies to reduce complications. Design We first determined the effects of long-term immobilization on joint pain and osteophyte formation in patients after an extraarticular fracture or ligament injury. We then developed a mouse model of joint immobilization and harvested the knee joint samples at 2, 4, and 8 weeks. We further determined the effects of remobilization on recovery of the osteoarthritis (OA) lesions induced by immobilization in mice. Results We found that the long-term (6 weeks) joint immobilization caused significant joint pain and osteophytes in patients. In mice, 2-week immobilization already induced moderate sensory innervation and increased pain sensitivity and infiltration in synovium without inducing marked osteophyte formation and cartilage loss. Long-term immobilization (4 and 8 weeks) induced more severe sensory innervation and inflammatory infiltration in synovium, massive osteophyte formation on both sides of the femoral condyle, and the edge of the tibial plateau and significant loss of the articular cartilage in mice. Remobilization, which ameliorates normal joint load and activity, restored to certain extent some of the OA lesions and joint function in mice. Conclusions Joint immobilization caused multiple OA-like lesions in both mice and humans. Joint immobilization induced progressive sensory innervation, synovitis, osteophyte formation, and cartilage loss in mice, which can be partially ameliorated by remobilization.

Background: The development of osteoarthritis after anterior cruciate ligament (ACL) reconstruction (ACLR) is an important issue. However, the appropriate rehabilitation protocol to prevent cartilage degeneration due to postoperative osteoarthritis is unclear. Purpose: To examine the effects of joint immobilization and treadmill exercise on articular cartilage after ACLR. Study Design: Controlled laboratory study. Methods: A total of 55 rats received unilateral knee ACL transection and reconstruction surgery using tail tendon autografts. After surgery, rats were reared without intervention, with joint immobilization, or with daily treadmill exercise (12 m/minute, 60 minutes/day, 6 days/week). Treadmill exercise was initiated at 3 or 14 days postoperatively. After 2 weeks of immobilization, the fixation device was removed from some of the immobilized rats, and the knee was allowed to move freely for 2 weeks. Untreated, age-matched rats (n = 8) were used as controls. At 2 or 4 weeks after starting the experiment, cartilage degeneration in the medial tibial plateau was histologically assessed using a modified Mankin score, cartilage thickness, chondrocyte density, and immunohistochemistry for cyclooxygenase-2 (COX-2) in the anterior, middle, and posterior regions. Results: After ACLR, cartilage degeneration in the anterior region characterized by increased Mankin score, accompanied with increased COX-2 expression, was detected. Joint immobilization after ACLR facilitated cartilage degeneration, which is detected by histological changes such as reductions in cartilage thickness, chondrocyte density, and high Mankin scores. Enhanced COX-2 expression in all degenerated cartilage regions was also detected. It was found that 2 weeks of remobilization could not restore cartilage degeneration induced by 2 weeks of immobilization after ACLR. Treadmill exercise after ACLR did not affect most articular cartilage parameters, regardless of the timing of exercise. Conclusion: Our results indicated that (1) immobilization after ACLR accelerates cartilage degeneration, even when applied only for 2 weeks, and (2) mild exercise during early phases after ACLR does not facilitate cartilage degeneration. Clinical Relevance: To reduce cartilage degeneration, periods of joint immobilization after ACLR should be minimized. Mild exercise during the early phases after ACLR will not negatively affect articular cartilage. [ABSTRACT FROM AUTHOR]

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. Antiinflammatory 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 cellproliferation 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. [ABSTRACT FROM AUTHOR]

Contractures -- limitation of passive movements in the joint -- are a fairly frequent complication after immobilization or limitation of mobility and loading of the limb due to injuries, but the exact cause of their formation has not been clarified. Objective. Based on the meta-analysis of the results of experimental modeling and clinical studies of immobilization contractures, create a conceptual model of their formation. Methods. Literature sources from scientific bases were analyzed: Cochrane Library, Scopus, National Library of Medicine, ReLAB-HS Rehabilitation Resources Repository, Mendeley Reference Manager, The Physiological Society library, Google Scholar. Results. A conceptual model of the development of contractures was created. It is shown that immobilization of the joint of the injured limb blocks the execution of the signal of motor impulses. The lack of movement in the joint leads to a decrease in muscle strength and a slowdown in blood circulation. These processes are interrelated: hypotonia of the muscle is due to the restriction of nutrition through the blood supply, and the lack of contractile activity of the muscles leads to the rearrangement of the blood vessels. Articular cartilage is nourished through the subchondral bone and due to osmosis from the synovial fluid during movements. The lack of movement limits nutrition, protein synthesis is disrupted, the surface of the cartilage, synovial membrane and fluid begins to be rebuilt, the joint capsule, ligaments, and tendons thicken. At the same time, the structure of the muscles changes, they shorten and become denser. With long-term immobilization, degenerative processes in the tissues of the joint worsen its general condition, which can eventually lead to complete immobilization. Conclusions. The created conceptual model of the formation of immobilization contractures of joints takes into account the morphological changes of tissues as a result of immobilization. Immobilization affects all components of the joint and adjacent tissues from the first days, the changes progress over time. The use of the model will allow the development of a system of treatment measures to prevent the development of contractures. [ABSTRACT FROM AUTHOR]

Abstract Background Joint hemorrhage is caused by trauma, ligament reconstruction surgery, and bleeding disorders such as hemophilia. Recurrence of hemorrhage in the joint space induces hemosiderotic synovitis and oxidative stress, resulting in both articular cartilage degeneration and arthropathy. Joint immobilization is a common treatment option for articular fractures accompanied by joint hemorrhage. Although joint hemorrhage has negative effects on the articular cartilage, there is no consensus on whether a reduction in joint hemorrhage would effectively prevent articular cartilage degeneration. The purpose of this study was to investigate the effect of joint hemorrhage combined with joint immobilization on articular cartilage degeneration in a rat immobilized knee model. Methods The knee joints of adult male rats were immobilized at the flexion using an internal fixator from 3 days to 8 weeks. The rats were randomly divided into the following groups: immobilized blood injection (Im-B) and immobilized-normal saline injection (Im-NS) groups. The cartilage was evaluated in two areas (contact and non-contact areas). The cartilage was used to assess chondrocyte count, Modified Mankin score, and cartilage thickness. The total RNA was extracted from the cartilage in both areas, and the expression of metalloproteinase (MMP)-8, MMP-13, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α was measured by quantitative real-time polymerase chain reaction. Results The number of chondrocytes in the Im-B group significantly decreased in both areas, compared with that in the Im-NS group. Modified Mankin score from 4 to 8 weeks of the Im-B group was significantly higher than that of the Im-NS group only in the contact area. The expression of MMP-8 and MMP-13 from 2 to 4 weeks and TNF-α from 2 to 8 weeks significantly increased in the Im-B group compared with those in the Im-NS group, but there was no significant difference in IL-1β expression. Conclusions The results showed that joint hemorrhage exacerbated immobilization-induced articular cartilage degeneration. Drainage of a joint hemorrhage or avoidance of loading may help prevent cartilage degeneration during joint immobilization with a hemorrhage.

Skeletal disuse can cause an accumulation of bone marrow adipose tissue (MAT) characterized by a combination of marrow adipocyte hyperplasia and/or hypertrophy. The malleability of MAT accumulation and of the hyperplasia and hypertrophy upon remobilization is unknown. In this study, we showed extensive hyperplasia and accelerated hypertrophy of bone marrow adipocytes in the proximal tibia epiphysis of rat knees immobilized for durations between 1 and 32 wk. Similar histomorphometric measures of adipocytes carried out in unoperated controls allowed distinguishing the effects of immobilization from the effects of aging. Although both knee immobilization and aging led to adipocyte hypertrophy, adipocyte hyperplasia was the hallmark signature effect of immobilization on MAT. Both bone marrow adipocyte hyperplasia and hypertrophy were sustained despite knee remobilization for durations up to four times the duration of immobilization. These results suggest that adipocyte hyperplasia is the predominant mechanism explaining MAT accumulation in skeletal disuse. In this model, the changes were unremitting for the investigated time points. Investigating the cellular and molecular mechanisms of marrow adipocyte mechanoregulation will be important to better understand how adipocytes adapt to changes in mechanical environments. NEW & NOTEWORTHY This longitudinal study elucidates the response of marrow adipose tissue adipocytes in weight-bearing joints to changes in different mechanical environments, and we provide insight on the malleability of the changes over time. In a rat animal model, knee immobilization induced hyperplasia and accelerated the age-dependent hypertrophy of adipocytes. Changes in adipocyte number and size were sustained despite unassisted remobilization. Multimodal distributions of cell size were characteristic of bone marrow adipocytes. [ABSTRACT FROM AUTHOR]

The treatment of joint contracture continues to represent a challenging problem in orthopedic surgery and rehabilitation medicine. Existing animal models of knee contracture for evaluating new treatments are mostly created by extensive joint tissue damage with Kirschner‐wire immobilization which requires a second surgery to remove Kirschner‐wires. This study aimed to develop a less invasive rabbit model of moderate knee contracture through a single surgery. Skeletally mature New Zealand White rabbits had their right knee operated to create surgical damage to the posterior capsule under direct visualization. Operated knees were then held in a flexed position by suturing the superficial flexion muscles with absorbable sutures. The flexion contracture (net extension loss) was determined by comparing the extension angles between the operated and non‐operated knees from 8 to 24 weeks post‐surgery. The flexion contracture of the operated knees was significantly greater (p < 0.01/0.001) than the non‐operated knees at each weekly measurement. The mean flexion contractures were 22° at 8 weeks, 19° at 16 weeks, and 18° at 24 weeks. No significant differences in the severity of flexion contracture were observed between 8‐week and each of the following weeks, suggesting that the flexion contracture was essentially stabilized by 8 weeks post‐surgery. Histopathologic analyses demonstrated intra‐articular and peri‐articular scar formation. This less invasive rabbit model of moderate knee contracture is more quickly established through a single surgery with lower risk of surgical complications compared to the previously reported invasive models, and could be an alternative animal model for joint contracture research. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:2687–2695, 2018. [ABSTRACT FROM AUTHOR]

Degenerative alterations in articular cartilage are involved in the pathogenesis of osteoarthritis. The present study aimed to evaluate the role of complement component 5a (C5a) in osteoarthritic alterations in the articular cartilage and synovialis via a joint immobilization (IM) rat model. Rats were assigned to three groups: Control, IM and IM+anti‑C5a antibody (IM+anti‑C5a) groups. A terminal deoxynucleotidyl transferase dUTP nick end labeling assay and hematoxylin and eosin staining were used to evaluate the morphological alterations in the articular cartilage and synovialis. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis, immunohistochemical analysis and western blotting were used to evaluate C5a expression in the articular cartilage and synovialis. An ELISA was used to evaluate C5a‑induced alterations in interleukin (IL)‑1β, IL‑17A and tumor necrosis factor (TNF)‑α levels in the serum and joint fluid. The results demonstrated that knee joint immobilization induced destruction of knee joint synovial fluid and cartilage in the IM and IM+anti‑C5a antibody groups. Immobilization significantly increased the expression levels of C5a in serum and joint fluid in the IM group. Immunohistochemistry, western blotting and RT‑qPCR analysis illustrated markedly increased expression of C5a in the IM group. Immobilization markedly increased the IL‑1β, IL‑17A and TNF‑α expression levels in the serum and joint fluid in the IM group. Anti‑C5a was able to decrease immobilization‑induced alterations in morphology and cytokines compared with the IM group. The expression of C5a was increased in synoviocytes and joint cartilage in the IM model. Pro‑inflammatory cytokines, including TNF‑α and IL‑1β were released in the activated synoviocytes via the induction of C5a, suggesting that C5a serves an important role in joint inflammatory processes. [ABSTRACT FROM AUTHOR]

The purpose of this study was to examine the effect of low-intensity pulsed ultrasound (LIPUS) in preventing joint stiffness. Unilateral knee joints were immobilized in two groups of rats (n = 6/period/group). Under general anesthesia, the immobilized knee joints were exposed to LIPUS for 20 min/d, 5 d/wk, using an existing LIPUS device (LIPUS group, 1.5-MHz frequency, 1.0-kHz repetition cycle, 200-µs burst width and 30-mW/cm2 power output) until endpoints (2, 4 or 6 wk). In the control group, general anesthesia alone was administered in the same manner as in the other group. The variables compared between the groups included joint angles; histologic, histomorphometric and immunohistochemical analyses; quantitative reverse transcription polymerase chain reactions; and tissue elasticity. LIPUS had a preventive effect on joint stiffness, resulting in decreased adhesion, fibrosis and inflammation and hypoxic response after joint immobilization. [ABSTRACT FROM AUTHOR]

This study investigated the effects of treadmill walking during remobilization on range of motion (ROM) and histopathology in rat knee joints, which were immobilized for 3 wk in a flexed position. After fixator removal, rats were divided into a no-intervention (RM) group and a group forced to walk on a treadmill daily at 12 m/min for 60 min (WALK group). Passive knee extension ROMs were measured before (m-ROM) and after (a-ROM) knee flexor myotomy on the first and last day of a 7-day remobilization period, with m-ROM mainly reflecting myogenic factors and a-ROM reflecting arthrogenic factors. Knee joints were histologically analyzed and gene expression of inflammatory or fibrosis-related mediators in the posterior joint capsule were examined. m-ROM and a-ROM restrictions were established after immobilization. m-ROM significantly increased following the remobilization period both in RM and WALK groups compared with that of immobilized (IM) group. Conversely, a-ROM decreased following the remobilization period in both RM and WALK groups compared with that of IM group. Importantly, a-ROM was smaller in the WALK group than the RM group. Remobilization without intervention induced inflammatory and fibrotic reactions in the posterior joint capsule after 1 and 7 days. Treadmill walking promoted these reactions and also increased the expression of fibrosis-related TGF-β1 and collagen type I and III genes. While free movement after immobilization improved myogenic contracture, arthrogenic contracture worsened. Treadmill walking further aggravated arthrogenic contracture through amplified inflammatory and fibrotic reactions. Thus active exercise immediately after immobilization may not improve immobilization-induced joint contracture. [ABSTRACT FROM AUTHOR]

Marrow adipose deposition is observed during aging and in association with extended periods of immobility. The objective of this study was to determine the contribution of adipocyte hypertrophy and hyperplasia to bone marrow fat deposition induced by immobilization of the rat knee joint for 2, 4, 16 or 32 weeks. Histomorphometric analyses compared immobilized to sham-operated proximal tibia from age and gender matched rats to assess the contribution of aging and duration of immobilization on the number and size of marrow adipocytes. Results indicated that marrow adipose tissue increased with the duration of immobilization and was significant larger at 16 weeks compared to the sham-operated group (0.09956 ± 0.13276 mm 2 vs 0.01990 ± 0.01100 mm 2 , p = 0.047). The marrow adipose tissue was characterized by hyperplasia of adipocytes with a smaller average size after 2 and 4 weeks of immobilization (at 2 weeks hyperplasia: 68.86 ± 33.62 vs 43.57 ± 24.47 adipocytes/mm 2 , p = 0.048; at 4 weeks hypotrophy: 0.00036 ± 0.00019 vs 0.00046 ± 0.00023 mm 2 , p = 0.027), and by adipocyte hypertrophy after 16 weeks of immobilization (0.00083 ± 0.00049 vs 0.00046 ± 0.00028 mm 2 , p = 0.027) compared to sham-operated. Both immobilized and sham-operated groups showed marrow adipose conversion with age; immobilized (p = 0.008; sham: p = 0.003). Overall, fat deposition in the bone marrow of the proximal rat tibia epiphysis and induced by knee joint immobilization was characterized by hyperplasia of small adipocytes in the early phase and by adipocyte hypertrophy in the later phase. Mediators of marrow fat deposition after immobilization and preventive countermeasures need to be investigated. [ABSTRACT FROM AUTHOR]

Marrow adipose tissue (MAT) adversely affects bone metabolism under certain conditions. Although mechanical stress is an important factor in regulating MAT and bone mass, how stress from different rehabilitation protocols after anterior cruciate ligament (ACL) reconstruction affects trabecular bone and MAT is unclear. We aimed to examine the effects of joint immobilization and treadmill exercise on trabecular bone and MAT after ACL reconstruction. Rats received unilateral knee ACL transection and reconstruction surgery. After surgery, rats were reared without intervention, with joint immobilization, or with treadmill exercise (12 m/min, 60 min/day, six days/week), with untreated rats as controls. At two or four weeks after starting experiments, we examined histological changes in trabecular bone and MAT in the proximal tibial epiphysis. After ACL reconstruction, there were no significant changes in trabecular bone area and MAT area at both time points. Joint immobilization after ACL reconstruction resulted in reduced trabecular bone area and MAT accumulation due to adipocyte hyperplasia and hypertrophy within four weeks. Treadmill exercise after ACL reconstruction did not affect any parameters in trabecular bone and MAT. We detected a moderate negative correlation between trabecular bone area and MAT area. Therefore, MAT accumulation induced by joint immobilization may contribute, at least in part, to reducing trabecular bone area. To minimize trabecular bone loss and MAT accumulation, joint immobilization after ACL reconstruction should be minimized. Exercise after ACL reconstruction did not alter trabecular bone and MAT. ● How stress from rehabilitation methods after ACLR affects bone and MAT is unclear. ● We examined the effects of immobilization and exercise on bone and MAT. ● Immobilization resulted in reduced trabecular bone and MAT accumulation. ● Treadmill exercise did not affect any parameters in trabecular bone and MAT. ● Immobilization should be minimized to minimize bone loss and MAT accumulation. [ABSTRACT FROM AUTHOR]

Both myogenic and arthrogenic factors contribute to contracture formation after anterior cruciate ligament reconstruction surgery. However, effects of immobilization duration on myogenic and arthrogenic contractures after surgery are unknown. We examined the effects of immobilization duration on contracture formation. Rats were divided into groups according to treatment received: untreated control, knee immobilization, anterior cruciate ligament reconstruction, and anterior cruciate ligament reconstruction plus immobilization. Extension range of motion before and after myotomy as well as histomorphological knee changes were assessed two or four weeks after experiment commencement. Range of motion before myotomy mainly represents contractures due to myogenic factors. Range of motion after myotomy represents arthrogenic factors. Range of motion before and after myotomy was decreased in the immobilization, reconstruction, and reconstruction plus immobilization groups at both timepoints. In the reconstruction plus immobilization group, range of motion before and after myotomy was significantly smaller than in the immobilization and reconstruction groups. Shortening and thickening of the posterior joint capsule was induced in the immobilization and reconstruction groups. In the reconstruction plus immobilization group, capsule shortening was facilitated via adhesion formation, as compared to the immobilization and reconstruction groups. Our results indicate that immobilization after anterior cruciate ligament reconstruction surgery facilitates contracture formation via exacerbation of both myogenic and arthrogenic contractures within two weeks. Capsule shortening would be one of the main mechanisms for severe arthrogenic contracture observed in the reconstruction plus immobilization group. Periods of joint immobilization after surgery should be minimized to reduce contracture. • Joint contracture develops after anterior cruciate ligament reconstruction surgery. • Effects of immobilization duration on contractures after surgery are unknown • Two weeks of immobilization facilitated formation of joint contracture • Four weeks of immobilization further developed joint contractures • Periods of immobilization after surgery should be minimized to reduce contracture [ABSTRACT FROM AUTHOR]

[Objectives]Pseudomonas taiwanensis LH-3 was immobilized successfully lo degrade lawsone and die possible underlying mechanism was anticipated to be elucidated in this study. [MethodsjThe strain was immobilized in sodium alginate beads in which biochar(the masson pine tree trunk were pyrolyzed at 700 °C )was added lo enhance the removal efficiency. The morphological analysis of the joint immobilized beads was conducted. The degradation behavior of the immobilized bacteria was tentatively investigated along with control assays in terms of different environmental conditions. In addition, the reuse ability was comparatively investigated. Finally, the operation performance of sequencing batch reactor ( SBR) with immobilized strain was systematically evaluated. [Results] Brunner-Eimnet-Teller( BET) results showed that the specific surface area of joint immobilization beads and SA+bacteria beads were 22.26 and 4.02 m2·g-1, respectively. The adsorption-degradation performance of joint immobilization strains favored the degradation process. The joint immobilized bacteria showed better abilities than free bacteria in adapting to a wide range of temperature, pll, initial concentration of lawsone and heavy metal. Moreover, joint immobilized strains can be successfully reused for more than 9 times. In laboratory-scale SBR, the joint immobilized strain can degrade lawsone in a stable way. [Conclusions] Biochar can increase the surface area of sodium alginate beads and enhance the overall degradation efficiency of immobilized strain. Finally, the jointed immobilized beads can adopt to boarder environmental conditions and possess better application capability. [ABSTRACT FROM AUTHOR]

Objective: To compare the pathological changes in cartilage derived from rats that developed osteoarthritis either by joint immobilization or by strenuous treadmill running in order to better understand their respective pathomechanism. Method: A total of 24 male Wistar rats were randomly assigned to three groups: sedentary control (CON), immobilization (IM), and strenuous running (SR). For rats in the IM group, unilateral knee joint was immobilized in flexion. Rats in the SR group underwent treadmill running with high intensity. Eight weeks later, all animals were sacrificed. Femoral condyles were collected to take histological observation for cartilage characteristic and immunohistochemistry for collagen type II. In addition, cartilage samples were obtained to assess gene expression of aggrecan, collagen type II, biglycan, and fibromodulin by quantitative RT-PCR. Results: Gross and histological observation showed osteoarthritic changes in groups SR and IM; however, more severe cartilage degradation was revealed in the latter. Proteoglycan and collagen II content decreased in groups SR and IM in comparison to group CON, with more loss in group IM. In group SR, mRNA levels in femoral cartilage were found to be unaltered for all the molecules measured. On the contrary, these molecules were significantly downregulated in group IM. Conclusion: Differences in gross observation, histological characteristics, and gene expression of proteoglycans and collagen II suggest that both knee immobilization and strenuous running would lead to degenerative change of cartilage, but at different stages of the degenerative process. [ABSTRACT FROM PUBLISHER]

The effects of immobilization on passive muscle mechanical properties are inconsistent between studies. Here, we investigated the mechanical properties of immobilized muscle by obtaining length-force curves within and beyond the physiological muscle-tendon length in a knee-contractured rat model. Unilateral rat knee joints were immobilized using an external fixator for up to 21 days. Length-passive force relationships in the immobilized and contralateral semitendinosus muscles were determined by tensile testing. The semitendinosus muscle-tendon length at end physiologic length in vivo was approximately at 5% strain of the slack length. Dynamic, elastic, and viscous force (three aspects of muscle mechanical properties) evoked by instantaneous constant stretch were higher than contralateral side within the physiological muscle-tendon length limit (strains of 5% or 5%–7.5% slack length). When beyond muscle-tendon length corresponding to the maximum knee extension (strains of 7.5% or 10%–20% slack length), there was no difference between the two sides. Dynamic and elastic stiffness were also larger, as estimated by tangent angles of length-force curves, at strains of 5% slack length, and matched contralateral levels at strains of 7.5% slack length on day 21. There were no differences in semitendinosus muscle-tendon lengths overtime. Despite significantly reductions in knee extension range of motion, collagen content only showed slight changes and correlation was hardly detected between collagen and mechanical properties on day 21. Viscoelasticity in immobilized semitendinosus muscle increased within the physiological muscle-tendon length. Collagen content may have little effect on passive force and stiffness. • Maximum semitendinosus muscle-tendon unit length in vivo was 105% slack length. • Knee immobilization decreased knee joint extension range of motion. • Immobilization stiffened muscle within limit of muscle-tendon unit length in vivo. • Muscle stiffness matched the control beyond limit of muscle-tendon unit length. • Collagen content of semitendinosus muscle slightly increased with immobilization. [ABSTRACT FROM AUTHOR]

The purpose of this study was to examine the hypoxic and inflammatory conditions after immobilization in the joint capsule of rat knees. The unilateral knee joints of adult male rats were immobilized with an internal fixator (Im group) for 1 day, 3 days, and 1, 2, 4, 8, and 16 weeks. Sham-operated animals had holes drilled in the femur and tibia and screws inserted without a plate (control group). The number of cells and blood vessels in the capsule were histologically examined. The hypoxic condition in the capsule was histologically examined with a Hypoxyprobe™-1. The gene expressions related to the hypoxic (hypoxia inducible factor-1α, vascular endothelial growth factor, and fibroblast growth factor 2) and inflammatory conditions [interleukin-6 (IL-6), IL-1α, IL-1β, tumor necrosis factor-α, and tumor necrosis factor-β] were evaluated by quantitative reverse transcription polymerase chain reaction. The number of cells was unchanged at 1 day in the two groups; however, the number significantly increased at 3 days in the Im group. The number of blood vessels in the Im group gradually decreased. Strong immunostaining of Hypoxyprobe™-1 around the blood vessels was observed in the Im group. The gene expressions of hypoxia inducible factor-1α and fibroblast growth factor 2 were significantly higher in the Im group compared with those in the control group. The gene expressions of IL-6, IL-1α, IL-1β, and tumor necrosis factor-β were significantly higher in the Im group compared with those in the control group. These data indicated that joint immobilization induced hypoxic and inflammatory conditions in the joint capsule, which might be an initiating factor for joint contracture. [ABSTRACT FROM AUTHOR]

The study was to evaluate the effects in the immobilization range on disuse-induced atrophy. Eighteen 6-week-old male Wistar rats were divided into 3 groups: control, 1-joint immobilization, and 2-joint immobilization groups (n=6). The right hindlimb muscles (extensor digitorum longus muscles of toes and soleus muscles) were immobilized. The talocrural joint was perpendicularly immobilized in the 1-joint immobilization group, while, the knee and talocrural joints were perpendicularly immobilized in the 2-joint immobilization group. The immobilization period was 2 weeks. After 2 weeks immobilization, the muscles were removed, and wet weight was measured. The muscle samples were treated by HE or ATPase staining (pH 10.6, 4.4, and 4.2), and the number and ratio of muscular fiber types and their cross-sectional areas were determined. The immobilization in a large range tended to increase the atrophy of all muscular fibers in both muscles. The fibers were significantly atrophied, on the type IIb fibers in the extensor digitorum longus muscles of toes and types I and IIa fibers in the soleus muscles. The joint immobilization over 2 weeks caused atrophy of rat hindlimb muscles, and a large immobilization range increased disuse-induced muscle atrophy. The fiber types in the test were greatly affected by joint immobilization with a large number of muscular fibers and large cross-sectional areas. [ABSTRACT FROM AUTHOR]

To elucidate the formation process and therapeutic targets of hip flexion contracture, we developed a rat model of hip flexion contracture induced by hip mono-articular immobilization. Kirschner wires inserted into the femur and hip bone were anchored at the hip in a flexed position in the immobilization groups and unanchored in the sham groups for up to four weeks. Age-matched untreated rats were used as controls. Hip extension range of motion (RoM) was measured at three different extension moments (7.5, 15, and 22.5 N•mm) in each successive myotomy step as follows: before myotomy, after sequential myotomy of the tensor fascia lata, quadriceps muscle, iliopsoas muscle, and after myotomy of all residual muscles (the gluteus medius and adductor muscles). Histological analysis of the hip joint was also performed. After four weeks of immobilization, the RoM before myotomy at 22.5 N•mm was significantly decreased by 29° compared with controls, and this value was unaltered in the sham group. Analyses following serial myotomy suggested that the structures responsible for myogenic contracture were the tensor fascia lata, iliopsoas, gluteus medius, and adductor muscles because the RoMs were increased by these myotomies. Unexpectedly, arthrogenic contracture was not detected at moments other than at 7.5 N•mm, even after four weeks of immobilization. Histological analysis confirmed that pathological changes were not apparent in the anterior capsule of the hip joint. The present findings suggest that myogenic contracture may be an important therapeutic target for immobilization-induced hip flexion contracture. • We developed a rat model of hip joint immobilization to induce flexion contracture. • K-wires inserted into the femur and hip bone were anchored to immobilize hip joint. • Myogenic contracture increased time-dependently for up to 4 weeks. • Unexpectedly, arthrogenic contracture was hardly seen even 4 weeks of immobilization. [ABSTRACT FROM AUTHOR]

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The myotendinous junction (MTJ) is the muscle-tendon interface and constitutes an integrated mechanical unit to force transmission. Joint immobilization promotes muscle atrophy via disuse, while physical exercise can be used as an adaptative stimulus. In this study, we aimed to investigate the components of the MTJ and their adaptations and the associated elements triggered with aquatic training after joint immobilization. Forty-four male Wistar rats were divided into sedentary (SD), aquatic training (AT), immobilization (IM), and immobilization/aquatic training (IMAT) groups. The samples were processed to measure fiber area, nuclear fractal dimension, MTJ nuclear density, identification of telocytes, sarcomeres, and MTJ perimeter length. In the AT group, the maintenance of ultrastructure and elements in the MTJ region were observed; the IM group presented muscle atrophy effects with reduced MTJ perimeter; the IMAT group demonstrated that aquatic training after joint immobilization promotes benefits in the muscle fiber area and fractal dimension, in the MTJ region shows longer sarcomeres and MTJ perimeter. We identified the presence of telocytes in the MTJ region in all experimental groups. We concluded that aquatic training is an effective rehabilitation method after joint immobilization due to reduced muscle atrophy and regeneration effects on MTJ in rats. [ABSTRACT FROM AUTHOR]

Range of motion restriction following immobilization is spontaneously recovered at least in part by remobilization. However, the mechanisms underlying how muscles change with range of motion recovery are poorly understood. This study aimed to reveal morphological and biomechanical changes in the knee flexor semitendinosus muscle that contribute to knee joint contracture following the relief of immobilization. To induce flexion contracture, we immobilized rat right knees by an external fixator at a flexed position for three weeks. After removal of the fixator, the joints were allowed to move freely (remobilization) for up to 14 days. We obtained muscle length and passive stiffness of the isolated semitendinosus muscles after measuring passive knee extension range of motion. Three weeks of immobilization induced range of motion reduction, as well as changes in morphological and biomechanical properties of the semitendinosus muscle, such as reduced muscle length and increment of passive stiffness leading to myogenic contracture. Joint immobilization-induced reduction of range of motion, representing flexion contracture, was partially reduced by 14 days of remobilization. Concomitantly, both muscle length and muscle stiffness returned to levels not significantly different from those in the contralateral side during this period. These results suggest that improvement of myogenic contracture during the early phase of remobilization occurs via both morphological and biomechanical adaptations. [ABSTRACT FROM AUTHOR]

Although knee immobilization may deteriorate the mechanical parameters of the anterior cruciate ligament, such as stiffness and failure strength, it is unknown whether it induces laxity in the whole joint. We examined the effects of immobilization on anterior-posterior joint laxity and mechanical properties of the anterior cruciate ligament, as well as histological and gene expression profiles of the joint capsule in rat knee joints. Unilateral rat knees were immobilized using an external fixator. Non-immobilized contralateral knees were used as controls. After 3 weeks, anterior-posterior laxity in the whole joint (i.e., a complex of bones, ligaments, and capsule) and stiffness and failure strength in the anterior cruciate ligament were examined using a universal testing machine. Moreover, the knee joint capsule was histologically analyzed, and the expression levels of genes related to collagen turnover in the posterior joint capsule were examined. Joint immobilization slightly but significantly increased anterior-posterior laxity compared with the contralateral side. Unexpectedly, the stiffness and failure strength of the anterior cruciate ligament were not altered by immobilization. There was no correlation found between anterior cruciate ligament stiffness and anterior-posterior joint laxity. In the posterior joint capsule, thinning of the collagen fiber bundles accompanied by a decrease in COL3A1 gene expression was observed after immobilization. These results suggest that 3 weeks of joint immobilization alters the biomechanical integrity in the knee joint without altering the mechanical properties of the anterior cruciate ligament. Changes in the joint capsule may contribute to the immobilization-induced increase in anterior-posterior laxity. • Joint immobilization may deteriorate the mechanical parameters of the ligament. • However, it is unknown whether immobilization induces laxity in the whole joint. • Immobilization slightly but significantly increased anterior-posterior laxity. • The mechanical parameters of the anterior cruciate ligament were not altered. • Joint capsule may contribute to the immobilization-induced joint laxity. [ABSTRACT FROM AUTHOR]