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

Kaneguchi, Akinori; Ozawa, Junya; Kawamata, Seiichi; Yamaoka, Kaoru

doi:10.1002/jor.23419

Cited by 75 publications

(59 citation statements)

References 48 publications

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“…4,56 Excessive active exercises or stretching might even aggravate the fibrosis and subsequent motion restriction. [57][58][59] Although the surgical treatment of joint stiffness can improve joint motion, there is an urgent need for a non invasive prophylactic or first-line treatment.…”

Section: Discussionmentioning

confidence: 99%

<p>Effects of losartan and atorvastatin on the development of early posttraumatic joint stiffness in a rat model</p>

Baranowski

Schlemmer

Förster

et al. 2019

DDDT

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Background After a trauma, exuberant tissue healing with fibrosis of the joint capsule can lead to posttraumatic joint stiffness (PTJS). Losartan and atorvastatin have both shown their antifibrotic effects in different organ systems. Objective The purpose of this study was the evaluation of the influence of losartan and atorvastatin on the early development of joint contracture. In addition to joint angles, the change in myofibroblast numbers and the distribution of bone sialoprotein (BSP) were assessed. Study design and methods In this randomized and blinded experimental study with 24 rats, losartan and atorvastatin were compared to a placebo. After an initial joint injury, rat knees were immobilized with a Kirschner wire. Rats received either losartan, atorvastatin or a placebo orally daily. After 14 days, joint angle measurements and histological assessments were performed. Results Losartan increased the length of the inferior joint capsule. Joint angle and other capsule length measurements did not reveal significant differences between both drugs and the placebo. At cellular level both losartan and atorvastatin reduced the total number of myofibroblasts (losartan: 191±77, atorvastatin: 98±58, placebo: 319±113 per counting field, p <0.01) and the percentage area of myofibroblasts (losartan: 2.8±1.8% [ p <0.05], atorvastatin: 2.5±1.7% [ p <0.01], vs control [6.4±4%], respectively). BSP was detectable in equivalent amounts in the joint capsules of all groups with only a trend toward a reduction of the BSP-stained area by atorvastatin. Conclusion Both atorvastatin and losartan reduced the number of myofibroblasts in the posterior knee joint capsule of rat knees 2 weeks after trauma and losartan increased the length of the inferior joint capsule. However, these changes at the cellular level did not translate an increase in range of motion of the rats´ knee joints during early contracture development.

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Section: Discussionmentioning

confidence: 99%

<p>Effects of losartan and atorvastatin on the development of early posttraumatic joint stiffness in a rat model</p>

Baranowski

Schlemmer

Förster

et al. 2019

DDDT

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“…Joint contracture is characterized by loss of passive range of motion (ROM) and restriction of the activities of daily living, and is an important clinical problem in orthopedics and rehabilitation medicine. The most common cause of joint contracture is immobilization, which is a common orthopedic treatment for patients with severe traumatic injuries of the joints or other musculoskeletal disorders . In addition, several studies demonstrated that patients with conditions limiting their mobility are at a high risk for joint contracture .…”

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confidence: 99%

Effects of joint immobilization on changes in myofibroblasts and collagen in the rat knee contracture model

et al. 2017

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The purpose of this study was to examine the time-dependent changes in the development of joint capsule fibrosis and in the number of myofibroblasts in the joint capsule after immobilization, using a rat knee contracture model. Both knee joints were fixed in full flexion for 1, 2, and 4 weeks (immobilization group). Untreated rats were bred for each immobilization period (control group). Histological analysis was performed to evaluate changes in the amount and density of collagen in the joint capsule. The changes in type I and III collagen mRNA were examined by in situ hybridization. The number of myofibroblasts in the joint capsule was assessed by immunohistochemical methods. In the immobilization group, the amount of collagen increased within 1 week and the density of collagen increased within 2 weeks, as compared with that in the control group. Type I collagen mRNA-positive cell numbers in the immobilization group increased at all time points. However, type III collagen mRNA-positive cell numbers did not increase. Myofibroblasts in the immobilization group significantly increased compared with those in the control group at all time points, and they increased significantly with the period of immobilization. These results suggest that joint capsule fibrosis with overexpression of type I collagen occurs and progresses within 1 week after immobilization, and an increase in myofibroblasts is related to the mechanism of joint capsule fibrosis. The findings suggest the need for a treatment targeting accumulation of type I collagen associated with an increase in myofibroblasts. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1998-2006, 2017.

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“…To clarify the fibrotic changes in the posterior joint capsules, we evaluated collagen density using the method described in our previous study. 4 In AFMG-stained sections, the posterior joint capsule was photographed just behind the meniscus at 20Â magnification with a light microscope (BX-51; Olympus, Tokyo, Japan) and a digital camera (DS-Fi1, Nikon, Tokyo, Japan) and analyzed with ImageJ software. Using the Split Channels function, the green areas, which represented collagen, were isolated from the original color image.…”

Section: Quantification Of Collagen Density In Joint Capsulementioning

confidence: 99%

“…Joint contracture, defined as a limitation in active and passive range of motion (ROM) on the affected joints, is a common complication of various nonphysiological conditions in joints of orthopedic patients, including neurological disorders, 1,2 prolonged immobilization, [3][4][5] and inflammation. [6][7][8] Restriction of ROM limits the performance of stable and functional movements and restricts activities of daily living in affected patients.…”

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confidence: 99%

Accumulation of advanced‐glycation end products (AGEs) accelerates arthrogenic joint contracture in immobilized rat knee

Ozawa

Kaneguchi

Minamimoto

et al. 2017

Journal Orthopaedic Research

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Joint mobility decreases in the elderly and in diabetics, this process is thought to be caused by accumulation of advanced-glycation end products (AGEs). Here, we aimed to elucidate the role of AGEs in joint contracture formation in rat knees. Rats were injected with ribose or saline into the knees twice weekly for 8 weeks. Pentosidine (AGE) levels were measured in the knee-joint tissues. After serial injections, rats were subjected to unilateral knee-joint immobilization in a flexion position for various periods. At day 21, the passive knee ranges of motions (ROMs) were measured. Knee joint histopathology were assessed, and the expression of fibrotic genes in the posterior joint capsules was examined using real-time PCR. Ribose injection induced a 7.0-fold increase in pentosidine levels relative to saline injection. Joint immobilization resulted in equal myogenic ROM restriction in both groups. Arthrogenic ROM restriction was greater with ribose injection in the immobilized joints (p < 0.05), but was not affected in nonimmobilized joints. Type-I (COL1A1) and type-III (COL3A1) collagen gene expression increased significantly in immobilized joints relative to nonimmobilized joints in the ribose group, but was not affected in the saline group. Ribose injection increased COL1A1 expression slightly and COL3A1 expression significantly in immobilized joints. Histologically, inflammatory changes appeared at day 3 of immobilization and peaked at day 7. These responses trended to be more severe and prolonged in the ribose group than in the saline group. Our data provide evidence for a causal relationship between AGEs and joint contracture formation following immobilization. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:854-863, 2018.

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

Cited by 75 publications

References 48 publications

<p>Effects of losartan and atorvastatin on the development of early posttraumatic joint stiffness in a rat model</p>

<p>Effects of losartan and atorvastatin on the development of early posttraumatic joint stiffness in a rat model</p>

Effects of joint immobilization on changes in myofibroblasts and collagen in the rat knee contracture model

Accumulation of advanced‐glycation end products (AGEs) accelerates arthrogenic joint contracture in immobilized rat knee

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