Prevention of arthrofibrosis by monoclonal antibody against vascular endothelial growth factor: A novel use of bevacizumab in rabbits

Emami, Mohammad Jafar; Jaberi, Fereidoon Mojtahed; Azarpira, Negar; Vosoughi, Amir Reza; Tanideh, Nader

doi:10.1016/j.otsr.2012.05.020

Cited by 26 publications

(22 citation statements)

References 39 publications

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“…Michelson and Hunneyball observed the development of inflammation in the immobilized joint capsules of rabbits, and found that subsequent remobilization further aggravated the synovitis. In general, joint inflammation can lead to arthrofibrosis, which is characterized by collagen deposition in joint components and results in loss of ROM . Based on these reports, we speculate that inflammation and subsequent arthrofibrosis observed early during remobilization may be a primary mechanism responsible for the progression of arthrogenic contracture.…”

mentioning

confidence: 76%

“…Intra‐articular injection of IL‐1 receptor antagonist anakinra could improve ROM in patients with arthrofibrosis . Fibroblasts produce extracellular matrix structural proteins, including collagens, and thus fibroblast proliferation is an important process in the development of arthrofibrosis . Indeed, IL‐1β has been shown to have proliferative effects on synovial fibroblasts sampled from arthritic joints .…”

Section: Discussionmentioning

confidence: 99%

“…In this study, only few genes were examined. Other factors such as vascular endothelial growth factor and prostaglandin F 2α have also been reported to contribute to the formation of arthrofibrosis in other situations. Therefore, these factors might also contribute to remobilization‐induced arthrofibrosis.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2017

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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.

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confidence: 76%

Section: Discussionmentioning

confidence: 99%

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

et al. 2017

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“…The biologic prevention or treatment of arthrofibrosis may provide alternative therapies to improve ROM. Experimental approaches to limit the formation of fibrotic tissue in injured joints have included blocking the profibrotic activity of tissue growth factor β1 (TGF‐β1) with neutralizing antibodies or decorin, inhibiting vascular endothelial growth factor and fibroblast growth factor 2, and applying ketotifen to reduce profibrotic processes in mast cells that invade the injured joint tissues …”

mentioning

confidence: 99%

“…Experimental approaches to limit the formation of fibrotic tissue in injured joints have included blocking the profibrotic activity of tissue growth factor b1 (TGF-b1) with neutralizing antibodies or decorin, inhibiting vascular endothelial growth factor and fibroblast growth factor 2, and applying ketotifen to reduce profibrotic processes in mast cells that invade the injured joint tissues. [4][5][6][7][8][9] In this study, we tested the feasibility of limiting post-traumatic joint contracture by reducing the formation of collagen-rich deposits in the capsules of injured knee joints in rabbits. We aimed to directly interfere with the extracellular process of collagen fibril formation by blocking the critical collagencollagen interaction mediated by the C-terminal telopeptide region of collagen I molecules.…”

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confidence: 99%

Blocking collagen fibril formation in injured knees reduces flexion contracture in a rabbit model

et al. 2016

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Post-traumatic joint contracture is a frequent orthopaedic complication that limits the movement of injured joints, thereby severely impairing affected patients. Non-surgical and surgical treatments for joint contracture often fail to improve the range of motion. In this study, we tested a hypothesis that limiting the formation of collagen-rich tissue in the capsules of injured joints would reduce the consequences of the fibrotic response and improve joint mobility. We targeted the formation of collagen fibrils, the main component of fibrotic deposits formed within the tissues of injured joints, by employing a relevant rabbit model to test the utility of a custom-engineered antibody. The antibody was delivered directly to the cavities of injured knees in order to block the formation of collagen fibrils produced in response to injury. In comparison to the non-treated control, mechanical tests of the antibody-treated knees demonstrated a significant reduction of flexion contracture. Detailed microscopic and biochemical studies verified that this reduction resulted from the antibody-mediated blocking of the assembly of collagen fibrils. These findings indicate that extracellular processes associated with excessive formation of fibrotic tissue represent a valid target for limiting post-traumatic joint stiffness. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1038-1046, 2017.

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Formation process of joint contracture after anterior cruciate ligament reconstruction in rats

Kaneguchi

Ozawa

Minamimoto

et al. 2020

Journal Orthopaedic Research

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Knee joint contracture is often induced by anterior cruciate ligament reconstruction (ACLR). However, the temporal and spatial arthrofibrotic changes following inflammatory events, which occur in parallel with the formation of joint contractures after ACLR, are unknown. This study aimed to reveal: (a) time-dependent changes in myogenic and arthrogenic contractures; and (b) the process of arthrofibrosis development after ACLR. ACLR was performed on knees of rats unilaterally. Passive ranges of motions (ROMs) before and after myotomy, as well as inflammatory and fibrotic reactions, were examined before and after the surgery at various periods up to 56 days. Both ROMs before and after myotomy exhibited their lowest value on day 7 and increased thereafter in a time-dependent manner; nevertheless,

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Prevention of arthrofibrosis by monoclonal antibody against vascular endothelial growth factor: A novel use of bevacizumab in rabbits

Abstract: Level II.

Cited by 26 publications

References 39 publications

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

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

Blocking collagen fibril formation in injured knees reduces flexion contracture in a rabbit model

Formation process of joint contracture after anterior cruciate ligament reconstruction in rats

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