Collagenolytic Protease Expression in Cranial Cruciate Ligament and Stifle Synovial Fluid in Dogs with Cranial Cruciate Ligament Rupture

Muir, Peter; Danova, Nichole A.; Argyle, David; Manley, Paul A.; Hao, Zhengling

doi:10.1111/j.1532-950x.2005.00073.x

Cited by 49 publications

(60 citation statements)

References 36 publications

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“…These results relate to the histopathological findings of Vasseur et al (1985), who found degenerative changes in the intact CrCL earlier in larger breed dogs than in small breed dogs. In dogs with cruciate disease, gene expression of MMP-1, -2, -3, -9 and -13 was detected in both the CrCL and SF cells, in particular the gelatinases (MMP-2 and -9) (Muir et al, 2005a). Significant higher levels of MMP-2 and -9 have also been detected in the SF of dogs with cruciate disease (Coughlan et al, 1998;Volk et al, 2003).…”

Section: Proteolytic Tissue Degradationmentioning

confidence: 67%

“…This suggests that stromelysin is produced locally in the degenerative tissues (Spreng et al, 1999). Recently, mRNA expression of MMP was examined in CrCL cells and SF cells from cruciate deficient dogs and dogs with intact CrCLs (Muir et al, 2005a). No MMP expression was found in the CrCL and SF cells of normal young small breed dogs.…”

Section: Proteolytic Tissue Degradationmentioning

confidence: 99%

“…Dysregulation of the MMPs, their inhibitors, or both, can be a key event in shifting the MMP cascade from physiologic to pathologic conditions (Martel-Pelletier et al, 2001). There is accumulating evidence that MMPs play a prominent role in degradation of tendons, ligaments and articular cartilage in various arthropathies (Pelletier et al, 1993b;Muir et al, 2005a;MartelPelletier et al, 2001;Dalton et al, 1995). In various joint diseases, an imbalance between MMPs and their inhibitors exists, in favor of the MMPs.…”

Section: Proteolytic Tissue Degradationmentioning

confidence: 99%

“…The synovial tissue of dogs with cruciate disease also express other collagenolytic enzymes, for instance cathepsins and TRAP (Muir et al, 2002(Muir et al, , 2005a. Cathepsins are cysteine proteinases that are able to cleave the N-terminal end of the collagen triple helix, creating access for other proteolytic enzymes (Kafienah et al, 1998).…”

Section: Proteolytic Tissue Degradationmentioning

confidence: 99%

“…Moreover, the joint tissues of cruciate patients (synovial tissue, cartilage and CrCL) express many degradative enzymes including MMPs, cathepsins and tartrate-resistant acid phosphatase (TRAP) (Spreng et al, 1999;Muir et al, 2002;Muir et al, 2005a).…”

Section: Proteolytic Tissue Degradationmentioning

confidence: 99%

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Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

Doom

Bruin

Rooster

et al. 2008

Veterinary Immunology and Immunopathology

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The majority of studies on cranial cruciate ligament (CrCL) disease to date have been carried out on dogs that already sustained a CrCL rupture, which is the end-stage of the disease. Investigations have recently been carried out to study humoral and cellular immunopathological mechanisms in predisposed dogs before clinical rupture of the contralateral CrCL. The cruciate ligaments are mainly composed of collagen type I, and immune responses to collagen have been suggested as a cause of CrCL degradation in dogs. None of these investigations showed evidence that anticollagen type I antibodies alone initiate CrCL damage. However, in predisposed dogs a distinct anticollagen type I antibody gradient was found towards the contralateral stifle joint that eventually sustained a CrCL rupture, suggesting that there was an inflammatory process present in these joints before detectable joint instability occurred. The importance of cellular reactivity to collagen type I in cruciate disease also remains unclear. Peripheral blood mononuclear cell proliferation to collagen type I was very diverse in dogs with cruciate disease whereas some sham operated dogs and healthy dogs tested positive as well. It is not yet determined whether cellular reactivity to collagen type I exists locally in the stifle joints nor whether this could initiate CrCL degradation.Inflammatory processes within the stifle joint can alter the composition of the cruciate ligaments. In animal models of immunemediated synovitis, the mechanical strength of the CrCL is significantly reduced. Immunohistochemical studies on synovial tissues from dogs with rheumatoid arthritis and dogs with cruciate disease revealed that the pathologic features are similar in both joint pathologies and that the differences are mainly quantitative. Joint inflammation induced by biochemical factors such as cytokines has been implied in CrCL degeneration. In several studies, the levels of pro-inflammatory and T helper cytokines were measured in dogs that sustained a CrCL rupture, but the exact role of the various cytokines in the pathogenesis of CrCL disease remains inconclusive. More recently, the levels of the cytokines have been investigated over time in predisposed dogs before and after CrCL rupture. IL-8 expression tended to be higher in stifle joints that will rupture their CrCL during the next 6 months than in those that will not, indicating an inflammatory process in these joints before clinical rupture.

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Section: Proteolytic Tissue Degradationmentioning

confidence: 67%

Section: Proteolytic Tissue Degradationmentioning

confidence: 99%