Evaluation of anticollagen type I antibody titers in synovial fluid of both stifle joints and the left shoulder joint of dogs with unilateral cranial cruciate disease

Bruin, Tanya de; Rooster, H. de; Bree, Henri van; Cox, Eric

doi:10.2460/ajvr.68.3.283

Cited by 24 publications

(21 citation statements)

References 30 publications

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“…In spite of these limitations, antibody titers were higher in dogs with partial compared with complete tears of the CCL, which may reflect continued antigenic stimulation and release of collagen type I from damaged ligament into the articular space. Titers tended to increase in contralateral stifles that became CCL deficient during the study 86 . Expression of IL‐8 also tended to increase in these joints, further supporting the concept of an inflammatory process preceding the clinical stage of CCLD in dogs 87 .…”

Section: Arthritissupporting

confidence: 55%

A Review of the Pathogenesis of Canine Cranial Cruciate Ligament Disease as a Basis for Future Preventive Strategies

Griffon

2010

Veterinary Surgery

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Cranial cruciate ligament (CCL) deficiency is the leading cause of lameness of the canine stifle and has important consequences in terms of morbidity and cost associated with its management. In spite of this impact, development of preventive strategies remains in its infancy, largely because of gaps in our understanding of the complex and likely multifactorial origin of CCL deficiency. The purpose of this article is to provide a critical review of the literature related to the pathogenesis of CCL deficiency and place this evidence in the context of potential preventive measures. Trauma accounts for a minority of CCL ruptures in dogs, whereas progressive degeneration of the ligament has been attributed to a variety of factors that may be broadly classified as genetic, conformational, environmental, immune-mediated, and inflammatory. Genetic screening appears promising as a long-term option in selected breeds while immunomodulating therapies may be implemented in the nearer future to reduce the incidence of contralateral disease in dogs with unilateral CCL deficiency. Preventive modification of conformation factors may be applicable to most breeds predisposed to CCL deficiency but requires further investigations into the relative contribution of individual factors, as well as into the feasibility, and potential risks of large-scale implementation.

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Section: Arthritissupporting

confidence: 55%

A Review of the Pathogenesis of Canine Cranial Cruciate Ligament Disease as a Basis for Future Preventive Strategies

Griffon

2010

Veterinary Surgery

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“…In predisposed dogs, higher anticollagen type I titers were found in the stifle joints that eventually sustained a CrCL rupture, compared to the titers in a remote joint. This finding suggests that there was an inflammatory process with production of collagen-specific antibodies, present in these joints before detectable joint instability occurred (de Bruin et al, 2007a). Antigens can also maintain joint inflammation by forming immune complexes with antibodies.…”

Section: Humoral Immunity In Cruciate Diseasementioning

confidence: 85%

“…Anticollagen type I and II antibodies have also been detected in the SF of stifle joints with OA secondary to arthropathies other than CrCL rupture, suggesting that these antibodies are not specific for the type of joint disorder (de Rooster et al, 2000). A prospective study in which anticollagen type I antibodies have been measured sequentially over a 12-18 months period in the SF of dogs initially presented with unilateral CrCL rupture, could not provide evidence that anticollagen antibodies initiated CrCL damage in dogs, since not all dogs with high antibodies developed a contralateral CrCL rupture (de Bruin et al, 2007a). Nevertheless, it is possible that anticollagen antibodies perpetuate chronic joint inflammation in some dogs with cruciate deterioration, even if collagen is not the primary arthritogenic agent.…”

Section: Humoral Immunity In Cruciate Diseasementioning

confidence: 99%

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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“…CCL deficiency in dogs typically develops during normal daily activities with a chronic history of progressive lameness consistent with degenerative joint disease 7,8 . In a recent study of the inheritance of CCL deficiency in Newfoundland dogs, only 27% of the phenotypic expression of CCL deficiency was attributed to genetics, while 73% was linked to environmental factors 9 .…”

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confidence: 99%

Morphometric Characteristics of the Pelvic Limb Musculature of Labrador Retrievers with and without Cranial Cruciate Ligament Deficiency

et al. 2010

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Evaluation of anticollagen type I antibody titers in synovial fluid of both stifle joints and the left shoulder joint of dogs with unilateral cranial cruciate disease

Cited by 24 publications

References 30 publications

A Review of the Pathogenesis of Canine Cranial Cruciate Ligament Disease as a Basis for Future Preventive Strategies

A Review of the Pathogenesis of Canine Cranial Cruciate Ligament Disease as a Basis for Future Preventive Strategies

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

Morphometric Characteristics of the Pelvic Limb Musculature of Labrador Retrievers with and without Cranial Cruciate Ligament Deficiency

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