Immunohistochemical characterization of inflammatory cell populations and adhesion molecule expression in synovial membranes from dogs with spontaneous cranial cruciate ligament rupture

Lemburg, A.K.; Meyer‐Lindenberg, Andrea; Hewicker‐Trautwein, M.

doi:10.1016/j.vetimm.2003.09.007

Cited by 60 publications

(62 citation statements)

References 20 publications

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“…Histological studies on synovial tissue from stifle joints of dogs with cruciate disease also support the belief that anticollagen antibodies are produced locally within the synovial tissue (Hewicker et al, 1999;Tirgari, 1977;Galloway and Lester, 1995;Lawrence et al, 1998). The main cell types detected in the synovial tissue are macrophages, T-lymphocytes, B-lymphocytes and plasma cells belonging predominantly to the IgG isotype (Hewicker et al, 1999;Tirgari, 1977;Galloway and Lester, 1995;Lawrence et al, 1998;Lemburg et al, 2004). A significant higher amount of IgG and IgM has been detected in the synovial tissue of stifle joints of dogs with cruciate disease compared to normal stifle joints (Lawrence et al, 1998).…”

Section: Humoral Immunity In Cruciate Diseasementioning

confidence: 79%

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: Humoral Immunity In Cruciate Diseasementioning

confidence: 79%

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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“…T cells and dendritic cells are major components of the inflammatory response. 38 While no causal relationship necessarily exists between synovial inflammation and the development of HS, there is ample evidence of progression of inflammation to neoplasia in many inflammatory disease states. 17 The immunophenotype of histiocytes in articular HS is identical to that of perivascular interstitial DCs (CD1aþ CD11c/CD18þ) rather than synovial type A cells (CD1a-CD11b/CD18þ), which are intercalated between synovial-type B cells (synovial fibroblasts) in the synovial lining.…”

Section: Distinctive Histiocytic Sarcoma Syndromesmentioning

confidence: 99%

A Review of Histiocytic Diseases of Dogs and Cats

2014

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Histiocytic proliferative disorders are commonly observed in dogs and less often cats. Histiocytic disorders occur in most of the dendritic cell (DC) lineages. Canine cutaneous histiocytoma originates from Langerhans cells (LCs) indicated by expression of CD1a, CD11c/CD18, and E-cadherin. When histiocytomas occur as multiple lesions in skin with optional metastasis to lymph nodes and internal organs, the disease resembles cutaneous Langerhans cell histiocytosis of humans. Langerhans cell disorders do not occur in feline skin. Feline pulmonary LCH has been recognized as a cause of respiratory failure due to diffuse pulmonary infiltration by histiocytes, which express CD18 and E-cadherin and contain Birbeck's granules. In dogs and cats, histiocytic sarcomas (HS) arise from interstitial DCs that occur in most tissues of the body. Histiocytic sarcomas begin as localized lesions, which rapidly disseminate to many organs. Primary sites include spleen, lung, skin, brain (meninges), lymph node, bone marrow, and synovial tissues of limbs. An indolent form of localized HS, progressive histiocytosis, originates in the skin of cats. Hemophagocytic HS originates in splenic red pulp and bone marrow macrophages in dogs and cats. In dogs, histiocytes in hemophagocytic HS express CD11d/CD18, which is a leuko-integrin highly expressed by macrophages in splenic red pulp and bone marrow. Canine reactive histiocytic diseases, systemic histiocytosis (SH) and cutaneous histiocytosis, are complex inflammatory diseases with underlying immune dysregulation. The lesions are dominated by activated interstitial DCs and lymphocytes, which invade vessel walls and extend as vasocentric infiltrates in skin, lymph nodes, and internal organs (SH).

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“…In cases with lymphoma, immunohistochemistry was performed with antibodies against human CD3 and human CD79a molecule as described elsewhere. 7 For cases with LPE or enterocolitis, a histologic grading system was used. 4 Biopsy samples of control dogs showed a regular histologic architecture as described elsewhere.…”

mentioning

confidence: 99%

Retrospective Study on the Diagnostic Value of Full-Thickness Biopsies from the Stomach and Intestines of Dogs with Chronic Gastrointestinal Disease Symptoms

Kleinschmidt¹,

Meneses²,

Nolte³

et al. 2006

Vet Pathol

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Abstract. An evaluation of histologic findings in full-thickness biopsies from the gastrointestinal tract (GIT) from 64 dogs with chronic GIT disease symptoms was performed. In the majority of cases (38/64; 59%), intestinal lymphangiectasia and mucosal edema of unknown etiology were present. In 10 dogs (16%) an eosinophilic colitis, either alone or together with gastritis and/or enteritis, was found. In 5 dogs (8%) lymphocytic-plasmacytic enteritis or enterocolitis was diagnosed. Five dogs (8%) had an intestinal T-cell lymphoma. Samples from the remaining cases were histologically normal or did not allow for a final diagnosis. In contrast to reports about findings in endoscopic biopsies (which often are of varying quality or inadequate for diagnosis), in the majority of cases of this study, examination of fullthickness biopsies from the GIT allowed us to make a definitive histopathologic diagnosis. Furthermore, the study revealed that transmural biopsies are very helpful for diagnosing lymphoma.

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Immunohistochemical characterization of inflammatory cell populations and adhesion molecule expression in synovial membranes from dogs with spontaneous cranial cruciate ligament rupture

Cited by 60 publications

References 20 publications

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

A Review of Histiocytic Diseases of Dogs and Cats

Retrospective Study on the Diagnostic Value of Full-Thickness Biopsies from the Stomach and Intestines of Dogs with Chronic Gastrointestinal Disease Symptoms

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