Analysis of Blood Clotting Factor Activities in Canine Legg-Calvé-Perthes’ Disease

Institute of Veterinary Medicine, University of Göttingen, Germany.
Journal of Veterinary Internal Medicine (Impact Factor: 1.88). 11/1999; 13(6):570-3. DOI: 10.1111/j.1939-1676.1999.tb02212.x
Source: PubMed


Legg-Calve-Perthes' (LCP) disease is a noninflammatory aseptic necrosis of the femoral head and neck in small-breed dogs. The etiology of the disease is not known, but ischemia resulting from vascular compression or occlusion has been proposed. A latent ischemic phase during development of the femoral epiphysis seems to be responsible for the onset of the typical clinical features of LCP disease. Ischemia might result from insufficient oxygen supply either caused by a reduced number of afferent arterial vessels or an occlusion of the efferent venous vessels by thrombosis. In humans, LCP disease has been linked to hypercoagulability and hypofibrinolysis caused by deficiencies of protein C, protein S, or resistance to activated protein C. To determine whether canine LCP disease is caused by similar deficiencies, we determined protein C, protein S, activated protein C, factor II, factor V, factor VIII:C, and AT III activities in plasma samples of 18 dogs with clinically and histopathologically verified LCP disease. All dogs had normal plasma activities of these factors, indicating that in these dogs LCP disease was not caused by deficiencies of the analyzed blood clotting factors.

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    • "Many factors can predispose to femoral head ischaemia and osteonecrosis. Osteonecrosis of the femoral head occurs spontaneously in hypertensive rats (Kikkawa et al., 2000), and has been associated with hypercoagulability disorders in humans, but not in dogs (Mickelson et al., 1981;Brenig et al., 1999). Steroid-induced osteonecrosis is a side-effect in up to 50% of human patients treated with long-term corticosteroids (Boss & Misselevich, 2003), a side-effect thought to be the result of changes in lipid mobilization and storage. "
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    ABSTRACT: Animal models of osteonecrosis of the femoral head are indispensable to the understanding of successful treatment modalities for avascular necrosis of the femoral head in adults and in children with Legg-Calvé-Perthes disease. Many of these models adequately reflect the current "vascular deprivation" theory regarding the etiology of the disease. In addition to spontaneous occurrence, surgical- and corticosteroid-induced models are suitable, common experimental ones. Osteonecrosis of spontaneously hypertensive rats appears to be due to defective bone formation and compression of the arteries entering the femoral head at its lateral facets by daily weight-bearing loads. Successful modeling of surgical-induced femoral capital necrosis can be a challenge in animals with a dual epiphyseal blood supply. High doses of corticosteroids are a pivotal risk factor in the development of osteonecrosis. The pathogenesis of corticosteroid-induced osteonecrosis likely resides in reduced blood flow. Steroids may reduce blood flow by numerous mechanisms, including marrow adipocytic hypertrophy leading to sinusoidal compression, venous stasis and, eventually, obstruction of the arteries, and arterial occlusion by fat emboli and lipid-loaded fibrin-platelet thrombi. Other, less common varieties of osteonecrosis include those secondary to endotoxin-induced disseminated intravascular coagulation, immune reactions, immoderately low or high temperatures, and high-impact-related injuries. Common to these diverse forms of osteonecrosis are fibrin thrombi clogging arterioles and small arteries.
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