Authors investigated the possible role of intravascular hypercoagulable states on the etiology of Kegg-Clave-Perthes diesease. Forty-five patients with Legg-Clave-Perthes disease(31 avascular stages and 14 reossification stages) and twenty-two normal control patients were subjected to study for evaluation of coagulation and fibrinolysis system by means of the tests which included antiphospholipid antibody(APA), Protein C, Protein S and antithrombin- III (AT- III) for evaluation of coagulation system, and tissue type PIasminogen activator(tPA), Plasminogen activator inhibitor(PAI), D-dimer for fibrinolytic system. APA increased significantly in Legg-Clave-Perthes patients(p=0.016) as compared with control group, while Protein C(p=0.040) and Protein S(P=0.0001) decreased significantly in Legg-Clave- Perthes disease. AT- III increased in Legg-Clave-Perthes disease(p=0.0000). In contrast, there were no statistically significant differences in PAI, tPA, D-dimer between the Legg-Clave-Perthes disease and control group. There were no differences in all parameters between the avascular stage and reossification stage in patients with Legg-Clave-Perthes disease, Suggestive of possible inherent effect in coagulation system(hypercoagulable states) which does not change with time. Based on the above findings authors presumed that hypercoagulable state may contribute to the development of Legg-Calve-Perthes disease. However, to elucidate the etiology of Legg-Calve-Perthes disease, further extensive investigation should be followed, which include the familial tendency of hypercoagulable state, relationship with other multifactorial causes such as alcohol and steroids, and confirmation of intravascular thrombosis or decreased blood perfusion in the femoral head. Also, the significance of abnormally elevated AT-III on the disease should be answered.