The precise pathogenetic basis of Legg-Calve-Perthes disease (LCPD) is currently unknown. Hemostatic abnormalities, i.e., hypercoagulability and/or hypofibrinolysis, were proposed in the genesis of the LCPD. Deficiency of tissue factor pathway inhibitor (TFPI), a critical natural anticoagulant. molecule, may lead to a prothrombotic state in a wide variety of conditions. The aim of this study is to assess the circulating TFPI pool in the LCPD. Group I consisted of 44 patients with LCPD and group H comprised 38 healthy children. Median (IQR) TPFI concentration was significantly higher in the group I (p<.0001). Enhanced TFPI response could be regarded as a compensatory defense mechanism against ongoing local microvascular events of occlusion, and revascularization of LCPD. 7741 molecule may be an important link between the crossroads of the LCPD genesis and pathogenetic microvascular changes in the disease course. further investigations are needed to shed light on the endothelial anticoagulant kinetics, the unique microvascular compromise, and the self-limiting nature of the disease.