Blood-induced joint damage: interaction between coagulation and inflammation

Abstract

Hemophilia is a hereditary coagulation disorder caused by a deficiency of either blood coagulation factor VIII (FVIII) in hemophilia A, or blood coagulation factor IX (FIX) in hemophilia B. Affected hemophilia individuals have a life-long bleeding tendency with a variable phenotype of spontaneous hemorrhages, easy bruising, and prolonged bleeding following trauma. Repeated joint bleedings results in blood-induced joint damage and ultimately in hemophilic arthropathy. The aim of this thesis is to gain more insight in the pathophysiology of blood-induced joint damage and to establish new therapeutic modalities for the treatment of bloodinduced arthropathy. Several human in vitro and ex vivo studies involving patients with hemophilia, as well as animal in vivo studies have been performed in light of this aim.