Optimizing interactions between biomaterials and blood

A cascade of biological events can be initiated at the blood-material interface leading to thrombosis and intimal hyperplasia. Thrombus formation can be initiated intrinsically by surface interactions with adsorbed proteins or extrinsically by clotting factors derived from damaged tissue. The interaction between clotting factors and platelet surface receptors leads to platelet activation. The cleavage of prothrombin via prothrombinase formation in which those two pathways converged into one common pathway generates thrombin. The common pathway converts fibrinogen to fibrin that forms a hemostatic clot. The intrinsic pathway also known as contact-clotting pathway, is considered as a more critical pathway in biomaterial-associated blood coagulation (Figure 3).