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).