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Biomaterials. 2004 Nov;25(26):5681-703.

Biomaterial-associated thrombosis: roles of coagulation factors, complement, platelets and leukocytes.

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  • 1Department of Chemical Engineering and Applied Chemistry, Institute of Biomaterials and Biomedical Engineering, University of Toronto, 4 Taddle Creek Road, Room 407D, Toronto, Ont., Canada M5S 3G9.


Our failure to produce truly non-thrombogenic materials may reflect a failure to fully understand the mechanisms of biomaterial-associated thrombosis. The community has focused on minimizing coagulation or minimizing platelet adhesion and activation. We have infrequently considered the interactions between the two although we are generally familiar with these interactions. However, we have rarely considered in the context of biomaterial-associated thrombosis the other major players in blood: complement and leukocytes. Biomaterials are known agonists of complement and leukocyte activation, but this is frequently studied only in the context of inflammation. For us, thrombosis is a special case of inflammation. Here we summarize current perspectives on all four of these components in thrombosis and with biomaterials and cardiovascular devices. We also briefly highlight a few features of biomaterial-associated thrombosis that are not often considered in the biomaterials literature: The importance of tissue factor and the extrinsic coagulation system. Complement activation as a prelude to platelet activation and its role in thrombosis. The role of leukocytes in thrombin formation. The differing time scales of these contributions.

[PubMed - indexed for MEDLINE]
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