Platelets contribute to the maintenance of the normal circulation of blood through the vasculature by taking care of the integrity of the vessel wall. They continuously ‘examine’ the inner lining of the vessel wall for leakage without adhering to the intact endothelial cell lining. They respond immediately, however, when the endothelium is injured and they rapidly adhere to the exposed subendothelial structures. After the adherence of a first layer of platelets a series of complicated reactions are initiated that finally result in the formation of a platelet plug stabilized by an insoluble fibrin network. This so-formed hemostatic plug prevents further loss of blood. Platelets, however, cannot distinguish between a dissected vessel wall, which results in bleeding wounds, and superficial lesions of the endothelium occurring in atherosclerosis. Adhesion of platelets to these superficial lesions may be the onset of the formation of a plug in an intact vessel, a mural thrombus that occludes a blood vessel and prevents the supply of blood to a vital organ, resulting in a serious pathological condition, such as heart attack and stroke.

Platelet adhesion is the first step in the hemostatic response and knowledge of the mechanisms of platelet adhesion is an important lead to the development of selective antithrombotic drugs. The adhesive proteins responsible for optimal platelet adhesion are different from adhesive proteins involved in the adhesion of other cells. Platelet adhesion has several unique features.