Platelets are cells with key function in primary haemostasis. They localise coagulation to the haemostatic thrombus. After injury of the vessel wall blood contacts subendothelial matrix proteins as well as cells constitutively exposing tissue factor (TF). Platelets adhere to the subendothelial matrix, become activated, spread and secrete the contents of their granules. On the surface of the TF exposing cells minute amounts of thrombin are formed. These amounts of thrombin are inadequate to yield in a stable fibrin clot, but activate platelets and factors XI, VIII, V. In that way the consolidation pathway is triggered. Activated platelets aggregate and bind leukocytes. On the surface of the activated platelets coagulation (co)factor complexes are formed and protected in an optimal way. Thus large amounts of prothrombin are converted to thrombin, creating a so-called thrombin burst. This leads to the formation of a stable platelet-fibrin-clot. Platelets are not always prothrombotic. They have their own mechanisms to stop activation processes and thrombus growth. Besides, its key role in haemostasis platelets are involved in inflammation and innative immune defence.