Early evidence has already shown that activated platelets play a role in the intrinsic pathway of coagulation, but the mechanism remained unclear. The finding that the dense granules of platelets contain polyphosphate (polyP), which has procoagulant effects, resolved this missing link between activated platelets and coagulation. PolyP secreted from platelets leads via activation of Factor XII to in vivo thrombin and fibrin formation. The relative importance of polyP in the process and stages of thrombus formation will require further investigation. In addition to its role in coagulation, polyP-induced Factor XII activation mediates the release of the inflammatory mediator bradykinin by activating the kallikrein-kinin system. This results in vascular leakage and edema formation in vivo. Together, polyP release from platelets has a physiological role in the thrombus-forming process, as well as in inflammatory reactions.