Both Crohn's disease (CD) and ulcerative colitis (UC) are associated with abnormalities of platelet number and function. In the peripheral circulation the state of platelet activation is typically increased, and inflammatory bowel disease (IBD)-involved mucosa frequently contains platelet aggregates within mucosal microthrombi. The relevance of platelet dysfunction to IBD pathogenesis is still unclear, but there is solid evidence demonstrating that platelets, in addition to their traditional role in hemostasis, can also function as potent proinflammatory cells. Upon activation, platelets secrete a large number of biologically active molecules able to induce or amplify an inflammatory process through many of the same cellular and molecular pathways conventionally utilized by immune cells mediating IBD. The aim of this article is to review data on the existence of platelet dysfunction in IBD, substantiate platelets' inflammatory potential, discuss the implications of abnormal platelet activity for chronic intestinal inflammation, and consider the potential benefits of platelet modulation for treatment of IBD.