Venous thrombosis is associated with a significant inflammatory response. Inflammatory cells, adhesion molecules (especially selectins), cytokines, and procoagulant microparticles appear to be associated with the thrombogenic process. Once thrombus forms, inflammatory cells are important to thrombus resolution along with fibrinolytic agents and proinflammatory mediators. Collagen and elastin breakdown by the DVT renders the vein wall stiff and non-compliant. Rapid and complete thrombus resolution should lessen vein wall damage and lessen or prevent the development of chronic venous insufficiency. Understanding the basic biology of thrombogenesis and thrombus resolution is important, as novel therapies to both prevent and treat venous thrombosis and hasten thrombus resolution should result from a better understanding of the basic biological mechanisms.