In recent years, the concepts of the pathogenesis of atherosclerosis and cardiovascular events have broadened from a lipid-centric view of etiology to the appreciation of the importance of the inflammatory processes. Although obesity, oxidized lipids, and other factors are known to contribute to cardiovascular inflammation, the role of infection is believed to serve as a critical inflammatory stimulus that contributes to both atherogenesis and acute events via plaque destabilization. This inflammatory process can involve the vasculature directly by interaction of the organisms or bacterial by-products with the vessel wall or indirectly via modulation of hemostasis or hepatic activation of the acute phase response that leads to increased circulating levels of acute-phase reactants such as C-reactive protein (CRP). Epidemiological studies have suggested a significant moderate association between periodontal infection and cardiovascular risk adjusting for traditional risk factors. The potential role of periodontal disease as a possible chronic source of infection and inflammation is supported by findings indicating an association of periodontal disease with elevated serum CRP and interleukin 6. Recently, periodontal therapy studies have shown a lowering of CRP and interleukin 6, and in this issue, a new report of an improvement of endothelial function, as measured by flow-mediated dilation. These studies raise the possibility that periodontal disease may represent a modifiable risk factor that merits further study.