Our current concept of the etiology of atherosclerosis is that it is a chronic inflammatory process. In support of this model serum markers of inflammation, such as high levels of C-reactive protein and fibrinogen, have been observed in numerous studies to be sensitive predictors of future cardiovascular adverse events. These markers are a group of serum proteins that are termed “acute phase reactants.” Their serum levels increase in the presence of any inflammatory process, the most common of which are infections. And indeed it has been suggested that atherosclerosis may be due to a focus of infection, such as periodontal disease. The infection then presumably spreads to the vascular tissues to initiate a local inflammatory process. Against this model it has been found in clinical trials that antibiotics do not prevent adverse vascular events. Furthermore, agents, such as statins, which have no antibacterial activity, have been shown in innumerable studies to be highly effective in the reduction of number of vascular events occuring in a vulnerable population. The apparent association between periodontal and vascular disease may be due to the fact that both conditions are much more common in smokers.