It is becoming increasingly clear that infections and chronic inflammatory conditions, such as periodontitis can be linked with atherosclerotic process. Periodontitis and atherosclerosis have many pathogenetic mechanisms in common. The objective of this based on current knowledge review is to present the putative mechanisms whereby periodontitis which is chronic and inflammatory in nature and initiated by microbial plaque can influence the atherosclerosis. Two main processes in particular are worthy of consideration and may provide the link between these two diseases. Induction of the chronic systemic inflammation has been proposed to be of pathogenetic relevance in the association of infection and atherosclerosis, and may rely in part on the endothelial toxicity of bacterial endotoxin and the action of proinflammatory cytokines (PGE-2, IL-1beta, TNF-alpha). Another well-founded proatherogenetic property of infectious illness may be the induction of autoimmunity and autoagression. It has been suggested that humoral immune cross-reaction of the same antibodies to heat shock proteins (HSP), both bacterial mHSP65 and human endothelial HSP60 may play an important role in the process of vascular endothelial injury. Both of these mechanisms are believed to be a key event in the pathogenesis of artheriosclerosis.