Periodontal Diseases' Contributions to Cardiovascular Disease: An Overview of Potential Mechanisms

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Abstract
Periodontitis and atherosclerosis have complex etiologies, genetic and gender predispositions, and potentially share many risk factors—the most significant of which may be smoking status. These diseases also have many pathogenic mechanisms in common. It is becoming increasingly clear that infections and chronic inflammatory conditions such as periodontitis may influence the atherosclerotic process. The severity and chronicity of periodontal disease provides a rich source of subgingival microbial and host response products and effects over a long time period. The objective of this review is to consider the mechanisms whereby diseases such as periodontitis, which is chronic and inflammatory in nature and initiated by microbial plaque, can predispose to atherosclerosis. In common with periodontal disease, the pathogenesis of atherosclerosis is not completely understood and both diseases are currently under intensive investigation. Two main processes in particular are worthy of consideration and may provide the link between these 2 diseases, namely the lipopolysaccharide‐related responses and the hyperresponsive monocyte phenomenon. Insufficient experimental evidence exists, however, to further support these hypotheses at present and clearly more research is needed on both of these processes and the interrelationships between both diseases. Ann Periodontol 1998;3:142–150.