How periodontal disease may contribute to cardiovascular disease.

Coronary artery disease is the major cause of premature death among men in industrialized countries, and its pathological basis is atherosclerosis. Hemostatic and rheological variables are associated with both prevalent and incident cardiovascular disease and may be mechanisms through which risk factors such as smoking, hyperlipidemia and infections (including periodontal disease) may promote vascular events. Rheological variables (which influence blood flow) are consistently associated with both prevalent and incident cardiovascular disease, possibly because they play a role in localizing atherosclerosis and thrombosis, as well as promoting ischemia. The associations of whole-blood viscosity with cardiovascular disease are partly explained by plasma viscosity and partly by hematocrit. White cell count, but not platelet count, predicts ischemic heart disease events. Cigarette smokers have higher levels of all rheological variables than nonsmokers; these increases are partly or wholly reversible in ex-smokers. Other risk factors such as blood lipids and blood pressure also influence rheological variables. Among hemostatic variables, fibrinogen, factor VIII, von Willebrand’s factor complex, tissue plasminogen activator antigen and fibrin D-dimer are associated with both prevalent and incident cardiovascular disease. These findings suggest that endothelial disturbance and increased fibrin turnover may play roles in cardiovascular disease. The association between dental infections and cardiovascular disease has been reviewed recently and will not be covered here (2). The multifactorial causation of cardiovascular disease and the many risk factors and associations attributed to this condition are shown in Fig. 1 (27). Periodontitis and atherosclerosis have many potential pathogenic mechanisms in common. Both diseases have complex causation, genetic and gender predispositions,