Editorial

Periodontal diseases are characterized by gingival inflammation, loss of bone support, and ultimate loss of the tooth, the underlying cause being the presence of bacterial plaque. Recent epidemiological studies indicate a correlation between infection, inflammation and cardiovascular disease. In 1998, the Research, Science and Therapy Committee of the American Academy of Periodontology presented a position paper in which it stated that patients with periodontitis have a potentially higher risk for systemic diseases such as infective endocarditis, cardiovascular diseases, atherosclerosis, and diabetes mellitus compared to periodontally healthy people, and that the risk increases with age. The background is bacterial metastatic infection (bacteremia) arising from inflamed periodontal tissues, circulating microbiological toxins and immunologically induced serum antibodies, cytokines, interleukines, and prostaglandins. Deepened periodontal pockets are known to act as a reservoir of different bacteria.

Known risk factors for cardiovascular and coronary heart diseases are smoking, cholesterol/APO-B, obesity, mental stress, acute exercise, cold exposure and increased plasma homocysteine. However, infection may also activate cytokine release, such as interleukins (IL-1, IL-6), and tumor necrosis factor-alpha (TNF-a) from monocytes, lymphocytes, endothelial cells, etc.  These might cause expression of adhesion molecules, which have been found in atherosclerotic lesions. Acute and chronic inflammatory reactions may cause release of leukocytes and platelets into the blood. Increased leukocyte count may promote atherosclerosis and thrombosis, being significant predictors of coronary heart disease. Release of C-reactive protein, serum amyloid A, fibrogen, as well as fibrin degrading products, such as fibrin D dimmer, are other important factors.

Available epidemiological studies identify some association between periodontal disease and cardiovascular disease, yet urge caution in interpreting results, indicating instead a need for further investigations which may in more predictable way demonstrate the association between the two diseases. One approach may be that traditional clinical measures of pocket depth and attachment level loss must be changed to instruments more linked to, and thus more reliable indicators of, infection and host response. There might be a need for intervention studies focusing on treatment of periodontal disease. However, while seeking greater clarification of the connection, we should not overlook the possibility that one indeed exists. Thus, if periodontitis can contribute to systemic diseases, oral hygiene should be stressed as strongly as is a low fat diet, exercise and cessation of smoking. In the Annals of Periodontology, Beck and Offenbacher (2001) stated that "it is time to enter the next phase of investigation by testing new hypotheses in molecular epidemiology studies that are appropriately designed to address periodontal disease, represented by the triad of clinical status, infectious burden, and host response, as an exposure for systemic pathology." In this way, it will be possible to verify or disprove whether periodontitis can cause cardiovascular disease

Axel Bergenholtz, DDS, Odont. Dr

Faculty of Odontology, Umeå University, Umeå,

Sweden.