Could periodontal disease be killing your patients? This seems, taken literally, an absurd statement. However evidence has been mounting that points to a link between chronic periodontal disease and an increased risk for coronary artery disease as well as stroke. And the risk level is not so small that it can be considered inconsequential. While smoking, hypertension, excessive lipids in the bloodstream and diabetes remain major determinants of risk for cardiovascular incidents, periodontal disease may rank above stress, sedentary lifestyle and obesity as a contributor to heart disease. During the past ten years at least 12 papers have appeared in the worldwide literature relating periodontal disease to heart disease. Some indicate periodontal disease to nearly double the risk of a coronary incident in those with other major risk factors. Since the major risk factors account for only 50% to 60% of the incidence of cardiovascular disease chronic periodontal infection may be a source of frequent bacterial challenge to heart and brain vessel walls, accelerating the disease process. Your patients with periodontal disease should be made aware of the interactions between periodontal disease, heart disease and stroke.They may have several questions regarding the relationship between periodontal disease and heart disease and the steps which should be taken tor educe their risk. This newsletter provides youwith the latest background inforrnation on the development of vascular disease and the influence periodontal disease may have on its progression.

When the endothelial layer becomes injured, the damaged endothelial cells develop wider inter-endothelial spaces. Injury can occur from smoking (reduced oxygen carrying by red blood cells produces endothelial cell hypoxia), hypertension (increased blood pressure on endothelial cells) and hyperlipidemia (primary mechanism related to lipid release into endothelial cells by lowdensity lipoproteins [LDL] circulating in bloodstream). These are identified primary factors. But bacteremias from chronic periodontal disease may serve as repeated sources of infection to the endothelium which has been conditioned by prior trauma. Dom and Progulske-Fox have demonstrated that two periodontal pathogens, P. Gingivalis and P. Intermedia, do invade endothelium in a laboratory setting. In addition, Herzberg and Meyer found the otherwise innocuous bacteria Streptococcus Sanguis to induce the aggregation of platelets. When introduced in experimental animals with hyperlipidemia the resulting red blood cell aggregations triggered signs of myocardial infarction.

The chronic nature of periodontal infection makes it a particularly significant factor in the process of plaque formation. In moderate periodontal disease with pockets of 4-5mm depth throughout the mouth the surface area of infection in the pockets added together would be equivalent to creating an ulcer the size of your palm with fingers extended on the side of your face. When this condition exists bacteremias occur over 40% of the times the teeth are brushed. It is the repeated introduction to the bloodstream of these bacteria which may increase periodontitis as a risk factor for myocardial infarction or stroke.

Repetitive challenges to the vascular endothelium from the periodontal bacteremias initiate the inflammatory cycle in the vascular endothelium already involved with plaque formation. Observations of myocardial infarction cases indicate that rupture of the atherosclerotic plaque (the fibrous plaque mentioned earlier) with superimposed thrombosis is the primary mechanism in myocardial infarction rather than a progressive, gradual enlargement of the fibrous plaque. The repetitive challenge produced by oral bacteremias may cause the production of more foam cells (in the presence of too many circulating low density lipoproteins [LDL]) and, at the same time, inhibit collagen synthesis increasing the likelihood of rupture of the fibrous plaque. As noted earlier some oral pathogens also cause alterations in the inflammatory process resulting in more sticking of platelet cells to the damaged endothelium.

Just as we attempt to treat hyperlipidemia to reduce the risk of atherlerosclerotic heart disease periodontal bacteremias need to be reduced in the coronary high risk patient. Patients who have high blood pressure, hyperlipidemia, diabetes or smoke are at greater risk for myocardial infarction and stroke when periodontal pockets are of moderate depth. In these cases good oral hygiene, pocket reduction and short interval maintenance may be the best method of reducing periodontal risk factors. In several of the studies the impact of periodontitis as a risk factor was greatest in males under 50. Since many of the studies were on male populations the impact on females may be similar but less well documented.

Our office welcomes the opportunity to assist you in assessing the periodontal status of those patients at risk for significant cardiac disease. Your patients who smoke, have high cholesterol, hypertension or diabetes should be closely scrutinized for periodontal disease and aggressively treated. Together we can improve not only the dental health status of patients but their overall health as well.