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Periodontal and Cardiovascular Disease

What is the connection between cardiovascular disease (heart attack, stroke) and periodontal disease?

Research has found that people with periodontal disease are almost twice as likely to suffer from coronary artery disease than those without periodontal disease. Studies focused on stroke appear to demonstrate even a stronger relationship with periodontal disease.

Mild forms of periodontal disease affect 75 percent of adults in the United States, and more severe forms affect 20 to 30 percent of adults. (1)

Traditional factors such as obesity, hyperlipidemia, diabetes, hypertension, and cigarette smoking account for only 50 to 60 percent of cases of cardiovascular disease.

The association between atherosclerosis and infections seems to be a rational one, as the process of development of atherosclerosis involves a chronic low-grade inflammation. (2)

Moreover, systemic markers of inflammation (that is C-reactive protein, leukocyte count, fibrinogen, cell adhesion molecules and proinflammatory cytokines) are predictors of present and future cardiovascular events and disease. (2)

The bulk of evidence and research supports a moderate association between cardiovascular disease and periodontal disease. There is not enough evidence at present to conclude that the association is causal. There are many studies that show a moderate relationship with an odds ratio (OR) between 1.5 to ? 3. 8. (1) For example, if the OR is 2 it means that a person with periodontal disease is twice as likely to have cardiovascular disease as compared to someone without periodontal disease. However, even a moderate risk contributed byperiodontal disease to heart disease could contribute to significant morbidity and mortality. (1)

Mounting evidence points to an association of periodontal disease at the biological, clinical, radiographic and microbiological levels in relation to clinical and subclinical vascular disease. (3)

Insurance company studies find fewer medical care needs in patients who maintain their periodontal health.

The time has come for the emergence of periodontal infections as a possible risk factor for cardiovascular disease leading to a convergence in oral and medical care. (3)

Periodontal disease can contribute to cardiovascular disease by either direct or indirect pathways. Oral Microbes and their byproducts can gain direct access to the circulatory system or they can stimulate the production of inflammatory components which will then indirectly affect the cardiovascular system. Either route can contribute to the initiation and propagation of the inflammatory process that potentiates the development of atherosclerosis.

I would like to conclude with explanations from two prominent scientific articles explaining the pathopsyiological nature of the relationship between these destructive and deleterious diseases.

Infectious agents may play a role in the pathogenesis of atherosclerosis by several mechanisms of action and at different stages. Microorganisms could infect vascular endothelial cells directly, initiating the inflammatory response needed for the initial process of inducing atherosclerosis. Furthermore, even if the induction or initial injury to the endothelium was caused by another inciting agent or factor (for example, hypercholesterolemia or hypertension), infectious agents could accelerate or enhance the process through several mechanisms of action. They include further recruitment and stimulation of proinflammatory cytokines and tissue growth factors in the arterial wall, as well as enhancement of lipid (low density lipoprotein, or LDL) accumulation through stimulation of macrophage scavenger or LDL – receptors. Microbes could indirectly influence the development and progression of atherosclerosis by a systemic effect without directly invading the arterial endothelium. Release of endotoxins or lipopolysaccharide into the circulation could indirectly damage vascular endothelium or the immune response and systemic cytokine release could result in lipid profile predisposing the arterial environment to a procoagulant state, resulting in acute thrombus on a preexistent unstable or critical plaque, thus causing an acute ischemic event, or heart attack. (2)

Periodontal pathogens are capable of invading the coronary and carotid endothelium in cell culture. Monocyte-derived cytokines such as tumor necrosis factor-alpha, and interleukins may be released in response to a series of stimuli secondary to periodontal infection. One of these potential stimuli, the endotoxin lipopolysaccharide, or LPS, is present in such gingival plaque associated with periodontal disease. LPS and other bacterial components can activate an impressive cascade of inflammatory cytokines that in turn, can play a role in atherosclerotic heart disease, either through a direct action on the vessel wall or by inducing the liver to produce acute-phase proteins.

For example, acute-phase proteins, such as C-reactive protein, or CRP, and fibrinogen, affect coagulation, platelet activation and aggregation. People with periodontal disease have increased systemic levels of CRP and fibrinogen. Both CRP and fibrinogen contribute to atheroma formation via several possible mechanisms, including CRP-triggered complement activation and fibrinogen-clotting effects. (1)

The bottom line is that periodontal disease is a pernicious disease that has far reaching destructive consequences both in the mouth and throughout the body. Periodontal treatment can be very effective in treating this disease. You owe it to yourself and your overall health to visit your dentist on a regular basis and to maintain proper dental home maintenance.

Your dentist needs to be a part of your health care team. Call today to reserve your consultation with Dr. Wesley P. Kandare. Our dental office is conveniently located in the Great Bridge Hickory area in Chesapeake, Virginia just north of the North Carolina border. We serve patients from Virginia Beach, Norfolk, Hampton Roads, Moyock, Elizabeth Chesapeake, Currituck, Outer Banks and beyond with personalized dental care.

1. Robert Gence, DDS, Ph.D; Stevan Offenbacher, DDS, Ph.D, M.Sci, James Beck, Ph.D Periodontal disease and cardiovascular disease Epidemiology and possible mechanisms JADA, vol. 133, June 2002

2. Ingnatius W. Fong, MD, BS, F.R.C.P.C. Infections and their role in atherosclerotic vascular disease JADA. Vol. 133, June 2002

3. Ryan T. Demmer, Ph.D and Moise Degueriaux, MD, Ph.D, Periodontal infections and cardiovascular disease. The heart of the matter. JADA, vol. 137, No suppl-2, 145-205


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