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The Link Between Periodontal Disease and Atherosclerotic Cardiovascular Disease
More than 20 years ago, epidemiologists reported significant associations between periodontitis and atherosclerotic cardiovascular diseases (CVD). Since the first reports many studies have replicated the findings, and recent meta-analyses (1-8) conclude that the association is significant and independent of standard CVD risk factors.
In general the association is stronger with more severe generalized periodontitis, is evident in multiple ethnic populations, and is stronger in stroke than coronary artery disease. Although the epidemiological studies are strong and there are plausible biological explanations for the association, to date there have been no prospective studies to assess whether periodontitis treatment reduces the incidence of CVD.
Periodontitis is a chronic inflammatory disease caused by bacterial biofilms that form at the gingival-tooth margins. (9) The bacterial biofilms (dental plaque), if not disrupted, change over time and a small set of highly pathogenic microorganisms emerge that are consistently associated with periodontitis ("peri" – around; "odont" – tooth; "itis" – inflammation.) These bacteria activate host immuno-inflammatory mechanisms that ultimately destroy the connective tissues and bone that support the teeth. The first sign of periodontal disease is gingivitis, a reversible inflammation of the gingival tissues. Mild to moderate periodontitis affects approximately 30% of U.S. adults, but more severe generalized forms affect 5% to 15%. (10,11)
Although specific bacteria are essential for initiating the disease, environmental and genetic modifying factors appear to determine disease severity. Smoking, diabetes, genetics, mental anxiety, depression, obesity, and physical inactivity are strongly linked with increased risk for and severity of periodontitis, with approximately 50% of the variation in disease severity attributable to genetic influences.
Periodontitis is a silent, painless disease that often occurs without any symptoms. Although periodontitis patients do not have an elevated body temperature, those with severe generalized disease often have increased C-reactive protein levels, as measured by high sensitivity assays. (12, 13)
Appropriate strategies for treating periodontitis focus on the resolution of inflammation by removing the bacterial biofilm attached to roots of the teeth, along with education to reinforce oral hygiene and reduce bacterial regrowth. Antibiotics may briefly improve sites of localized periodontal infection when combined with professional tooth cleaning to disrupt the biofilm. While antibiotics markedly reduce bacterial amounts, taken alone they do not usually eliminate the disease-causing strains that may be resident in a patient's mouth.
Drugs that modulate or damp down the inflammatory response have been shown to reduce the progression of periodontal disease. (14) Low-dose doxycycline, which has an anti-inflammatory effect, is the only FDA-approved drug for treating certain forms of periodontitis. Certain non-steroidal anti-inflammatory drugs (e.g., aspirin and ibuprofen) and bisphosphonate drugs for osteoporosis (e.g. alendronate) are also effective in treating periodontitis, but are not routinely used due to potential long-term systemic effects.
Advanced periodontitis may require surgery to gain adequate access to contaminated root surfaces for removal of the bacterial biofilm. In some instances, surgical approaches include bone and soft tissue regeneration to
regain at least some support for the teeth and to facilitate bacterial control.
Based on the frequency of periodontitis in the population and the potential implications of the disease for cardiovascular disease, a group of periodontists and cardiologists recently reviewed the evidence for linkage between the two diseases and made some recommendations for how such information should be used clinically with our patients. (15)
The first recommendations were for dentists who have patients with periodontitis to encourage them to: a) advise their patients of the potential risk for cardiovascular disease, b) to counsel on control of risk factors common to both diseases, such as smoking, and c) to refer for medical evaluations of CVD risk. Dentists were also encouraged to do a comprehensive examination of periodontal tissues in all patients with a history of cardiovascular disease.
The second set of recommendations encouraged physicians to consider referrals for periodontal evaluation in patients with CVD who have signs of periodontal disease, such as bad breath, multiple missing teeth, loose teeth, and unexplained elevations of CRP or other inflammatory markers.
While evidence is not yet available to show that treatment of periodontitis reduces the incidence of CVD, current evidence supports a role for periodontitis as an independent risk factor for cardiovascular disease, and there is much that physicians and dentists can do to modify this risk factor.
—Kenneth Kornman DMD, PhD & Nadeem Karimbux DDS, MMSc
BIOS
Kenneth S. Kornman, DDS, PhD: Emory University, Dental School 1973; MS periodontics, 1978 and PhD, microbiology/immunology, 1980, University of Michigan. He was Professor and Chairman of the Department of Periodontics and Professor of Microbiology at the University of Texas Health Science Center at San Antonio 1984-1990. He retains an academic appointment at Harvard University School of Dental Medicine. He has published 125 manuscripts, including papers in Science and the New England Journal of Medicine, and authored 3 textbooks. He is Editor-in-Chief of the Journal of Periodontology and actively involved in genomics research. Dr. Kornman is currently the Chief Scientific Officer at Interleukin Genetics, a molecular diagnostics company focused on genetic variations that influence inflammatory mechanisms and chronic diseases.
Nadeem Karimbux, DMD, MMSc: DMD, 1991; MMSc Oral Biology and Certificate in Periodontology, 1993, Harvard School of Dental Medicine. He is Associate Professor of Periodontology in the Department of Oral Medicine Infection and Immunity at Harvard University School of Dental Medicine. He is a Board Certified periodontist, seeing patients at Children's Hospital Boston and at the Harvard Dental Center. He has published 60 manuscripts, and authored 2 textbooks. He is Associate Editor of the Journal of Periodontology and MedEdPORTAL and is actively involved in research with the oral-systemic links.
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