by Trisha E. O'Hehir
Heart disease — including blood vessel disorders, hypertension, and arteriosclerosis — is the number one cause of death in the Western World. Medical researchers are now suggesting that heart disease is really a bacterial infection, similar in many ways to periodontitis. Isn't it interesting that "plaques" accumulate in blood vessels and on the teeth and under the gums?
For several years now, periodontal researchers have been evaluating the possibility of a link between the two. It's tempting to assume a cause and effect relationship in educating people to take better care of their mouths. Caution is urged here. Good oral health is desirable in and of itself. Telling people that flossing will prevent heart disease is stretching it just a bit. Good oral hygiene will do a lot of things — from eliminating bad breath to avoiding tooth loss.
We just don't have sufficient research to claim that good oral hygiene will prevent heart disease. On the other hand, who wants the byproducts of oral infection being dumped into the body's circulatory system all day, every day, or 24/7 as they say?
Periodontal care interacts with three areas relating to cardiovascular disease: effects of medications, infective endocarditis (IE), and the potential for periodontal disease to contribute to heart disease. Here's a quick review of the research to date in these areas.
o Calcium-channel blockers — In 1984, calcium-channel blockers were determined to contribute to gingival overgrowth, occurring in 3 to 43 percent of cases, depending on the study. Men are three times more likely to experience gingival overgrowth than women. The overgrowth can be controlled with meticulous oral hygiene, professional dental hygiene care, and chlorhexidine rinses. Surgical elimination of the tissue is often needed, with recurrence in some patients.
o Beta-blockers and diuretics — Beta-blockers and diuretics are associated with a reduction in calculus formation, but an increase in cervical caries. The exact mechanisms for each of these side effects are unknown. It is thought that the drug is excreted into saliva or alters saliva, leading to a reduced rate of crystallization. Patients on these drugs should be carefully screened for root caries.
o Anticoagulants — Traditionally, patients have been taken off anticoagulants for periodontal procedures. There is some evidence now that the risks of this may outweigh the benefits. In a study of 950 patients continuing on coagulant medications and receiving a total of 2,400 surgical procedures, only 12 required attention for hemorrhage.
In contrast, of 526 patients who stopped anticoagulant medications, five suffered serious embolic complications and four of them died. Based on this evidence, current recommendations in the United Kingdom are to continue anticoagulant medications rather than stopping them prior to dental treatment.
o Bacterial endocarditis — The American Heart Association recommends antibiotic prophylaxis prior to dental treatment for those with heart valve problems. This is the current standard, despite a lack of evidence. Unanswered questions include:
• Are dental procedures really the cause of IE, or can chewing or toothbrushing be the cause of spontaneous bacteremia?
• Who is at risk for IE?
• Which procedures require antibiotic coverage?
• Are the risks of antibiotic allergy higher than the risks of IE?• Are the antibiotics used effective?
Although oral Streptococci are responsible for 50 percent of IE cases, according to one study, only 15 percent of patients with IE received dental treatment within the previous three months. According to other research, only 4 percent of all IE cases are related to dental-induced bacteremia, suggesting that 96 percent of cases are caused by spontaneous bacteremia. One theory suggests that repeated spontaneous bacteremia primes the blood vessel lining, making it susceptible to further significant bacteremia from dental procedures.
o Mitral valve prolapse — The main problem in determining who is at risk of IE is the diagnosis of mitral valve prolapse (MVP), a common condition affecting 5 percent of the population. Only those with regurgitation and/or thickening are considered at risk. Proper diagnosis requires angiography or echocardiograms. It is not surprising that the great majority of cases will be undiagnosed and therefore not brought to the attention of the dental team.
In the United States, 400 to 800 deaths occur each year due to anaphylactic reactions to penicillin. Putting this figure into perspective, 1.36 people per million will die from anaphylactic reaction to prophylactic antibiotic compared to 0.26 deaths per million due to IE from dental procedures.
According to these figures, people taking prophylactic antibiotics for dental procedures are five times more likely to die from the antibiotic than from contracting endocarditis.
The prevalence of IE is 15 cases per million, but this figure has not been reduced with the advent of antibiotic prophylaxis. Randomized, placebo-controlled clinical trials have not been done to determine the effectiveness of antibiotic prophylaxis. In fact, studies suggest that current doses do not reduce bacteremia, but may instead decrease bacterial adherence to damaged cardiac valves.
It doesn't seem feasible to undertake a large-scale study to answer these questions, due in part to the ethical risk of not providing antibiotic coverage to the controls. Despite lack of evidence to support the need and/or the effectiveness of antibiotic coverage, it remains the current standard.
Based on numerous studies, it is clear that periodontal disease and heart disease occur more frequently together than purely by chance. That may be due to a similar set of risk factors, including smoking and lifestyle. Separating out the risk factors to determine a direct cause and effect is nearly impossible. Intervention studies are needed to determine cause and effect. Various explanations have been suggested for a connection: bacterial, hyperlipidemia, genetic, and acute phase response.
o Bacterial — Oral bacteria are known to trigger platelet aggregations and have a thrombogenic role. The bacteria seem to be able to insert themselves into blood vessel walls. This may be significant or it may be what researchers consider a "bystander" effect. The finding of P gingivalis within atheromatous plaques suggests they could precipitate rupture of the fibrous membranes through the release of inflammatory cytokines.
o Hyperlipidemia — High cholesterol levels are linked with cardiovascular disease and now periodontitis is also linked with high cholesterol. The cytokines released by periodontal pathogens are known to alter lipid metabolism and lead to increased cholesterol levels. If this is significant, it remains to be determined by research.
o Genetics — Genetic factors play a role. The IL-1 genotype in pattern 1 is associated with severe periodontitis, but not atherosclerosis. IL-1 genotype pattern 2 is associated with atherosclerosis, but not periodontitis. Both affect the immune response, so there may actually be a biological link. More research is ongoing in this area.
o Acute phase response — The most convincing evidence relates to the inflammatory process. It's hard to imagine that the reactions taking place in the gingival tissue are confined to that area. Subgingival biofilm activates an acute phase response from the immune system, resulting in an increase in white blood cells, fibrinogen, C-reactive protein, and other substances. For example, one of these substances, C-reactive protein, is also a marker for cardiovascular disease. Bacterial lippopolysaccharide triggers IL-1 and TNF and other mediators capable of platelet adhesion and aggregation and promotes formation of lipid laden foam cells. Dr. Offenbacher and colleagues suggest that both diseases could form a syndrome, the Periodontitis-Atherosclerosis Syndrome.
Although we can't say with any certainty that periodontal disease causes heart disease, it is still a good idea to keep periodontal tissues healthy and to encourage patients to effectively control bacterial biofilm on a daily basis.
References available upon request
Trisha E. O'Hehir, RDH, BS, is a senior consulting editor of RDH. She is also an international speaker, author, instrument designer, inventor, and oral health detective. Her Web sites are www.perioreports.com and www.toothpastesecret.com. She can be reached at (800) 374-4290 or at [email protected].