Embargoed by the American Association for the Advancement of Science until 1 p.m. EST Monday, Feb. 16. Sound bites will be available at that time on the Newsline at (612) 625-6666.
Contacts:
Dr. Mark Herzberg, Preventive Sciences, (612) 625-8404
Deane Morrison, University News Service, (612) 624-2346, [email protected]
Good Dental Hygiene may Prevent Heart Attacks,
U of Minnesota Study Finds
Bacteria found in dental plaque near diseased gums can induce clumping of blood platelets, a University of Minnesota study has found. Such clumping is an early step in the formation of blood clots, the precipitating event in heart attacks. Working with rabbits, Dr. Mark Herzberg, professor of preventive sciences, and Dr. Maurice Meyer, professor emeritus of oral sciences, physiology and neurology, found that the bacteria can also cause abnormalities in heart function. While previous reports have linked bacterial infections to the buildup of atherosclerotic plaque in coronary arteries, the researchers believe this to be the first evidence linking bacteria to the event that directly causes most heart attacks. The work will be presented Monday, Feb. 16, at the American Association for the Advancement of Science meeting in Philadelphia.
"We know a great deal about risk factors for atherosclerosis and heart attacks, but not the actual causes," said Herzberg. "Risk factors include high LDL cholesterol, lack of exercise and smoking. But our data suggest that two different 'bugs' may trigger the formation of blood platelet clots, which is the actual artery-blocking event." The researchers say that rabbits infused with the clot-inducing bacteria make a good animal model of events leading up to or predicting human heart attacks.
There is currently no way to estimate the extent to which the presence of these bacteria in blood contributes to heart attacks, but several epidemiological studies implicate poor dental health, particularly periodontitis (gum disease), as a risk factor in heart attacks, Herzberg said.
"Severe periodontitis is the equivalent of about nine square inches of chronic wound around the teeth," he said. "It offers considerable opportunity over time for these bacteria to enter the blood." The researchers studied certain strains of the bacteria Streptococcus sanguis (S. sanguis), the most numerous organism found in dental plaque, and Porphyromonas gingivalis (P. gingivalis), a major pathogen in periodontitis. After S. sanguis was infused into rabbits, blood platelets clumped together. The bacteria appear to do this, said Herzberg, by producing a protein called PAAP (platelet aggregation associated protein) and displaying it on their outer cell walls. In test-tube experiments, only PAAP-producing strains of S. sanguis triggered platelet clumping.
These events mimic an early step in the development of clots. When injury rips open blood vessels, blood is exposed to collagen, a protein found in blood vessel walls and connective tissue. To stop the bleeding, platelets stick to collagen, which activates them to "grab" molecules of the blood protein fibrinogen. Each fibrinogen molecule can attach to two platelets, and soon these "bridges" of fibrinogen create a clump of platelets. Clotting factors convert fibrinogen to another protein--fibrin--which forms the solid meshlike framework of a blood clot. Herzberg and colleagues have previously shown that PAAP bears a chemical resemblance to collagen, and both mediate platelet clumping in much the same way, Herzberg said.
The researchers also found that infusions of PAAP-producing S. sanguis quickly caused dose-related platelet clotting, faster heart and breathing rates, and intermittent abnormalities in the rabbits' electrocardiograms. (A similar bacterium that doesn't produce PAAP caused no changes.) Some of these pathological changes persisted for 30 minutes. The abnormal EKGs suggest that platelet clots formed in the coronary arteries, said Herzberg. As a result of these obstructions, part of the heart muscle suffers from a lack of blood and oxygen. If the clots persist, heart muscle in that area dies--a heart attack.
Herzberg said there is also evidence implicating mouth bacteria in coronary artery disease, including a preliminary study at the State University of New York at Buffalo that found P. gingivalis in atherosclerotic deposits in coronary arteries. But the absence of bacteria in arterial lesions or blood clots wouldn't rule them out as a factor, Herzberg maintained. Bacterial cells might cause inflammation that leads to atherosclerosis, but the cells may be removed by the immune system during the process of building up deposits. Also, Herzberg pointed out that the process of clotting in response to PAAP-producing bacteria is self-propagating. These bacteria would act only as "seeds" and may never be found associated with damaging clots.
Herzberg estimated that about 60 percent of S. sanguis strains found in the human mouth are PAAP-producing, but cautioned that much more research is needed before it is known whether these mechanisms occur in humans. He plans to continue studying rabbits for periods longer than 30 minutes to see if heart attacks could occur as a result of clotting caused by the PAAP-producing bacteria.
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