Periodontal bacteria linked to heart disease
People who test positive for bacteria that cause periodontal disease also have increased thickness of the carotid artery, which suggests there is a direct relationship between periodontal infection and atherosclerosis, investigators report.
However, “there is no guarantee that treating periodontal disease would reverse it, because the damage might be preventable but not reversible,” Dr. Moise Desvarieux told AMN Health.
While there have been numerous studies linking periodontal health and the risk of vascular disease, this is the first to directly measure oral bacteria and thickness of the arteries, Dr. Desvarieux explained.
Desvarieux, an epidemiologist at Columbia University in New York City, and colleagues obtained up to eight subgingival plaque samples from each of 657 subjects 55 years or older with no history of stroke or heart attack. The samples were analyzed for 11 different types of bacteria. Carotid artery thickness was measured using high-resolution ultrasound.
After adjusting the data to factor out conventional risk factors, the researchers found that carotid artery thickness corresponded with bacterial levels. Five specific types of bacteria that cause periodontal disease were detected.
Furthermore, there was no association between artery thickness and bacteria not associated with periodontal disease, the authors report in Circulation: Journal of the American Heart Association.
These differences in arterial thickness are “clinically relevant,” Desvarieux said. For example, he noted, a difference of 0.03 mm is associated with a 15-mm Hg increase in systolic blood pressure, or twice the risk of heart attack or coronary death.
Because this analysis was a cross-sectional study, it does not prove the periodontal bacteria cause atherosclerosis, Desvarieux added. It’s not clear which one comes first, the increased bacterial levels or artery thickening, “so it becomes critical for us to follow up those patients to see if the progression in microbial burden would also follow the progression of atherosclerosis and translate into clinical events.”
SOURCE: Circulation, February 16, 2005.
Revision date: June 18, 2011
Last revised: by Janet A. Staessen, MD, PhD