Published: Nov 5, 2013 | Updated: Nov 6, 2013
By Todd Neale, Senior Staff Writer, MedPage Today
Full Story: http://www.medpagetoday.com/Cardiology/Atherosclerosis/42727
Action Points
- Previous studies have indicated that the burden of periodontal disease-causing bacteria was cross-sectionally related to increased carotid intima-media thickness.
- In this study, longitudinal improvement in clinical and microbial periodontal status was related to a decreased rate of carotid artery intima-medial thickness progression at 3-year average follow-up.
Older adults who had improvements in periodontal health also had smaller increases in subclinical atherosclerosis, a longitudinal study showed.
Reductions in the percentage of periodontal sites with a high probing depth and in the burden of periodontal disease-causing bacteria over about 3 years were associated with less progression of carotid intima-media thickness (P<0.0001 for trends), according to Moïse Desvarieux, MD, PhD, of Columbia University’s Mailman School of Public Health in New York City, and colleagues.
The findings remained significant after adjustment for sociodemographic factors and several established cardiovascular risk factors, including diabetes, smoking status, body mass index, systolic blood pressure, and LDL and HDL cholesterol, they reported online in the Journal of the American Heart Association.
“We report the first evidence that improvement in periodontal status — defined both clinically and microbiologically — is associated with less progression in carotid atherosclerosis in a randomly selected population-based sample of men and women,” they wrote. “These findings were observed during a relatively short period, strengthening the hypothesis that accelerated atherosclerotic progression is a mechanistic explanation for previous reports linking periodontal disease and clinical cardiovascular disease.”
They said, however, that randomized trials are needed to test whether treating periodontal infections can reduce the progression of atherosclerosis and prevent cardiovascular events.
Desvarieux’s group previously reported that the burden of periodontal disease-causing bacteria was cross-sectionally related to increased carotid intima-media thickness. But there are no data on the relationship between changes in chronic periodontal infections and progression of subclinical atherosclerosis.
“Prospective studies of this nature are important for establishing or refuting causality, thus, filling a critical gap, as recently summarized in an American Heart Association statementregarding the association between periodontal disease and atherosclerotic vascular disease,” the authors wrote.
The researchers examined data from 420 participants (mean age 68) in the Oral Infections and Vascular Disease Epidemiology Study (INVEST) who did not have a history of stroke, myocardial infarction, or chronic inflammatory conditions at baseline.
Through a median follow-up of 3.1 years, all participants had their periodontal health assessed at two visits. High-resolution ultrasound was used to measure carotid intima-media thickness.
On average, carotid intima-media thickness was 0.847 mm at baseline and increased by 0.139 mm during follow-up.
Progression was significantly slower, however, when periodontal health improved.
As the percentage of sites within the mouth with a probing depth of 3 mm or more decreased, so did the degree of intima-media thickness progression, which was 0.18 mm in the patients with an increase in the percentage of sites over time and 0.07 mm in those with the largest reduction in the percentage of sites (P<0.0001 for trend).
Similarly, intima-media thickness progression declined as the percentage of oral bacteria believed to cause periodontal disease decreased. Patients with the highest percentage of disease-causing bacteria had a progression of 0.20 mm and those with the lowest had a progression of 0.12 mm (P<0.0001 for trend).
The roughly 0.1-mm difference identified between the top and bottom quartiles for both comparisons appears “to meet the threshold of clinical significance” based on prior studies showing that such a change was associated with an increased risk of coronary events, the authors noted.
“The potential for oral microbes to contribute to atherogenesis is biologically plausible,” they wrote. “Oral bacterial species can induce immune system activation characterized by chronic elevations in systemic inflammatory markers, possibly resulting from bacteremias of oral origin, which may in turn initiate or exacerbate the inflammatory aspect of atherogenesis, as in animal models.”
“In humans,” they added, “anti-infective periodontal therapy improves endothelial function in as little as 2 months.”
They acknowledged some limitations of their study, including possible bias resulting from loss to follow-up and the limited number of bacterial species examined.
This research is supported by grants from the NIH. It is also partially supported by an INSERM Chair of Excellence from the Institut National de la Santé et de la Recherche Médicale (INSERM), a Chair in Chronic Disease from École des Hautes Études en Santé Publique, and a Mayo Chair Endowment from the University of Minnesota School of Public Health. Two of the authors reported additional support from the NIH and the National Institute of Neurological Disorders and Stroke.
The authors reported that they had no conflicts of interest.
From the American Heart Association:
Primary source: Journal of the American Heart Association