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Gum and Heart link-‘Most direct evidence yet’

Research has shown for the first time that as gum health improves, progression of atherosclerosis slows to a clinically significant degree.

Atherosclerosis, or the narrowing of arteries through the build-up of plaque, is a major risk factor for heart disease, stroke, and death.

The researchers followed 420 adults as part of the Oral Infections and Vascular Disease Epidemiology Study (INVEST), a randomly sampled prospective cohort of Northern Manhattan residents.

Participants were examined for periodontal infection. Overall, 5,008 plaque samples were taken from several teeth, beneath the gum, and analysed for 11 bacterial strains linked to periodontal disease and seven control bacteria.

Fluid around the gums was sampled to assess levels of Interleukin-1β, a marker of inflammation.

Atherosclerosis in both carotid arteries was measured using high-resolution ultrasound.

Over a median follow-up period of three years, the researchers found that improvement in periodontal health and a reduction in the proportion of specific bacteria linked to periodontal disease correlated to a slower intima-medial thickness (IMT) progression, and worsening periodontal infections paralleled the progression of IMT.

Results were adjusted for potential confounders such as body mass index, cholesterol levels, diabetes, and smoking status.

Co-author Panos N Papapanou, DDS, PhD, professor of Dental Medicine at Columbia University’s College of Dental Medicine, whose laboratory assessed the bacterial profiles in the gums, said: ‘Our results show a clear relationship between what is happening in the mouth and thickening of the carotid artery, even before the onset of full-fledged periodontal disease. This suggests that incipient periodontal disease should not be ignored.’

Bacteria in the mouth may contribute to the onset of atherosclerosis in a number of ways, scientists speculate. Animal studies indicate that they may trigger immune response and high levels of inflammatory markers, which may initiate or exacerbate the inflammatory aspect of atherosclerosis.