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Treating Dental Disease Improves Vascular Function

Article

FARMINGTON, Conn. -- Treating periodontal disease may pay off for cardiovascular health, researchers here found.

FARMINGTON, Conn., Feb. 28 -- Treating severe periodontal disease may pay off for cardiovascular health, researchers here found.

Intense treatment to remove pockets of bacteria and plaque around affected teeth significantly improved vascular endothelial function six months later, according to a randomized, controlled trial reported in the March 1 issue of the New England Journal of Medicine.

The findings support epidemiologic evidence suggesting that chronic infection of tissue around the teeth may contribute to cardiovascular disorders, said Maurizio S. Tonetti, D.M.D., Ph.D., of the University of Connecticut Health Center here, and colleagues.

The researchers had previously reported that similar treatment improved periodontal and systemic inflammation.

Because endothelial dysfunction may be how inflammation influences arterial plaque formation and thus acute cardiovascular events, the researchers studied it in 120 patients with severe periodontitis referred to University College London.

Patients had more than 6 mm deep pockets and over 30% marginal alveolar bone loss around at least half of their teeth.

They were randomized to standard above-the-gum scaling and polishing or to intensive treatment including below-the-gum scaling and root planing, extraction of teeth that could not be saved, and administration of minocycline (Arestin) into periodontal pockets.

Endothelial function was indirectly measured with ultrasound as the diameter of the brachial artery during flow. For this primary endpoint, the researchers reported:

  • At 24 hours after treatment, significantly lower flow-mediated dilatation in the intensive-treatment group compared with the control group (absolute difference 1.4%, 95% confidence interval 0.5 to 2.3, P=0.002),
  • At two months, significantly improved endothelial function for the treatment group (absolute difference 0.9%, 95% CI 0.1 to 1.7, P=0.02), and
  • At six months, further improvements in flow-mediated dilation were seen in the intensive-treatment group (difference 2.0%, 95% CI 1.2 to 2.8, P

The endothelial function improvements at six months appeared to be in response to therapy. The improvements were significantly correlated with a reduction in the number of periodontal lesions (P=0.002) and with a reduction in gum bleeding scores (P=0.003).

Neither group experienced any serious adverse effects or cardiovascular events.

The researchers concluded, "This study showed that intensive treatment of periodontitis, a common potential source of low-grade inflammation, results in an improvement in endothelial function."

The mechanism remains uncertain, they added, but may include direct effects from the gram-negative bacteria and their product invading periodontal tissue or indirectly acting as triggers for a systemic inflammatory response that harms the vascular walls.

They noted that severe periodontitis of the sort seen in the study may affect 0.5% to 1.0% of the adult U.S. population though up to 80% may have some form of periodontal disease.

However, "it remains uncertain whether those with less severe disease would have improvements in vascular function that would be similar to the improvements in our study population," Dr. Tonetti and colleagues wrote.

"Further studies are required to determine whether the treatment of severe periodontitis could contribute to the prevention of atherosclerosis and cardiovascular events in adults," they added.

Dr. Tonetti reported serving on the advisory boards of Ora-Pharma (Johnson & Johnson) and ITI Biologics, which is financially supported by Straumann, and receiving consulting fees from Thommen Medical. Another author reported that he is now senior vice president for drug discovery at GlaxoSmithKline.

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