Make sure to floss! Intensive treatment of periodontal disease improves endothelial function

February 28, 2007

Farmington, CT - A new study appears to suggest that treating periodontal disease can improve endothelial dysfunction, with investigators showing that aggressively treating periodontal disease, a potential source of low-grade inflammation, results in a long-term improvement in vascular function [1].

"Local intensive mechanical treatment of periodontitis, without the use of systemic drug therapy, resulted in a transient acute inflammatory response and a transient impairment of endothelial function," write lead author Dr Maurizio Tonetti (University of Connecticut Health Center, Farmington, CT) and colleagues in the March 1, 2007 issue of the New England Journal of Medicine. "At six months, however, intensive treatment of the periodontitis, as compared with control treatment, was associated with reduced indexes of periodontal disease severity and significantly better endothelial function."

Periodontitis is a very common chronic infection of the tissue surrounding the teeth and has been shown to be associated with elevated levels of C-reactive protein (CRP) and other inflammatory biomarkers, the authors point out. Cohort and case-control studies have also shown that periodontitis is associated with endothelial dysfunction, atherosclerosis, and an increased risk of MI and stroke. Other studies have shown that aggressively treating periodontal disease can reduce inflammation of the gums as well as systemic inflammation.

In the present study, the authors sought to determine the effect of treatment of severe periodontitis on endothelial function, an end point through which a range of risk factors, including inflammation, could influence long-term atherogenesis and possibly trigger acute cardiovascular events.

In total, 59 patients were assigned to community-based periodontal care, which included instructions in basic oral hygiene as well as a standard cycle of supragingival mechanical scaling and polishing, and 61 patients to intensive periodontal treatment. Those in the intensive-treatment arm also received instruction in oral hygiene as well as full-mouth removal of subgingival dental plaque with the use of scaling and root planing after local anesthesia and the local administration of a tetracycline antibiotic into periodontal pockets. Teeth that could not be saved were extracted.

Twenty-four hours after treatment, flow-mediated dilatation, a measure of endothelial function, was significantly lower in the intensive-treatment arm than in the control group, and levels of CRP, interleukin-6, and E-selectin and von Willebrand factor, both markers of endothelial activation, were significantly higher. However, flow-mediated dilatation was significantly greater and plasma levels of soluble E-selectin significantly lower 60 and 180 days after therapy in the intensive-treatment arm. This improvement was associated with improvements in various measures of periodontal disease.

Between-group differences in serum levels of CRP and interleukin-6 did not reach statistical significance at two or six months, and the effect on these measures was not associated with the difference in flow-mediated dilatation between the groups, report investigators. CRP and interleukin-6 levels did decrease six months after therapy in both treatment groups, but Tonetti and colleagues suggest that CRP and other markers might not adequately reflect the relevant inflammatory pathways or that the long-term improvements were independent of the systemic inflammatory response.

The authors note that the severe periodontitis of patients in this study affects 0.5% to 1.0% of the adult population in the US, with as many as 80% of US adults having some form of periodontal disease. They add that it remains unclear whether those with less-severe disease would have similar improvements in vascular function and whether the treatment of severe periodontitis could aid in the prevention of atherosclerosis and cardiovascular events.

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