Up-to-date medical news, research results, and treatment options, intended for the general public and their health care professionals, brought to you by the Web-based Health Education Foundation (WHEF). All information provided is balanced, fact-based and totally uninfluenced by our sponsors.
September 6, 2008 go to public site
   [Suggest to a Friend]
[Subscribe to Newsletter]






  RSS



Choose Font Size
Normal
Large
Extra Large

Other Center

[ Health Centers >  Other >  PERIODONTITIS ]

Periodontitis - How it Causes Cardiovascular Problems

Summarized by Robert W. Griffith, MD
March 22, 2007

Summary

Intensive treatment of periodontitis can, after an initial short inflammatory response, lead to measurable improvements in endothelial function, suggesting a slowing or reversal of the atherosclerotic process.

Introduction

It's been recognized in recent years that inflammation plays an important role in the causation of atherosclerosis.1 A common chronic infection of the tissue surrounding the teeth, called periodontitis, has been associated with raised C-reactive protein (CRP) blood levels, along with those of other biomarkers of inflammation, such as soluble E-secretin. And periodontitis is linked clinically to atherosclerosis and an increased risk of heart attack and stroke.

A detailed study of the way in which periodontitis exerts its effect on the blood vessels has been reported in the New England Journal of Medicine. It goes a long way to explaining how intensive treatment of the disease can reverse the initial change that leads to atherosclerosis - disruption of endothelial function.2 Here's a summary of the study.

What was done

Patients referred to a dental hospital in London, UK, were invited to participate if they had severe generalized periodontitis. They had to be free of general disease and any other acute or chronic infections. They were randomly assigned to receive intensive periodontal treatment or community-based periodontal care.

The degree of periodontitis was scored using recognized methods for quantifying the disease process. The intensive treatment group had the plaques below their gums removed using scaling and root planing, under local anesthesia; teeth that could not be saved were removed. Minocycline (a tetracycline antibiotic) in a slow-release form was placed in the periodontal pockets. Patients in the control (community-based care) group had a standard cycle of mechanical scaling and polishing, without extension below the gum margins.

Endothelial function was measured by flow-mediated dilatation (FMD) of the brachial (arm) artery assessed by high-resolution ultrasound. Endothelial dysfunction is usually diagnosed if the FMD is less than 4.5%.

The patients had blood sampling and FMD exams at days 1, 7, 30, 60, and 180 days after administration of treatment. Blood levels of CRP, interleukin-6, and other markers of endothelial inflammation (soluble E-selectin, tissue plasminogen activator, plasminogen-activator inhibitor type 1, and von Willebrand factor) were determined, along with glucose and lipid levels. Dental exams were done at 60 and 180 days.

What was found

Of the 120 patients with periodontitis entering the study, half were assigned to intensive treatment and half to control treatment. Their average age was 48, with men and women equally represented. The clinical characteristics of the patients in the two groups were similar at baseline. Systolic blood pressure was raised in the intensive treatment group 24 hours after the treatment was given, compared with those in the control group. No other clinical differences were seen between the groups.

On dental examination, the intensive treatment group had lower scores for plaque at both post-treatment exams (2 months and 6 months). They also had lower scores for gingival bleeding.

On the first day following treatment, FMD was significantly lower in the intensive treatment group; the difference amounted to 1.4% to that of the control group score. The CRP, interleukin-6, soluble E-selectin and von Willibrand factor levels were all significantly increased. These changes represented an acute inflammatory response to the treatment.

By day 2 the FMD was similar in both groups. At 60 days after treatment, FMD was significantly greater and the blood levels of soluble E-selectin were lower in the intensive treatment group. And at 180 days after treatment the difference in FMD in favor of intensive treatment had increased to +2%, along with a corresponding further decrease in soluble E-selectin.

What the findings show

The intensive treatment of periodontitis was clearly associated with a short (24-hour) episode of acute generalized inflammation along with a decrease in endothelial function. This had resolved by day 2, and by 60 days the reverse was seen: there was an increase in endothelial function coupled with a decrease in soluble E-selectin, the most sensitive of the inflammatory markers.

Six months after the intensive treatment, as compared with control treatment there were reduced periodontitis scores, reduced soluble E-secretin levels, and a 2% increase in flow-mediated dilatation, which signifies much better endothelial function - i.e. a reduction in an early stage of atherosclerosis.

There are two conclusions to be drawn from this study. On the scientific level, the data provide further evidence of the path leading from localized bacterial infection (periodontitis) to systemic (whole-body or generalized) inflammation, to initial changes of atherosclerosis. On a more practical level, the findings point up the need for people with periodontitis to have it treated energetically, if they are to reduce their risk of heart attack or stroke. Better still, avoid periodontitis by brushing, flossing and antiseptic rinsing.

Source

  • Treatment of periodontitis and endothelial function. MS. Tonetti , F. D'Aiuto, L. Nibali,  et al., N Engl J Med, 2007, vol. 356, pp. 911--920


Footnotes
1. In atherosclerosis deposits of fatty substances, cholesterol, cellular waste products, and calcium build up in the inner lining (the intima) of an artery; this buildup is called plaque.
2. The endothelium consists of the cells that line the inner surface of all blood vessels including arteries and veins. The cells' functions include mediation of coagulation, platelet adhesion, immune function, and control of volume and mineral content of the vessels. Endothelial dysfunction is a key early event in the development of atherosclerosis. One feature is the inability of arteries to dilate fully in response to an appropriate stimulus, such as temporary inflation of a blood pressure cuff to high pressures, as was done here.

Related Links
Tooth Brushing, Flossing, AND a Mouthwash Can Help Prevent Stroke
Tip of the Month 2: Looking After Your Teeth and Gums
Brush Up on Oral Health

Please take a moment to give us your comments. For questions about Health matters you may check our "Questions & Answers" Portal and Service.





Copyright © 2006. All rights reserved. [ Privacy Policy | Terms of Use | About Us | Site Map ]