Periodontal disease and C-reactive protein-associated cardiovascular risk

Authors

  • Francesco D'Aiuto,

    1. Department of Periodontology, Eastman Dental Institute and Hospital, University College London
    2. Eastman Clinical Investigation Center, Eastman Dental Institute and Hospital, University College London
    Search for more papers by this author
  • Derren Ready,

    1. Microbiology Unit, Eastman Dental Hospital, University College London Hospitals NHS Trust, London, UK
    Search for more papers by this author
  • Maurizio S. Tonetti

    1. Department of Periodontology, Eastman Dental Institute and Hospital, University College London
    2. Eastman Clinical Investigation Center, Eastman Dental Institute and Hospital, University College London
    Search for more papers by this author

Professor Maurizio S. Tonetti, Department of Periodontology, Eastman Dental Institute and Hospital, 256 Gray's Inn Road, London WC1X 8LD, UK
Tel: + 44 20 79151075
Fax: + 44 20 79151137
e-mail: M.Tonetti@eastman.ucl.ac.uk

Abstract

Background:  Periodontitis has been associated with a moderate systemic inflammatory response. Successful periodontal therapy could decrease serum inflammatory parameters. The aim of this report was to explore the outcomes of periodontal therapy in terms of changes in C-reactive protein (CRP)-associated cardiovascular disease (CVD) risk as defined in a recent American Heart Association (AHA) consensus conference.

Methods:  Ninety-four systemically healthy subjects suffering from severe generalized periodontitis received standard non-surgical periodontal therapy. Periodontal parameters and serum inflammatory responses [interleukin-6 (IL-6) and CRP] were monitored 2 and 6 months after therapy.

Results:  At baseline, subjects with more severe and widespread periodontitis had a higher chance of having high CRP-associated CVD risk (OR 5.6, 95% CI 1.2–27.4). Age and body mass index were also significant in the analysis. After therapy, a significant decrease in number of subjects associated with a medium and high CRP-associated risk was observed (p < 0.001 χ2), with 40 of 94 subjects displaying a decrease in their class of risk. Patients who had a better oral response to periodontal therapy were also more likely to have decreased their inflammatory risk category (OR 4.8, 95% CI 1.4–15.8) after correcting for age, gender, ethnicity and cigarette smoking.

Conclusions:  This study indicated that periodontitis may add to the inflammatory burden of the individual and may result in increased levels of cardiovascular risk based on serum CRP concentrations. These observations will need to be confirmed in a definitive trial. Given the high prevalence of periodontitis in the population, these data would caution physicians to be aware of the possible oral source of an increased inflammatory burden.

Ancillary