Smoking-related cotinine levels and host responses in chronic periodontitis

J. L. Ebersole, M. J. Steffen, M. V. Thomas, M. Al-Sabbagh

    Research output: Contribution to journalArticlepeer-review

    31 Scopus citations

    Abstract

    Background and Objective: Smoking has been reported to increase the risk of periodontal disease by disrupting the balance of immune responses and tissue repair processes; however, this risk varies among smokers. Cotinine levels in saliva are routinely used to measure the level of smoking, and reflect the quantity of nicotine, and other smoking-related xenobiotics that challenge host systems. This study delineated characteristics of inflammatory mediators in saliva and serum antibody responses to both periodontal pathogens and commensal bacteria in smokers as they related to cotinine levels. Materials and Methods: This case-control study (n = 279) examined salivary inflammatory mediator responses [interleukin (IL)-1ß, IL-10, prostaglandin E2, myeloperoxidase and plasminogen activator inhibitor-1], and serum IgG antibody responses to three periodontal pathogens (Aggregatibacter actinomyce-temcomitans, Porphyromonas gingivalis, Treponema denticola) and five commensal oral microorganisms (Veillonella parvula, Streptococcus sanguis, Prevotella loescheii, Actinomyces naeslundii, Capnocytophaga ochracea). Results: The patients were stratified into health (n = 30), gingivitis (n = 55) and periodontitis (n = 184); cotinine levels correlated with reported smoking habits in health, less so with gingivitis, and were not correlated in periodontitis. Of the inflammatory mediators/acute phase proteins, only IL-1ß levels were positively associated (p < 0.001) with the pack years and cotinine levels. As might be predicted, patients with periodontitis smoked more (p < 0.001) and had higher levels of cotinine. IL-1ß and antibody to A. actinomycetemcomitans, P. gingivalis and T. denticola were significantly higher in the patients with periodontitis than either patients with gingivitis or who were healthy. Conclusions: Generally, antibody to the pathogens and commensals was lower with decreased cotinine levels. Smoking exacerbated differences in both inflammatory mediators and three antibody in periodontal disease compared to healthy subjects.

    Original languageEnglish
    Pages (from-to)642-651
    Number of pages10
    JournalJournal of Periodontal Research
    Volume49
    Issue number5
    DOIs
    StatePublished - Oct 1 2014

    Bibliographical note

    Publisher Copyright:
    © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

    Funding

    FundersFunder number
    National Center for Research Resources
    National Institutes of Health (NIH)P20 RR020145, UL1 RR033173
    National Center for Research ResourcesP20RR020145

      Keywords

      • Cotinine
      • Inflammation
      • Periodontitis
      • Smoking

      ASJC Scopus subject areas

      • Periodontics

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