Smoking-related cotinine levels and host responses in chronic periodontitis
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...
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Published in | Journal of periodontal research Vol. 49; no. 5; pp. 642 - 651 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Blackwell Publishing Ltd
01.10.2014
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Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | NCRR and the National Center for Advancing Translational Sciences - No. NIH UL1 RR033173 National Institutes of Health - No. P20 GM103538; No. UL1 TR000117 ark:/67375/WNG-QHHNBDXF-H istex:99ABE56F2CEF50CEBA22AD98941A5D76B4E77672 Center for Clinical and Translational Sciences at the University of Kentucky NIH/NCRR - No. P20 RR020145 ArticleID:JRE12146 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0022-3484 1600-0765 |
DOI: | 10.1111/jre.12146 |