Abstract
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. 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). 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. 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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