Cotinine Related to Inflammatory Mediators and Antibody to Oral Bacteria

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 is routinely used to measure the level of smoking, and reflects the quantity of nictotine, and other smoking related xenobiotics that challenge host systems .  Objective: This study delineated characteristics of inflammatory mediators in saliva and antibody responses to both periodontal pathogens and commensal bacteria in smokers as they related to cotinine levels.  Methods: This case-control study (n=326; 68% Caucasians, 28% African-Americans; 39% males; age range 21-65 years) examined salivary inflammatory mediator responses (IL-1ß, IL-10, PGE₂, MPO, PAI-1).  Serum IgG antibody responses were analyzed for 3 periodontal pathogens (A. actinomycetemcomitans, P. gingivalis, T. denticola) and 5 commensal oral microorganisms (V. parvula, S. sanguis, P. loescheii, A. naeslundii, C. ochracea). Results:   Irrespective of periodontal disease, salivary cotinine levels did not correlate to amount smoked daily, length of smoking, or pack years.  A subset of the patients were stratified into health (n=30), gingivitis (n=55) and periodontitis (n=184); continine 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 amount smoked, years smoked, and age of the patients.  As might be predicted, patients with periodontitis smoked more (p<0.001) and had higher levels of cotinine.  IL-1ß, and antibody to Pg, Td, Pl and An were significantly higher in the periodontitis patients than either gingivitis or healthy patients.  Conclusions:   Salivary cotinine levels as a measure of smoking may be adversely affected by oral inflammation and disease (ie. periodontitis).  Moreover, smoking exacerbated differences in both inflammatory mediators and antibody in periodontal disease compared to healthy subjects.  Supported by 5PRR020145 from the NIH/NCRR.