Find in Library

Aim and objective Cigarette smoking presents oral health professionals with a clinical conundrum: reduced vascular responsiveness in response to the oral biofilm (often incongruously equated to decreased gingival inflammation per se), accompanied by increased susceptibility to destructive periodontal diseases. The aim of this review was to summarize contemporary hypotheses that help explain the suppressed bleeding response in the oral cavity of smokers. Methods The core of this review was informed by a PubMed search for “(smok* OR cigar* OR nicotine OR tobacco) AND (periodont* OR gingiv* ) AND (blood OR vascul*)” generating n = 958 hits on March 17, 2018. Results and conclusions Smoke exposure influences angiogenesis, innate cell function, the production of inflammatory mediators including cytokines and proteases and tobacco-bacterial interactions, while concomitant smoking and specific genetic traits predispose to destructive periodontal diseases. Funding The tobacco-related research in D.A. Scott’s lab is currently funded by the U.S. Department of Health and Human Services via the National Institute for Dental and Craniofacial Research (R01DE026963 [DAS]; R01DE017680 [DAS]; and R01DE026963 [P.I., H. Wang]); and via the National Institute for General Medical Sciences (P20GM125504 [P.I., R.J. Lamont]).