Nicotine promotes pathogenic bacterial growth and biofilm formation in peri-implant

<b>Introduction.</b> Peri-implantitis is a plaque-associated disease that leads to implant loss and arises from bacterial biofilms on the surface of the implant. Smoking is a risk factor for peri-implantitis and impedes treatment effectiveness. Additionally, aryl hydrocarbon receptor (AHR), IL-6, and IL-22 levels are related to peri-implantitis.<b>Aim.</b> We aimed to investigate the effects of nicotine on inflammatory response, bacterial growth and biofilm formation.<b>Hypothesis/Gap Statement.</b> We hypothesized that nicotine promoted pathogenic bacterial growth and biofilm formation, thereby aggravating inflammation.<b>Methodology.</b> The expression of AHR, IL-6 and IL-22 was measured in peri-implant sulci fluid using quantitative PCR and Western blot analyses. The cementum was incubated with bacterial suspension including <i>Porphyromonas gingivalis</i>, <i>Streptococcus sanguinis</i> and <i>Fusobacterium nucleatum</i> and treated with 100, 200, 250 and 300 µg ml^-1 nicotine, and then, the absorbance and number of colony-forming units were detected. Biofilm formation was evaluated using the tissue culture plate method and safranin O staining. Carbohydrates and proteins were measured by the phenol-sulfuric acid method and the bicinchoninic acid method, respectively.<b>Results.</b> The results indicated that smoking increased the levels of AHR, IL-6 and IL-22. Functionally, nicotine promoted the growth of <i>P. gingivalis</i>, <i>S. sanguinis</i> and <i>F. nucleatum</i>. Additionally, it promoted the biofilm formation of these bacteria and increased the contents of carbohydrates and proteins.<b>Conclusion.</b> Nicotine promoted bacterial growth and biofilm build-up, suggesting that smoking may aggravate the progression of peri-implantitis.