Barão, Valentim A. R.Ricomini-Filho, Antonio P.Faverani, Leonardo P. [UNESP]Del Bel Cury, Altair A.Sukotjo, CortinoMonteiro, Douglas R. [UNESP]Yuan, Judy Chia-ChunMathew, Mathew T.Amaral, Regiane C. doMesquita, Marcelo F.Silva, Wander J. daAssunção, Wirley G. [UNESP]2015-12-072015-12-072015-11-01Materials Science & Engineering. C, Materials For Biological Applications, v. 56, p. 114-124, 2015.1873-0191http://hdl.handle.net/11449/131678Although smoking promotes deleterious effect to bone healing, there is a lack of study investigating its role on the implant structure and biofilm growth. We hypothesized that nicotine, cotinine and caffeine would impair the corrosion resistance of commercially-pure titanium (cp-Ti) and would enhance Streptococcus sanguinis biofilm growth. Neither the smoking products nor the caffeine affected the corrosion tendency (P>.05) and the oxide layer resistance (P=.762) of cp-Ti. Lower capacitance values were noted in the presence of nicotine (P=.001) and cotinine (P=.0006). SEM showed no pitting corrosion, and the EDS spectra did not differ among groups. Nicotine (300μg/mL) induced higher surface roughness (P=.03) and greater surface change of cp-Ti. Nicotine at 3μg/mL, and cotinine at 0.3 and 3μg/mL increased the number of viable cells (P<.05). Biofilm exposed to nicotine (0.3, 3 and 30μg/mL) (P=.025, .030, .040, respectively) and cotinine (3 and 30μg/mL) (P=.027, .049, respectively) enhanced carbohydrate content. Biofilm biomass and protein content were similar among groups (P>.05). These findings suggest a greater biofilm accumulation in smokers, a risk factor that may lead to peri-implantitis.114-124engBiofilmCaffeineCorrosionCotinineDental implantsElectrochemistryNicotineArtigo10.1016/j.msec.2015.06.026Acesso restrito26249572