The Impact of Nicotine and Cigarette Smoke Condensate on Metabolic Activity and Biofilm Formation of Candida albicans on Acrylic Denture Material.

Abstract

Smokers have increased denture stomatitis caused primarily by Candida albicans. The primary aim of this study was to demonstrate the impact of a wide range of nicotine and cigarette smoke condensate (CSC) concentrations on biofilm formation and metabolic activity of C. albicans on acrylic denture material. C. albicans (ATCC strain 10231) was used. Standardized denture acrylic (PMMA) specimens (total of 135 specimens) were incubated with C. albicans and exposed to nicotine and CSC at different concentrations (0, 0.25, 0.5, 1, 2, 4, 8, 16, and 32mg/ml) and (0, 0.25, 0.5, 1, 2, and 4mg/ml), respectively. For each experiment, 3 samples per nicotine and CSC concentration and a total of 45 specimens (27 specimens for the nicotine and 18 specimens for the CSC-treated samples) were used and were selected randomly for each group. The control group consisted of 0mg/ml of nicotine or CSC. The viability of C. albicans was measured using spiral plating on blood agar plates. The effect of nicotine and CSC concentrations on planktonic cells was were measured using a microplate reader. Metabolic activity of 24-hour-old established C. albicans biofilm exposed to nicotine and CSC for 24hours in microtiter plates was determined using a 2,3-bis (2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-carboxanilide (XTT) reduction assay. The viability of C. albicans increased concomitant with increasing concentrations of CSC and nicotine, particularly at 0.5 and 2mg/ml, respectively. Concentrations of CSC and nicotine above this resulted in an inhibitory effect on C. albicans viability. CSC and nicotine at 4 and 16mg/ml, respectively, increased C. albicans biofilm metabolic activity. Nicotine and CSC up to certain concentrations caused increases in biofilm formation, metabolic activity, viability, and planktonic cell absorbance of C. albicans. This in vitro study demonstrates the effectiveness of tobacco on promoting the growth of C. albicans and suggests their potential contributing factor in C. albicans biofilm related infections in smokers.