Methods: S. mutans UA159 was treated with nicotine (0-8 mg/ml), EGCG (0.25 mg/ml), and ECG (0.25 mg/ml) in combination with and without nicotine. Growth effects were measured kinetically in microtiter plates over a 12 h period. Lag time, time to maximal absorbance (Tmax), maximal absorbance, and maximal velocity (Vmax) of planktonic cells were measured. Biofilm formation was measured using a crystal violet dye staining assay.
Results: S. mutans exposed to nicotine and EGCG demonstrated significantly increased Tmax (0-1 mg/ml of nicotine; p < 0.05) and a decrease in Vmax (0-1 mg/ml) in planktonic cells. S. mutans exposed to ECG and nicotine displayed an increase in Tmax (0.25-1 mg/ml) and a decrease in Vmax (0- 2 mg/ml). Biofilm formation of S. mutans with EGCG and nicotine exhibited a decrease in biofilm formation at 0.25, 1, 2, and 4 mg/ml of nicotine and an increase in biofilm formation at 0.5 mg/ml of nicotine. Biofilm formation of S. mutans with ECG and nicotine demonstrated that ECG abrogates nicotine’s effect on S. mutans growth (0.25-4 mg/ml).
Conclusions: These results suggest that both EGCG and ECG slowed the growth of planktonic S. mutans with no nicotine and at low concentrations of nicotine. EGCG exhibited a biphasic response on biofilm formation. ECG diminished nicotine’s stimulatory effect on S. mutans in biofilm formation. This study provides evidence for the beneficial aspects of tea polyphenols on S. mutans treated with nicotine.
Keywords: Antimicrobial agents/inhibitors, Caries, Microbiology and Tobacco