Antibacterial activity of resin composites containing surface pre-reacted glass-ionomer (S-PRG) filler

Abstract

ObjectiveA surface pre-reacted glass-ionomer (S-PRG) filler is a technology of interest for providing bio-functions to restorative materials. Resin composites containing S-PRG filler have been reported to show less plaque accumulation and reduced bacterial attachment. In this study, experimental resin composites containing S-PRG filler at various concentrations were fabricated, and the inhibitory effects on bacterial growth on their surface and the association of ions released from S-PRG filler with antibacterial activity were evaluated. MethodsFive kinds of experimental resin composites containing S-PRG filler at 0, 13.9, 27.3, 41.8, or 55.9 (vol.%) were fabricated. Streptococcus mutans was cultured on the cured discs for 18h to examine the growth of bacteria in contact with the surface of the experimental resins. The concentrations of Al3+, BO33−, F−, Na+, SiO32−, or Sr2+ released from each experimental resin into water were measured. The standardized solutions of each ion were prepared at the concentrations determined to be released from the experimental resin, and their inhibitory effects of single ion species on S. mutans growth were evaluated by using each standardized solution. ResultsResin composites containing S-PRG filler at 13.9 (vol.%) or greater inhibited S. mutans growth on their surface. When S. mutans was incubated in the presence of six kinds of ions at the concentrations released from the resin composite containing S-PRG filler at 55.9 (vol.%), a significant reduction in bacterial number was observed for BO33−, F−, Al3+, and SiO32−. Among these four ions, BO33− and F− demonstrated the strongest inhibitory effect on S. mutans growth. SignificanceOur findings suggest that resin composites containing S-PRG filler inhibit the growth of S. mutans on their surface. BO33−, F−, Al3+ and SiO32− released from S-PRG filler have the ability to inhibit S. mutans growth, and the inhibitory effects are mainly attributed to release of BO33− and F−.