In vitro caries inhibition effects by conventional and resin-modified glass-ionomer restorations

The ability of a material to inhibit recurrent caries formation is an important clinical therapeutic property. The objectives of this study were to develop an initial anticariogenicity profile (from fluoride release, to fluoride uptake, to resistance to an artificial caries challenge), testing the ability of conventional versus resin-modified glass-ionomer restorations to resist decay, and to study the effect of using intermediary dentin bonding agent components on the development of surface and wall carious lesions adjacent to a resin-modified glass-ionomer restoration. Cumulative fluoride release was measured from the immersion of disk-shaped specimens into deionized distilled water for 24 hours, 1, 2, 4, and 10 weeks. For the fluoride uptake and artificial caries test, standardized restorations were placed along the cementoenamel junction of extracted human molars. Secondary ion mass spectroscopy was used to determine the depth of fluoride uptake into the adjacent axial dentin from the restoration after 1 and 10 weeks. For the artificial caries test, the teeth were immersed into an acidified gelatin gel, pH 4.0, for 10 weeks. The development of recurrent decay was assessed using polarizing light microscopy. Statistical analyses were conducted using ANOVA and Fishers' LSD test (P < or = 0.05). There was generally greater fluoride release and uptake from the conventional glass ionomers, equivalent or less from the resin-modified glass ionomers, and none from the resin composite restorations. The use of an acid conditioner and primer from a dentin bonding system significantly increased the depth of fluoride uptake at 1 week. The additional use of an intermediary adhesive resin layer, however, significantly decreased the depth of fluoride uptake. The maximum depth of fluoride uptake into dentin was 300 microns at 10 weeks. Both conventional and resin-modified glass-ionomer restorations imparted resistance to dentin against the development of recurrent wall carious lesions in vitro. This was attributed to material fluoride release and uptake.