The mechanism responsible for hydrogenperoxide- or sodium-hypochlorite-induced reductions in dentin bond strength is unknown. This in vitro study tested the hypothesis that these oxidizing agents were responsible by attempting to reverse the effect with sodium ascorbate, a reducing agent. Human dentin was treated with these oxidants before or after being acid-etched and with or without post-treatment with sodium ascorbate. They were bonded with either Single Bond or Excite. Hydrogen peroxide reduced the bond strengths of both adhesives, while sodium hypochlorite produced reduction in adhesion of only Single Bond (p < 0.05). Following treatment with sodium ascorbate, reductions in bond strength were reversed. Transmission and scanning electron microscopy showed partial removal of the demineralized collagen matrix only by sodium hypochlorite. The observed compromised bond strengths cannot be attributed to incomplete deproteinization and may be related to changes in the redox potential of the bonding substrates.
Resin cement diffusion into dentin may differ as a function of the pre-treatment regimen. Since self-adhesive cements do not require substrate pre-treatment for luting, penetration of and interaction with the underlying dentin are questioned. We hypothesized that differences in the resin cement diffusion into dentin may exist among current commercial adhesive cements. Composite cylinders were luted on mid-coronal dentinal surfaces by an etch-and-rinse cement (Calibra), a self-etching system (Panavia F 2.0), and 4 self-adhesive cements (Multilink Sprint, Rely X Unicem, G-Cem, Bis-Cem). Dentin/cement interfacial characteristics were analyzed by a staining technique (Masson’s trichrome) and by scanning electron microscopy. Conventional acid etching resulted in partially infiltrated adhesive interfaces differing from those achieved with the application of self-etching primer. No hybrid layer and/or resin tag formation was detectable at the interfaces bonded with self-adhesive cements. Limited decalcification/infiltration was observed for self-adhesive cements into the underlying dentin. Self-adhesive cements were not able to demineralize/dissolve the smear layer completely.
Oxygen inhibits polymerization of resin-based materials. We hypothesized that compromised bonding to bleached enamel can be reversed with sodium ascorbate, an anti-oxidant. Sandblasted human enamel specimens were treated with distilled water (control) and 10% carbamide peroxide gel with or without further treatment with 10% sodium ascorbate. They were bonded with Single Bond (3M-ESPE) or Prime&Bond NT (Dentsply DeTrey) and restored with a composite. Specimens were prepared for microtensile bond testing and transmission electron microscopy after immersion in ammoniacal silver nitrate for nanoleakage evaluation. Bond strengths of both adhesives were reduced after bleaching but were reversed following sodium ascorbate treatment (P < 0.001). Resin-enamel interfaces in bleached enamel exhibited more extensive nanoleakage in the form of isolated silver grains and bubble-like silver deposits. Reduction of resin-enamel bond strength in bleached etched enamel is likely to be caused by a delayed release of oxygen that affects the polymerization of resin components.