The mechanism responsible for hydrogen-peroxide- 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.
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.
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.
Er-YAG laser irradiation has been claimed to improve the adhesive properties of dentin. We tested the hypothesis that dentin adhesion is affected by Er-YAG laser conditioning. Superficial or deep dentin from human molars was: (a) acid-etched with 35% H3PO4; (b) irradiated with an Er-YAG laser (KaVo) at 2 Hz and 180 mJ, with water-cooling; and (c) laser- and acid-etched. Single Bond (3M ESPE) and Z100 composite (3M ESPE) were bonded to the prepared surfaces. After storage, specimens were tested in shear to failure. Bonded interfaces were demineralized in EDTA and processed for transmission electron microscopy. Two-way ANOVA revealed that conditioning treatment and interaction between treatment and dentin depth significantly influenced shear bond strength results. Acid-etching alone yielded shear bond strength values that were significantly higher than those achieved with laser ablation alone, or in combination with acid-etching. The Er-YAG laser created a laser-modified layer that adversely affects adhesion to dentin, so it does not constitute an alternative bonding strategy to conventional acid etching.
Dentin matrix metalloproteinases (MMPs) are involved in collagen degradation of resin-dentin interfaces. This study evaluated if collagen degradation can be prevented by chlorhexidine after different dentin demineralization procedures. Human dentin demineralization was performed with phosphoric acid (PA), EDTA, or acidic monomers (ClearfilSEBond and XENOV). Specimens were stored (24 h, 1 wk or 3 wk) in the presence or absence of chlorhexidine. In half of the groups, active MMP-2 was incorporated into the storing solution. C-terminal telopeptide determination (ICTP) was performed in the supernatants. Collagen degradation was higher in PA and EDTA-demineralized dentin. Chlorhexidine reduced collagen degradation in these groups only for 24 h. When dentin was demineralized with SEBond or Xeno, collagen degradation was reduced up to 30%, but addition of exogenous MMP-2 significantly increased collagen degradation. In self-etchant treated dentin the inhibitory effect of chlorhexidine on MMPs lasted up to 3 wk. Treating dentin with EDTA, PA or self-etching agents produces enough demineralization to permit cleavage of the exposed collagen. Monomers infiltration may exert protection on demineralized collagen, probably through immobilization of MMPs. The partial inhibitory action of CHX on MMP activity produced by self-etching adhesives was prolonged compared to the short-acting in PA or EDTA-treated dentin.
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