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.

Water sorption into resin-dentin interfaces precedes hydrolytic degradation. We hypothesized that these processes are morphologically manifested by the uptake of ammoniacal silver nitrate, which is thought to trace hydrophilic domains and water-filled channels within matrices. Water sorption is thought to be nonuniform and can be traced by the use of silver nitrate. Human teeth bonded with an experimental filled-adhesive were aged in artificial saliva (experimental) or non-aqueous mineral oil (control). Specimens retrieved for up to a 12-month period were immersed in 50 wt% ammoniacal silver nitrate and examined by transmission electron microscopy for identification of the changes in their silver uptake. Reticular silver deposits initially identified within the bulk of hybrid layers in the experimental group were gradually reduced over time, but were subsequently replaced by similar deposits that were located along the hybrid layer-adhesive interface. Silver uptake in water-binding domains of the adhesive layers increased with aging, resulting in water tree formation. These water-filled channels may act as potential sites for hydrolytic degradation of resin-dentin bonds.

The survival of the vital pulp in teeth restored with a single-unit CMC was significantly higher than those serving as an abutment of a fixed-fixed bridge. Maxillary anterior teeth used as bridge abutments had a higher rate of pulpal necrosis than any other tooth types.

Compromised bonding of total-etch adhesives to dentin treated with oxalate desensitizers results from the interference of a surface layer of acid-resistant crystals of calcium oxalate. We hypothesize that effective tubular occlusion and dentin bonding may be simultaneously achieved by depleting dentin surfaces of calcium with acids before desensitizer application. Dentin specimens treated with 4 oxalate desensitizers before or after being acid-etched were bonded with a two-step adhesive. Microtensile bond strengths ( micro TBS) were significantly lower, compared with the control, when oxalates were used before the specimens were acid-etched; in contrast, when oxalates were used after acid-etching. micro TBS were similar to nonoxalate-treated controls. Dentin surfaces and tubular orifices were covered with a surface layer of crystals when desensitizers were applied to fractured dentin and smear-layer-covered dentin before specimens were acid-etched. However, when the dentin was acid-etched prior to the application of oxalate desensitizers, the crystals were largely limited to the subsurface of dentinal tubules, where they did not interfere with subsequent resin bonding.

No abstract

The mechanism responsible for sodium-hypochlorite-induced reduction in dentin bond strength and its reversal with reducing agents is unknown. This study examined the relationship between nanoleakage and reversal of compromised bonding to oxidized dentin. Acid-etched dentin was completely depleted of demineralized collagen matrix when sodium hypochlorite was used. Specimens were bonded with two single-bottle dentin adhesives. They were immersed in ammoniacal silver nitrate for 24 hrs before being processed for transmission electron microscopy. For both adhesives, tensile bond strengths of acid-etched dentin were significantly reduced after sodium hypochlorite treatment, but were reversed when sodium ascorbate was used. After sodium hypochlorite application, reticular nanoleakge patterns in hybrid layers were replaced by vertical, shag-carpet-like patterns along the demineralization front. This type of nanoleakage was completely eliminated after sodium ascorbate treatment with the materials tested. Residual sodium hypochlorite within the porosities of mineralized dentin may result in incomplete resin polymerization, and hence compromised bond strength.