Fluoride bioactive glass paste improves bond durability and remineralizes tooth structure prior to adhesive restoration

ObjectiveThe current study aimed at examining a fluoride containing bioactive glass (BiominF®) paste as a temporary filling material capable of remineralizing the demineralized enamel or dentin, and its ability to decrease a simulated dentinal fluids pressure on the resin/dentin interface, without affecting the shear bond strength of a universal bonding agent to enamel and dentin.Methods60 premolars were utilized for the acid resistance, trans-microradiography (TMR) and shear bond strength (SBS) experiments. Enamel and dentin discs were demineralized for 4 days to create a subsurface demineralized zone followed by applying BiominF® paste, 1.23% acidulated phosphate fluoride, or a temporary filling material for 24 h.30 extracted human non-carious third molars were utilized for the pulpal pressure experiment in which direct communication to the pulp chamber was created by cutting at a level approximately 1 mm below the cemento-enamel junction while the coronal enamel was ground to expose mid coronal dentin. The dentin surface was exposed to a simulated pulpal pressure. The dentin surfaces had BiominF® paste, an oxalate desensitizing agent, or temporary filling material followed by application of a universal adhesive system.ResultsOne way ANOVA showed that BiominF® paste remineralized effectively the demineralized enamel or dentin, did not affect the bond strength of the enamel and dentin surfaces to the tested adhesive system p < 0.05, and improved the acid resistance of the demineralized enamel and dentin against a secondary erosive challenge. Moreover, BiominF® paste decreased the nanoleakage expression in the dentin/adhesive interface exposed to a simulated pulpal pressure.SignificanceBiominF® paste may serve as a temporary filling material that may improve the longevity of adhesive restorations and help to conserve tooth structures by preserving the demineralized enamel and dentin form cutting during cavity preparation.     

Excitatory Synaptic Function and Plasticity is Persistently Altered in Ventral Tegmental Area Dopamine Neurons after Prenatal Ethanol Exposure

Prenatal ethanol exposure (PE) is one of the developmental factors leading to increased addiction propensity (risk). However, the neuronal mechanisms underlying this effect remain unknown. We examined whether increased excitatory synaptic transmission in ventral tegmental area (VTA) dopamine (DA) neurons, which is associated with drug addiction, was impacted by PE. Pregnant rats were exposed to ethanol (0 or 6 g/kg/day) via intragastric intubation from gestational day 8–20. Amphetamine self-administration, whole-cell recordings, and electron microscopy were performed in male offspring between 2 and 12-week-old. The results showed enhanced amphetamine self-administration in PE animals. In PE animals, we observed a persistent augmentation in calcium-permeable AMPA receptor (CP-AMPAR) expression, indicated by increased rectification and reduced decay time of AMPAR-mediated excitatory postsynaptic currents (AMPAR-EPSCs), enhanced depression of AMPAR-EPSCs by NASPM (a selective CP-AMPAR antagonist), and increased GluA3 subunits in VTA DA neuron dendrites. Increased CP-AMPAR expression in PE animals led to enhanced excitatory synaptic strength and the induction of CP-AMPAR-dependent long-term potentiation (LTP), an anti-Hebbian form of LTP. These observations suggest that, in PE animals, increased excitatory synaptic strength in VTA DA neurons might be susceptible to further strengthening even in the absence of impulse flow. The PE-induced persistent increase in CP-AMPAR expression, the resulting enhancement in excitatory synaptic strength, and CP-AMPAR-dependent LTP are similar to effects observed after repeated exposure to drugs of abuse, conditions known to increase addiction risk. Therefore, these mechanisms could be important neuronal substrates underlying PE-induced enhancement in amphetamine self-administration and increased addiction risk in individuals with fetal alcohol spectrum disorders.