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The effect of post-space treatment on the retention of fiber posts in different root regions was evaluated using two self-etching systems. Post spaces were prepared in extracted premolars and then the root canals were subjected to one of the following post-space treatments: (i) water irrigation (control); (ii) etching with 35% phosphoric acid for 30 s; (iii) irrigation with 17% EDTA followed by 5.25% sodium hypochlorite (NaOCl); and (iv) ultrasonic agitation associated with 17% EDTA and 5.25% NaOCl irrigating solutions. The dentin surfaces were examined under scanning electron microscopy (SEM) after different post-space treatments. Fiber posts were then luted in the treated roots using resin cement with either Clearfil SE Bond or Clearfil DC Bond, and the thin-slice push-out test was performed. Scanning electron microscopy showed that all the post-space treatments tested were effective in removal of the smear layer of debris, or sealer/gutta-percha remnants, on the root canal. The apical push-out strength was affected by post-space treatment. Both 35% phosphoric acid etching and ultrasonic agitation in combination with EDTA/NaOCl irrigation improved the apical push-out strength of the fiber post, regardless of the type of self-etching system. A solo irrigation with an EDTA/NaOCl solution resulted in a lower apical push-out strength compared with the other two experimental groups.

Highlights d FiNad responds to subtle changes of NAD + metabolism in live cells and animals d The role of NAD + precursors in boosting NAD + levels is mapped in various organisms d Increased NAD + synthesis controls morphofunctional changes of activated macrophages d FiNad enables live-cell and in vivo imaging of NAD + decline during aging

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PurposeTo investigate the involvement of intrinsic mitochondrial apoptosis in dental monomer-induced cytotoxicity and the influences of N-acetyl cysteine (NAC) on this process.MethodsHuman dental pulp cells (hDPCs) were exposed to several dental monomers in the absence or presence of NAC, and cell viability, intracellular redox balance, morphology and function of mitochondria and key indicators of intrinsic mitochondrial apoptosis were evaluated using various commercial kits.ResultsDental monomers exerted dose-dependent cytotoxic effects on hDPCs. Concomitant to the over-production of reactive oxygen species (ROS) and depletion of glutathione (GSH), differential changes in activities of superoxide dismutase, glutathione peroxidase, and catalase were detected. Apoptosis, as indicated by positive Annexin V/propidium iodide (PI) staining and activation of caspase-3, was observed after dental monomer treatment. Dental monomers impaired the morphology and function of mitochondria, and induced intrinsic mitochondrial apoptosis in hDPCs via up-regulation of p53, Bax and cleaved caspase-3, and down-regulation of Bcl-2. NAC restored cell viability, relieved oxidative stress and blocked the apoptotic effects of dental monomers.ConclusionsDental monomers induced oxidative stress and mitochondrial intrinsic apoptosis in hDPCs. NAC could reduce the oxidative stress and thus protect hDPCs against dental monomer-induced apoptosis.