Erbium:yttrium-aluminum-garnet (Er:YAG) laser preparation of tooth cavities for restoration is an increasingly popular method, but its compatibility with existing composite material bonding protocols has not been fully defined. This study evaluated the effect of laser and etchant pretreatments on the performance of one-bottle self-etch adhesives in Er:YAG laser-prepared dentin. Eight groups of 20 extracted teeth were established to investigate bonding in tested dentin disks. Various combinations of laser preparation (with/without), pretreatment (none/acid-etch/low-fluence Er:YAG irradiation), and self-etching adhesive (G-Bond Plus or Xeno V) were tested. Samples were then restored with composite resin and subjected to a tensile bond strength (TBS) test. We also performed scanning electron microscopy (SEM) on dentin disks from some of these groups before and after adhesive application to evaluate their microscopic morphological appearance. Statistical analysis (Dunnett T3 test coupled with the general linear model at 5% significance level) revealed that the laser preparation of dentin did not impact on TBS (p = 0.914), whereas pretreatment with either phosphoric acid (p < 0.0001) or low-fluence Er:YAG laser irradiation (p < 0.0001) significantly increased TBS, although there was no difference between them in their respective elevation of TBS. SEM analysis demonstrated that both acid and laser pretreatments reduced irregularities and produced a more homogeneous surface. Er:YAG laser preparation does not compromise the efficacy of one-step self-etch dentin adhesives, and pretreatment with phosphoric acid or low-fluence Er:YAG laser can significantly increase the TBS of adhesion to this irradiated dentin.

This study aimed to investigate the interaction of current one-bottle self-etching adhesives and Er:YAG laser with dentin using a tensile bond strength (TBS) test and scanning electron microscopy (SEM) in vitro. Two hundred and thirteen dentin discs were randomly distributed to the Control Group using bur cutting and to the Laser Group using an Er:YAG laser (200 mJ, VSP, 20 Hz). The following adhesives were investigated: one two-step total-etch adhesive [Prime & Bond NT (Dentsply)] and four one-step self-etch adhesives [G-Bond plus (GC), XENO V (Dentsply), iBond Self Etch (Heraeus) and Adper Easy One (3 M ESPE)]. Samples were restored with composite resin, and after 24-hour storage in distilled water, subjected to the TBS test. For morphological analysis, 12 dentin specimens were prepared for SEM. No significant differences were found between the control group and laser group (p = 0.899); dentin subjected to Prime & Bond NT, XENOV and Adper Easy One produced higher TBS. In conclusion, this study indicates that Er:YAG laser-prepared dentin can perform as well as bur on TBS, and some of the one-step one-bottle adhesives are comparable to the total-etch adhesives in TBS on dentin.

Objective: The study aimed to evaluate the ability of optical coherence tomography (OCT) to guide and identify pulp exposure using an erbium: yttrium-aluminum-garnet (Er:YAG) laser.

Organogenesis, including renal development, requires an appropriate retinoic acid concentration, which is established by differential expression of aldehyde dehydrogenase 1 family member A2 (ALDH1A2) and cytochrome P450 family 26 subfamily A/B/C member 1 (CYP26A1/B1/C1). In the fetal kidney, ALDH1A2 expresses in the developing stroma and renal vesicle and its derivatives but does not present in the ureteric bud. It remains unclear what may contribute to this expression pattern. Here we show that the glycogen synthase kinase 3 alpha/beta (GSK3A/B) inhibitor CHIR99021 significantly represses ALDH1A2 expression in WiT49, which is a Wilms' tumor cell line that exhibits "triphasic" differential potential and is used as a fetal kidney cell model. CHIR99021 fails to suppress ALDH1A2 as β-catenin is inhibited, suggesting that the downregulation of ALDH1A2 by CHIR99021 is through Wnt/β-catenin signaling. Ectopic expression of mouse Wnt1, Wnt3a, Wnt4, and Wnt9b represses ALDH1A2 expression in WiT49 cells. Using immunohistochemistry, we show an inverse correlation of Aldh1a2 expression with β-catenin in rat E18.5 kidney. ChIP demonstrated that β-catenin is recruited to the ALDH1A2 promoter, the conserved intron1G, and another site within intron 1 of ALDH1A2. Using a luciferase assay, we further show that the ALDH1A2 promoter and the intron1G element are involved in the repression of ALDH1A2 expression by CHIR99021. Our work demonstrates that ALDH1A2 expression can be directly repressed by the Wnt/β-catenin signaling in fetal kidney cells, suggesting that Wnt/β-catenin may play a role in maintaining the expression pattern of ALDH1A2 in the fetal kidney, thus controlling the availability and localization of retinoic acid and regulating aspects of kidney development.