Search

A tricalcium-silicate-nanoparticle-containing cement (Biodentine) was developed to overcome the disadvantages of existing mineral trioxide aggregate (MTA) dental materials. This study aimed at evaluating the effects of Biodentine on the osteogenic differentiation of human periodontal ligament fibroblasts (HPLFs) in vitro and the healing of furcal perforations created experimentally in rat molars in vivo, in comparison to MTA. The in vitro studies performed the following assays: pH measurement using a pH meter, the release of calcium ions using a calcium assay kit, cell attachment and morphology using SEM, cell proliferation using a coulter counter, marker expression using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and cell mineralized deposit formation using Alizarin Red S (ARS) staining. In the in vivo studies, MTA and Biodentine were used to fill the rat molar perforations. Rat molars were processed at 7, 14 and 28 days for analysis of inflammatory processes using hematoxylin and eosin (HE) staining, immunohistochemical staining of Runx2 and tartrate-resistant acid phosphate (TRAP) staining. The results demonstrate that the nanoparticle size distribution of Biodentine is critical for osteogenic potential at an earlier stage compared to MTA. Further studies are required to elucidate the mechanism of action of Biodentine in osteogenic differentiation. [ABSTRACT FROM AUTHOR]

Odontoblasts are involved in sensory generation as sensory receptor cells and in dentin formation. We previously reported that an increase in intracellular cAMP levels by cannabinoid 1 receptor activation induces Ca2+ influx via transient receptor potential vanilloid subfamily member 1 channels in odontoblasts, indicating that intracellular cAMP/Ca2+ signal coupling is involved in dentinal pain generation and reactionary dentin formation. Here, intracellular cAMP dynamics in cultured human odontoblasts were investigated to understand the detailed expression patterns of the intracellular cAMP signaling pathway activated by the Gs protein-coupled receptor and to clarify its role in cellular functions. The presence of plasma membrane Gαs as well as prostaglandin I2 (IP), 5-hydroxytryptamine 5-HT4 (5-HT4), dopamine D1 (D1), adenosine A2A (A2A), and vasoactive intestinal polypeptide (VIP) receptor immunoreactivity was observed in human odontoblasts. In the presence of extracellular Ca2+, the application of agonists for the IP (beraprost), 5-HT4 (BIMU8), D1 (SKF83959), A2A (PSB0777), and VIP (VIP) receptors increased intracellular cAMP levels. This increase in cAMP levels was inhibited by the application of the adenylyl cyclase (AC) inhibitor SQ22536 and each receptor antagonist, dose-dependently. These results suggested that odontoblasts express Gs protein-coupled IP, 5-HT4, D1, A2A, and VIP receptors. In addition, activation of these receptors increased intracellular cAMP levels by activating AC in odontoblasts. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate whether atmospheric-pressure plasma (APP) or ultraviolet (UV) irradiation could alter the hydrophilicity of a computer-aided design/computer-aided manufacturing (CAD/CAM) glass ceramic surface, and thereby enhance the repair bond strength between the ceramic and a resin composite. Forty-eight leucite-reinforced glass ceramic discs were treated with 40% phosphoric acid and randomly assigned into one of six groups: Group 1, control; Group 2, treated with a mixture of Clearfil SE Bond primer (SEP) and Clearfil Porcelain Bond Activator (PBA); Group 3, subjected to APP irradiation for 10 s; Group 4, subjected to UV irradiation for 60 min; Group 5, APP irradiation followed by SEP/PBA; and Group 6, UV irradiation followed by SEP/PBA. After treatment, discs were bonded with resin composite using Clearfil SE Bond and stored in water at 37 °C for 1 week. We then tested how these treatments affected the microtensile bond strength (µTBS) and measured changes in the water contact angle (CA). Samples from Group 2 showed the highest µTBS (44.3 ± 6.0 MPa) and CA (33.8 ± 2.3°), with no significant differences measured between Groups 1, 3, and 4 (p < 0.05). Furthermore, the additional treatments of APP or UV before SEP/PBA had no effect (Group 5, p = 0.229) or a reduced effect (Group 6, p = 0.006), respectively, on µTBS. Overall, APP or UV irradiation before SEP/PBA treatment did not enhance the repair bond strength. [ABSTRACT FROM AUTHOR]