Evaluation of hypermobile teeth deviation during impression taking in a partially edentulous dental arch: An in vitro study comparing digital and conventional impression techniques.

PURPOSE: This study aimed to compare the deviation of hypermobile teeth in partially edentulous dental arches during impression taking using digital and conventional techniques. METHODS: A partially edentulous mandibular model with three target hypermobile teeth (including the left first premolar, #34; left second molar, #37; and right first premolar, #44), was used as the simulation model. After reference data were acquired using a desktop scanner, impressions of the simulation model were obtained using a digital intraoral scanner (IOS) and two conventional techniques (hydrocolloid material with a stock tray and silicone material with a custom tray as impression data (n=12/group). The three-dimensional accuracy (root mean square value) and two-dimensional accuracy (mesiodistal and buccolingual displacements) of the target teeth in each impression dataset were calculated based on the reference data. The comparison among three impression techniques was statistically performed using the Kruskal-Wallis test (α=0.05). RESULTS: For #34 and #44, the three- and two-dimensional accuracies of the impressions fabricated through data acquired through digital scanning (digital impression) were significantly superior to those of the hydrocolloid impression (P < 0.05), whereas no significant difference was found between the digital and silicone impressions. For #37, no significant difference in the accuracy of the impression data for the target teeth was observed among the three impression techniques. CONCLUSIONS: Digital impression acquiring using an IOS is recommended over using a conventional hydrocolloid impression to prevent the deviation of hypermobile teeth in partially edentulous dental arches. Hypermobile tooth deviation in digital impression data depends on the tooth location.

GPR110, a receptor for synaptamide, expressed in osteoclasts negatively regulates osteoclastogenesis.

Bone remodeling is precisely regulated mainly by osteoblasts and osteoclasts. Although some G-protein coupled receptors (GPCRs) were reported to play roles in osteoblast function, little is known about the roles in osteoclasts. In this study, we found, for the first time, that the expression of GPR110 increased during osteoclastogenesis. GPR110 belongs to adhesion GPCR and was the functional receptor of N-docosahexaenoyl ethanolamine (also called synaptamide). Synaptamide suppressed osteoclastogenesis induced by receptor activator of nuclear factor-kappa B ligand. Considering that synaptamide is the endogenous metabolite of DHA, we hypothesized that DHA may inhibit osteoclastogenesis by affecting synaptamide/GPR110 signaling. But GPR110 knockout and subsequent rescue experiments revealed a pivotal role of GPR110 in the attenuation of osteoclastogenesis by synaptamide but not by DHA. These results suggest that synaptamide/GPR110 signaling negatively regulates osteoclastogenesis. Our study suggested that ligands of GPR110, such as synaptamide, might be a useful drug for osteoporotic patients.

Mechanotransduction via the Piezo1-Akt pathway underlies Sost suppression in osteocytes.

Osteocytes function as critical regulators of bone homeostasis by coordinating the functions of osteoblasts and osteoclasts, and are constantly exposed to mechanical force. However, the molecular mechanism underlying the mechanical signal transduction in osteocytes is not well understood. Here, we found that Yoda1, a selective Piezo1 agonist, increased intracellular calcium mobilization and dose-dependently decreased the expression of Sost (encoding Sclerostin) in the osteocytic cell line IDG-SW3. We also demonstrated that mechanical stretch of IDG-SW3 suppressed Sost expression, a result which was abrogated by treatment with the Piezo1 inhibitor GsMTx4, and the deficiency of Piezo1. Furthermore, the suppression of Sost expression was abolished by treatment with an Akt inhibitor. Taken together, these results indicate that the activation of the Piezo1-Akt pathway in osteocytes is required for mechanical stretch-induced downregulation of Sost expression.