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WNT10A is a signaling molecule involved in tooth development, and WNT10A defects are associated with tooth agenesis. We characterized Wnt10a null mice generated by the knockout mouse project (KOMP) and six families with WNT10A mutations, including a novel p.Arg104Cys defect, in the absence of EDA,EDAR, or EDARADD variations. Wnt10a null mice exhibited supernumerary mandibular fourth molars, and smaller molars with abnormal cusp patterning and root taurodontism. Wnt10a (-/-) incisors showed distinctive apical-lingual wedge-shaped defects. These findings spurred us to closely examine the dental phenotypes of our WNT10A families. WNT10A heterozygotes exhibited molar root taurodontism and mild tooth agenesis (with incomplete penetrance) in their permanent dentitions. Individuals with two defective WNT10A alleles showed severe tooth agenesis and had fewer cusps on their molars. The misshapened molar crowns and roots were consistent with the Wnt10a null phenotype and were not previously associated with WNT10A defects. The missing teeth contrasted with the presence of supplemental teeth in the Wnt10a null mice and demonstrated mammalian species differences in the roles of Wnt signaling in early tooth development. We conclude that molar crown and root dysmorphologies are caused by WNT10A defects and that the severity of the tooth agenesis correlates with the number of defective WNT10A alleles.

Truncation mutations in FAM83H (family with sequence similarity 83, member H) cause autosomal dominant hypocalcified amelogenesis imperfecta ( ADHCAI), but little is known about FAM83H function and the pathogenesis of ADHCAI. We recruited three ADHCAI families and identified two novel (p.Gln457*; p.Lys639*) and one previously documented (p.Q452*) disease-causing FAM83H mutations. We generated and characterized Fam83h-knockout/ lacZ-knockin mice. Surprisingly, enamel thickness, density, Knoop hardness, morphology, and prism patterns were similar in Fam83h+/+, Fam83h+/−, and Fam83h−/− mice. The histology of ameloblasts in all stages of development, in both molars and incisors, was virtually identical in all three genotypes and showed no signs of pathology, although the Fam83h−/− mice usually died after 2 weeks and rarely survived to 7 weeks. LacZ expression in the knockin mice was used to report Fam83h expression in the epithelial tissues of many organs, notably in skin and hair follicles, which manifested a disease phenotype. Pull-down studies determined that FAM83H dimerizes through its N-terminal phospholipase D-like ( PLD-like) domain and identified potential FAM83H interacting proteins. Casein kinase 1 ( CK1) interacts with the FAM83H PLD-like domain via an F270-X-X-X-F274-X-X-X-F278 motif. CK1 can phosphorylate FAM83H in vitro , and many phosphorylation sites were identified in the FAM83H C-terminus. Truncation of FAM83H alters its subcellular localization and that of CK1. Our results support the conclusion that FAM83H is not necessary for proper dental enamel formation in mice, but may act as a scaffold protein that localizes CK1. ADHCAI is likely caused by gain-of-function effects mediated by truncated FAM83H, which potentially mislocalizes CK1 as part of its pathological mechanism. [ABSTRACT FROM AUTHOR]

The traditional method of preparing partial-stabilized cement (PSC), which is a kind of calcium silicate cement, is through power mixing method. Low reaction efficiency and initial strength limited the application of PSC as a dental root-end filling material. This study provides a one-step sol-gel process for the synthesis of PSC. A complexing ligand is used for tuning down the activity of aluminum sec-butoxide (ASB) in order to avoid possible self-polymerization. After the modification with complex ligand, there is no residue of reactant observed on the analysis of SDT, and bonding between metal atoms is observed in the FTIR spectrum. Each component of PSC is identified using XRD. The hydration product, which is called portlandite, of sol-gel-synthesized PSC is observed after 1 day of hydration, and crystallinity of portlandite increases much faster than that of traditional PSC. The initial strength of sol-gel-synthesized PSC achieves detectable level 24 h earlier than that of traditional PSC; microhardness value of sol-gel-synthesized PSC at 7th day is 2.98 HV, which is much higher than that of traditional PSC (2.05 HV). PSC is successfully synthesized and the initial strength of PSC is improved by this modified sol-gel process.

Laser ablation has been proposed as an alternative method to acid etching: however, previous studies have obtained contrasting results. The purpose of this study was to compare the bond strengths after acid etching, laser ablation, acid etching followed by laser ablation, and laser ablation followed by acid etching. Forty specimens were randomly assigned to one of the four groups. Two more specimens in each group did not undergo bond test and were prepared for observation with scanning electron microscope (SEM) after the four kinds of surface treatment. After the bond test, all specimens were inspected under the digital stereomicroscope and SEM to record the bond failure mode. Student's t-test results showed that the mean bond strength (13.0 +/- 2.4 N) of the laser group was not significantly different from that of the acid-etched group (11.8 +/- 1.8 N) (P > .05). However, this strength was significantly higher than that of the acid-etched then laser-ablated group (10.4 +/- 1.4 N) or that of the laser-ablated then acid-etched group (9.1 +/- 1.8 N). The failure modes occurred predominantly at the bracket-resin interface. Er:YAG laser ablation consumed less time compared with the acid-etching technique. Therefore, Er:YAG laser ablation can be an alternative tool to conventional acid etching.

Various glass ionomer cements (GICs) and resin-modified GICs are widely used as tooth-colored restorative materials. However, their potential effects on pulp tissues are not fully understood. In this study, the authors compared the toxicity of nine types of GICs on cultured human dental pulp cells. Exposure of pulp cells to GICs for five days led to differential growth inhibition as analyzed by 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. Exposure of pulp cells to ProTec CEM, Fuji II LC, Compoglass and GC Lining cement for five days decreased the cell numbers to 11%, 12%, 19% and 25%, respectively, of the control. Exposure of pulp cells to Fuji IX, GIC FX and Fuji II SC also decreased cell numbers by 62%, 33% and 24%, respectively. By contrast, Hy-Bond and Fuji I showed only mild suppression on the growth of pulp cells, with 12% and 16% decreased cell numbers. Morphologically, marked retraction and rounding of pulp cells were noted following exposure to GC Lining cement; in addition, cell surface blebbing was noted following exposure to Compoglass, Fuji II LC and ProTec CEM. Exposure of the pulp cells to Fuji II SC and Fuji IX, however, led to decreases in the cell density, with no obvious morphological changes. These results indicate that resin-modified GICs, such as Compoglass, Fuji II LC, ProTec CEM and GC Lining cements, are more toxic to pulp cells than conventional GICs. It is not recommended that resin-modified GICs be directly applied onto dental pulp cells. However, additional in vivo studies are needed to evaluate the potential toxicities of these resin-modified GICs during clinical operative procedures.