Background The purpose of this study was to evaluate the treatment effectiveness of Carriere Distalizer in comparison to Class II intermaxillary elastics and Forsus. Methods Three groups of patients treated with Class II intermaxillary elastics ( n = 18), Carriere Distalizer ( n = 18), and Forsus appliance ( n = 18) were collected from three private orthodontic practices. Inclusion criteria were as follows: (1) 10–14 years old of start age with permanent dentition, (2) no history of previous orthodontic treatment, (3) complete pre- and post-treatment records, (4) dental Class II division 1 (end-to-end or more), (5) no pre-treatment transverse discrepancy, (6) non-extraction treatment plan, and (7) Class I post-treatment occlusal relationship. The data consisted of cephalometric and study model measurements from pre- and post-treatment records and treatment time. Two-tail Student t test was used to analyze the differences in cephalometric changes and dental corrections between Carriere Distalizer group and Class II elastics/Forsus group. Results All three groups of patients showed no differences in the age of treatment initiation, pre-treatment cephalometric measurements and discrepancy index (DI). The time of Class II correction for Carriere Distalizer was significantly shorter than that for Class II elastics; there was no difference in the length of Class II correction between Carriere Distalizer and Forsus groups. The amount of Class II correction (canine/molar relationship) was significantly lower for Carriere Distalizer when compared with Forsus appliance. Carriere Distalizer, similarly to Class II elastics, did not induce any statistically significant correction in skeletal component (ANB and Wits appraisal). Conclusions There is no clinically significant skeletal correction induced by Carriere Distalizer in growing patients. Carriere Distalizer can be applied to treatment of mild to moderate Class II dental malocclusion over 6 months on average, although the total treatment time may be prolonged due to various side effects. Overall, the Carriere Distalizer appears to be no more effective or efficient than alternatives in the treatment of Class II malocclusion.

BackgroundIn the rodent incisor during amelogenesis, as ameloblast cells transition from secretory stage to maturation stage, their morphology and transcriptome profiles change dramatically. Prior whole genome transcriptome analysis has given a broad picture of the molecular activities dominating both stages of amelogenesis, but this type of analysis has not included miRNA transcript profiling. In this study, we set out to document which miRNAs and corresponding target genes change significantly as ameloblasts transition from secretory- to maturation-stage amelogenesis.ResultsTotal RNA samples from both secretory- and maturation-stage rat enamel organs were subjected to genome-wide miRNA and mRNA transcript profiling. We identified 59 miRNAs that were differentially expressed at the maturation stage relative to the secretory stage of enamel development (False Discovery Rate (FDR) < 0.05, fold change (FC) ≥ 1.8). In parallel, transcriptome profiling experiments identified 1,729 mRNA transcripts that were differentially expressed in the maturation stage compared to the secretory stage (FDR < 0.05, FC ≥1.8). Based on bioinformatics analyses, 5.8% (629 total) of these differentially expressed genes (DEGS) were highlighted as being the potential targets of 59 miRNAs that were differentially expressed in the opposite direction, in the same tissue samples. Although the number of predicted target DEGs was not higher than baseline expectations generated by examination of stably expressed miRNAs, Gene Ontology (GO) analysis showed that these 629 DEGS were enriched for ion transport, pH regulation, calcium handling, endocytotic, and apoptotic activities. Seven differentially expressed miRNAs (miR-21, miR-31, miR-488, miR-153, miR-135b, miR-135a and miR298) in secretory- and/or maturation-stage enamel organs were confirmed by in situ hybridization. Further, we used luciferase reporter assays to provide evidence that two of these differentially expressed miRNAs, miR-153 and miR-31, are potential regulators for their predicated target mRNAs, Lamp1 (miR-153) and Tfrc (miR-31).ConclusionsIn conclusion, these data indicate that miRNAs exhibit a dynamic expression pattern during the transition from secretory-stage to maturation-stage tooth enamel formation. Although they represent only one of numerous mechanisms influencing gene activities, miRNAs specific to the maturation stage could be involved in regulating several key processes of enamel maturation by influencing mRNA stability and translation.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-998) contains supplementary material, which is available to authorized users.

The bicarbonate transport activities of Slc26a1, Slc26a6 and Slc26a7 are essential to physiological processes in multiple organs. Although mutations of Slc26a1, Slc26a6 and Slc26a7 have not been linked to any human diseases, disruption of Slc26a1, Slc26a6 or Slc26a7 expression in animals causes severe dysregulation of acid-base balance and disorder of anion homeostasis. Amelogenesis, especially the enamel formation during maturation stage, requires complex pH regulation mechanisms based on ion transport. The disruption of stage-specific ion transporters frequently results in enamel pathosis in animals. Here we present evidence that Slc26a1, Slc26a6 and Slc26a7 are highly expressed in rodent incisor ameloblasts during maturation-stage tooth development. In maturation-stage ameloblasts, Slc26a1, Slc26a6 and Slc26a7 show a similar cellular distribution as the cystic fibrosis transmembrane conductance regulator (Cftr) to the apical region of cytoplasmic membrane, and the distribution of Slc26a7 is also seen in the cytoplasmic/subapical region, presumably on the lysosomal membrane. We have also examined Slc26a1 and Slc26a7 null mice, and although no overt abnormal enamel phenotypes were observed in Slc26a1 -/- or Slc26a7 -/- animals, absence of Slc26a1 or Slc26a7 results in up-regulation of Cftr, Ca2, Slc4a4, Slc4a9 and Slc26a9, all of which are involved in pH homeostasis, indicating that this might be a compensatory mechanism used by ameloblasts cells in the absence of Slc26 genes. Together, our data show that Slc26a1, Slc26a6 and Slc26a7 are novel participants in the extracellular transport of bicarbonate during enamel maturation, and that their functional roles may be achieved by forming interaction units with Cftr.

Calcium export is a key function for the enamel organ during all stages of amelogenesis. Expression of a number of ATPase calcium transporting, plasma membrane genes (ATP2B1-4/PMCA1-4), solute carrier SLC8A genes (sodium/calcium exchanger or NCX1-3), and SLC24A gene family members (sodium/potassium/calcium exchanger or NCKX1-6) have been investigated in the developing enamel organ in earlier studies. This paper reviews the calcium export pathways that have been described and adds novel insights to the spatiotemporal expression patterns of PMCA1, PMCA4, and NCKX3 during amelogenesis. New data are presented to show the mRNA expression profiles for the four Atp2b1-4 gene family members (PMCA1-4) in secretory-stage and maturation-stage rat enamel organs. These data are compared to expression profiles for all Slc8a and Slc24a gene family members. PMCA1, PMCA4, and NCKX3 immunolocalization data is also presented. Gene expression profiles quantitated by real time PCR show that: (1) PMCA1, 3, and 4, and NCKX3 are most highly expressed during secretory-stage amelogenesis; (2) NCX1 and 3, and NCKX6 are expressed during secretory and maturation stages; (3) NCKX4 is most highly expressed during maturation-stage amelogenesis; and (4) expression levels of PMCA2, NCX2, NCKX1, NCKX2, and NCKX5 are negligible throughout amelogenesis. In the enamel organ PMCA1 localizes to the basolateral membrane of both secretory and maturation ameloblasts; PMCA4 expression is seen in the basolateral membrane of secretory and maturation ameloblasts, and also cells of the stratum intermedium and papillary layer; while NCKX3 expression is limited to Tomes' processes, and the apical membrane of maturation-stage ameloblasts. These new findings are discussed in the perspective of data already present in the literature, and highlight the multiplicity of calcium export systems in the enamel organ needed to regulate biomineralization.

Amelogenesis (tooth enamel formation) is a biomineralization process consisting primarily of two stages (secretory stage and maturation stage) with unique features. During the secretory stage, the inner epithelium of the enamel organ (i.e., the ameloblast cells) synthesizes and secretes enamel matrix proteins (EMPs) into the enamel space. The protein-rich enamel matrix forms a highly organized architecture in a pH-neutral microenvironment. As amelogenesis transitions to maturation stage, EMPs are degraded and internalized by ameloblasts through endosomal-lysosomal pathways. Enamel crystallite formation is initiated early in the secretory stage, however, during maturation stage the more rapid deposition of calcium and phosphate into the enamel space results in a rapid expansion of crystallite length and mineral volume. During maturation-stage amelogenesis, the pH value of enamel varies considerably from slightly above neutral to acidic. Extracellular acid-base balance during enamel maturation is tightly controlled by ameloblast-mediated regulatory networks, which include significant synthesis and movement of bicarbonate ions from both the enamel papillary layer cells and ameloblasts. In this review we summarize the carbonic anhydrases and the carbonate transporters/exchangers involved in pH regulation in maturation-stage amelogenesis. Proteins that have been shown to be instrumental in this process include CA2, CA6, CFTR, AE2, NBCe1, SLC26A1/SAT1, SLC26A3/DRA, SLC26A4/PDS, SLC26A6/PAT1, and SLC26A7/SUT2. In addition, we discuss the association of miRNA regulation with bicarbonate transport in tooth enamel formation.

IntroductionThis systematic review evaluated the use of buffered versus non-buffered lidocaine to increase the efficacy of inferior alveolar nerve block (IANB).Materials and MethodsRandomized, double-blinded studies from PubMed, Web of Science, Cochrane Library, Embase, and ProQuest were identified. Two of the authors assessed the studies for risk of bias. Outcomes included onset time, injection pain on a visual analog scale (VAS), percentage of painless injections, and anesthetic success rate of IANB.ResultsThe search strategy yielded 19 references. Eleven could be included in meta-analyses. Risk of bias was unclear in ten and high in one study. Buffered lidocaine showed 48 seconds faster onset time (95% confidence interval [CI], −42.06 to −54.40; P < 0.001) and 5.0 units lower (on a scale 0–100) VAS injection pain (95% CI, −9.13 to −0.77; P=0.02) than non-buffered. No significant difference was found on percentage of people with painless injection (P = 0.059), nor success rate (P = 0.290).ConclusionBuffered lidocaine significantly decreased onset time and injection pain (VAS) compared with non-buffered lidocaine in IANB. However due to statistical heterogeneity and low sample size, quality of the evidence was low to moderate, additional studies with larger numbers of participants and low risk of bias are needed to confirm these results.

BackgroundFine osseointegration is the basis of long-term survival of implant. In our previous study, we observed a strong correlation between hyperlipidemia and compromised osseointegration. MicroRNA-29a-3p (miR-29a-3p) has been discovered to participate in bone marrow mesenchymal stem cells (BMSCs) differentiation. However, the role and the underlying mechanisms of hyperlipidemia and miR-29a-3p in osseointegration still remain obscure.ResultsIn peri-implant bone tissues of hyperlipidemia rats, bone mass, mineralization and bone trabecula formation were weakened. Alkaline phosphatase (ALP) and runt-related transcription factor 2 (Runx2), and miR-29a-3p expression were reduced. While in normal rats, implant-bone interfaces were filled with dense new bone and ALP, Runx2 and miR-29a-3p were up-regulated. Overexpressed miR-29a-3p can reverse the adverse effect of hyperlipidemia on osseointegration. Implants were tightly integrated with the surrounding dense new bone tissues, and ALP as well as Runx2 mRNAs were enhanced in miR-29a-3p overexpressed and hyperlipidemia rats, while little peri-implant bone tissue existed, ALP and Runx2 deregulated on miR-29a-3p inhibited rats. Dishevelled 2 (Dvl2) mRNA was declined in peri-implant bone tissue of high-fat (HF) group than normal group, while frizzled 4 (Fzd4) mRNA declined on day 5 and increased from day 10 to day 20 after implantation in hyperlipidemia rats than in normal rats. Next, BMSCs were cultured under HF or normal medium in vitro. In the HF group, ALP activity and mineralization, ALP and Runx2 mRNAs and proteins expression, and miR-29a-3p expression were suppressed, while adipogenesis was increased, as a result, cytoskeletons were sparse and disordered compared to control group. However, when miR-29a-3p was overexpressed in BMSCs, ALP activity, ALP, Runx2, Dvl2 and Fzd4 mRNAs and proteins expressions were up-regulated. As miR-29a-3p was inhibited in BMSCs, the reverse results were obtained. In addition, promoter assay revealed that miR-29a-3p can directly suppress Wnt/β-catenin pathway related Dvl2 and Fzd4 through binding to their 3′-UTR.ConclusionsMiR-29a-3p facilitated implant osseointegration via targeting Wnt/β-catenin pathway-related Dvl2 and Fzd4. MiR-29a-3p/Dvl2/Fzd4 may serve as a promising therapeutic target for hyperlipidemia osseointegration.

The aim was to investigate the osseointegration of a novel coating-plasma-sprayed nanostructured zirconia (NSZ) in dental implant. Nanostructured zirconia coating on non-thread titanium implant was prepared by plasma spraying, the implant surface morphology, surface roughness and wettability were measured. In vivo, nanostructured zirconia-coated implants were inserted in rabbit tibia and animals were respectively sacrificed at 2, 4, 8 and 12 weeks after implantation. The bond strength between implant and bone was measured by removal torque (RTQ) test. The osseointegration was observed by scanning electron microscopy (SEM), micro computed tomography (Micro CT) and histological analyses. Quantified parameters were calculated, including removal torque, Bone Volume to Tissue Volume (BV/TV), Trabecular Thickness (Tb. Th), Trabecular Number (Tb. N), Trabecular Separation/Spacing (Tb. Sp), and Bone-Implant contact (BIC) percentage. The statistical differences were detected by two-tail Mann-Whitney U test (SPSS 20.0). The surface roughness (1.58µm) and wettability (54.61°) of nanostructured zirconia coated implant was more suitable than those of titanium implant (0.598µm and 74.38°) for osseointegration and hierarchical surface morphology could be seen on zirconia coating. The histological analyses showed that zirconia coated implant induced earlier and more condensed bone formation than titanium implant at 2 and 4 weeks. Quantified parameters showed the significant differences between these two groups at early healing period, but the differences between these two groups decreased with the increase of healing period. All these results demonstrated that plasma sprayed zirconia coated implant induced better bone formation than titanium implant at early stage.