Background A method for assessing dental maturity in different populations was first developed in 1973 by Demirjian and has been widely used and accepted since then. While the accuracy for evaluating dental age using Demirjian’s method compared to children’s chronological age has been extensively studied in recent years, the results currently available remain controversial and ambiguous. Methods A literature search of PubMed, Embase, Web of Science, CNKI and CBM databases was conducted to identify all eligible studies published before July 12th, 2013. Weighted mean difference (WMD) with corresponding 95% confidence interval (95% CI) was used to evaluate the applicability of Demirjian’s method for estimating chronological age in children. Results: A meta-analysis was conducted on 26 studies with a total of 11,499 children (5,301 boys and 6,198 girls) aged 3.5 to 16.9 years. Overall, we found that Demirjian’s method overestimated dental age by 0.35 (4.2 months) and 0.39 (4.68 months) years in males and females, respectively. A subgroup analysis by age revealed that boys and girls between the ages of 5 to 14 were given a dental age estimate that was significantly more advanced than their chronological age. Differences between underestimated dental ages and actual chronological ages were lower for male and female 15- and 16-year-old subgroups, though a significant difference was found in the 16-year-old subgroup. Conclusions Demirjian’s method’s overestimation of actual chronological tooth age reveals the need for population-specific standards to better estimate the rate of human dental maturation.

We investigated the therapeutic effects of microRNA-139-5p in relation to osteoporosis of bone marrow-derived mesenchymal stem cell (BMSCs) and its underlying mechanisms. In this study we used a dexamethasone-induced in vivo model of osteoporosis and BMSCs were used for the in vitro model. Real-time quantitative polymerase chain reaction (RT-PCR) and gene chip were used to analyze the expression of microRNA-139-5p. In an osteoporosis rat model, the expression of microRNA-139-5p was increased, compared with normal group. Downregulation of microRNA-139-5p promotes cell proliferation and osteogenic differentiation in BMSCs. Especially, up-regulation of microRNA-139-5p reduced cell proliferation and osteogenic differentiation in BMSCs. Overexpression of miR-139-5p induced Wnt/β-catenin and down-regulated NOTCH1 signaling in BMSCs. Down-regulation of miR-139-5p suppressed Wnt/β-catenin and induced NOTCH1 signaling in BMSCs. The inhibition of NOTCH1 reduced the effects of anti-miR-139-5p on cell proliferation and osteogenic differentiation in BMSCs. Activation of Wnt/β-catenin also inhibited the effects of anti-miR-139-5p on cell proliferation and osteogenic differentiation in BMSCs. Taken together, our results suggested that the inhibition of microRNA-139-5p promotes osteogenic differentiation of BMSCs via targeting Wnt/β-catenin signaling pathway by NOTCH1.

Periodontal ligament stem cells (PDLSCs) are considered a promising cell source for dental tissue regeneration. Stromal cell-derived factor 1 [SDF‑1, also known as chemokine (C‑X‑C motif) ligand 12] is regarded as a critical cytokine involved in stem/progenitor cell chemotaxis and homing during tissue regeneration. The present study described a previously unsuspected role for SDF‑1 in the protection of PDLSCs against oxidative stress‑induced apoptosis. In the present study, apoptosis was induced by exposure of PDLSCs to various concentrations of H2O2 for 12 h, following which cell viability was assessed, and cleaved caspase‑3 and ‑9 expression levels were evaluated. To investigate the potential mechanism underlying this protection, the protein expression levels of total and phosphorylated extracellular signal‑regulated kinase (ERK), a key protein of the mitogen‑activated protein kinase (MAPK) signaling pathway, were examined. The results of the present study revealed that SDF‑1 pretreatment increased cell viability following H2O2 administration, and downregulated protein expression levels of activated caspase‑3 and ‑9. Furthermore, treatment with SDF‑1 increased the phosphorylation of ERK. The protective effect of SDF‑1 was partially inhibited by treatment with PD98059, a MAPK/ERK inhibitor, which decreased cell viability. The results of the present study suggested that SDF‑1 treatment is a potential strategy to improve the survival of PDLSCs, which may be beneficial for dental tissue regeneration.

No abstract