Research on the association between dental caries and body mass index (BMI) in children has shown contradictory results; thus we aimed to examine the association between dental caries and the full range of BMI classes among children. We comprehensively searched PubMed, Embase, and the Cochrane Library for studies published prior to March 2017. Articles comparing dental caries among the full range of BMI classes for children below 18 years of both genders were included. Fourteen studies were eligible for this study. Basic information - i.e., first author, published year, study design, country, sample size, age, type of dental caries index and BMI, main results and conclusions, and means and standard deviations of the dental caries indexes used - was pooled. The weighted mean differences and corresponding 95% confidence intervals for dental caries between children with abnormal weight and those with normal weight were analyzed. Generally, no significant differences in caries were found between any abnormal-weight group and the normal-weight group for both primary and permanent teeth. Sensitivity analyses showed that the obese group had more caries than the normal-weight group in their primary teeth. Significantly more caries was found among the overweight and obese children in both primary and permanent teeth in high-income countries, but not in low- and middle-income countries. We recommend that further studies use suitable sample sizes, unify the criteria for BMI categorization and the dental caries index, and investigate the confounding factors that might influence dental caries and BMI.

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There are signs that amyloid fibers exist in Streptococcus mutans biofilm recently. However, the characteristics of amyloid fibers and fibrillation influencing factors are unknown. In this study, we firstly used transmission electron microscopy (TEM) and atomic force microscopy (AFM) to observe the morphology of amyloid fibers in S. mutans . Then the extracted amyloid fibers from biofilm were studied for their characteristics. Further, the influencing factors, PH, temperature and eDNA, were investigated. Results showed there were mainly two morphologies of amyloid fibers in S. mutans , different in width. Amyloid fibers inhibitor-EGCG obviously destroyed biofilm at different stages, which is dose-dependent. The amount of amyloid fibers positively correlated with biofilm biomass in clinical isolates. Acidic pH and high temperature obviously accelerated amyloid fibrillation. During amyloid fibrillation, amyloid growth morphologies were observed by TEM and results showed two growth morphologies. Amyloid fibers formed complex with eDNA, which we call (a)eDNA. The molecular weight of (a)eDNA was similar to genomic DNA, greatly larger than that of eDNA in matrix. Combined use of DNase I and EGCG was more efficiently in inhibiting amyloid fibers and biofilm biomass. In conclusion, amyloid fibers are the crucial structures for S. mutans biofilm formation, showing two types of morphology. Acidic pH and temperature can obviously accelerate amyloid fibrillation. Amyloid fibers form complex with (a)eDNA and combined use of DNase and amyloid fiber inhibitor is more efficiently in inhibiting S. mutans biofilm formation. Electronic supplementary material The online version of this article (10.1186/s13568-019-0753-1) contains supplementary material, which is available to authorized users.

Hypoxia‑inducible factor‑1α (HIF‑1α) is essential for regulating the osteogenic differentiation of periodontal ligament cells (PDLCs). The regulatory mechanism of HIF‑1α transcription is still not clear. Recently, two long non‑coding RNAs, HIF1A antisense RNA 1 (HIF1A‑AS1) and HIF1A antisense RNA 2 (HIF1A‑AS2), were found to regulate HIF‑1α mRNA, but the regulatory mechanisms among HIF‑1α, HIF1A‑AS1 and HIF1A‑AS2 have not been well studied. We hypothesized that HIF1A‑AS1 and HIF1A‑AS2 play important roles in the osteogenic differentiation of PDLCs by regulating HIF‑1α. In the present study, we showed that expression levels of HIF1A‑AS1, HIF1A‑AS2, HIF‑1α and osteogenic biomarkers were time‑dependent under hypoxia. Even though both HIF1A‑AS1 and HIF1A‑AS2 were complementary to HIF‑1α mRNA, only HIF1A‑AS2 showed an inhibitory effect on HIF‑1α in PDLCs. Moreover, HIF‑1α had positive regulatory effects on HIF1A‑AS1 and HIF1A‑AS2. HIF‑1α promoted the osteogenic differentiation of PDLCs, and HIF1A‑AS2 had a negative effect on the osteogenic differentiation of PDLCs. Altogether, the present study revealed the complex relationships among HIF1A‑AS1, HIF1A‑AS2 and HIF‑1α, as well as their roles in regulating the osteogenic differentiation of PDLCs. These findings provide a theoretical basis for promoting periodontal tissue regeneration and repair during orthodontic tooth movement.

Three-dimensional printed (3DP) scaffolds have become an excellent resource in alveolar bone regeneration. However, selecting suitable printable materials remains a challenge. In the present study, 3DP scaffolds were fabricated using three different ratios of poly (ε-caprolactone) (PCL) and poly-lactic-co-glycolic acid (PLGA), which were 0.1PCL/0.9PLGA, 0.5PCL/0.5PLGA and 0.9PCL/0.1PLGA. The surface characteristics and degradative properties of the scaffolds, and the response of human periodontal ligament stem cells (hPDLSCs) on the scaffolds, were assessed to examine the preferable ratio of PCL and PLGA for alveolar bone regeneration. The results demonstrated that the increased proportion of PLGA markedly accelerated the degradation, smoothed the surface and increased the wettability of the hybrid scaffold. Furthermore, the flow cytometry and Cell Counting Kit-8 assay revealed that the adhesion and proliferation of hPDLSCs were markedlyincreased on the 0.5PCL/0.5PLGA and 0.1PCL/0.9PLGA scaffolds. Additionally, the alkaline phosphatase activity detection and reverse-transcription quantitative polymerase chain reaction demonstrated that the hPDLSCs on the 0.5PCL/0.5PLGA scaffold exhibited the best osteogenic capacity. Consequently, PCL/PLGA composite scaffolds may represent a candidate focus for future bone regeneration studies, and the 0.5PCL/0.5PLGA scaffold demonstrated the best bio-response from the hPDLSCs.

Dental follicle (DF) can develop into periodontal tissues including periodontal ligament, cementum, and alveolar bone. Possessing superior pluripotency and osteogenic capacity, dental follicle stem cells (DFSCs) have become a promising stem cell source for bone regeneration and periodontal engineering. However, the mechanisms underlying DFSCs‐mediated osteogenesis remain elusive. Our previous long noncoding RNA (lncRNA) microarray revealed that lncRNA HOTAIRM1 was significantly higher expressed in human DFSCs (hDFSCs) compared with human periodontal ligament stem cells (hPDLSCs). lncRNA HOTAIRM1, an antisense transcript of the HOXA1/2 intergenic region, can epigenetically regulate proximal and distant HOXA genes through histone and DNA methylation. HOXA2, a target of HOTAIRM1, is crucial for cranial neural crest morphogenesis, branchial arches development, and osteogenesis. However, the roles of both HOTAIRM1 and HOXA2 in odontogenic stem cells remain unknown. Here, we investigated the functions and regulatory mechanisms of these two genes in hDFSCs. Both genes were confirmed highly expressed in hDFSCs compared with hPDLSCs, and they displayed similar expression patterns in the DF and surrounding periodontium during mice tooth morphogenesis. Knockdown of either HOTAIRM1 or HOXA2 inhibited osteogenic differentiation of hDFSCs, while overexpressed HOTAIRM1 inhibited hDFSCs proliferation and promoted osteogenesis. Furthermore, HOTAIRM1 inhibited both overall DNMT1 expression and DNMT1 enrichment on HOXA2 promoter, mechanically binding to the CpG islands of the HOXA2 promoter region, leading to hypomethylation and HOXA2 induction. These findings suggested that HOTAIRM1 promoted the osteogenesis of hDFSCs by epigenetically regulating HOXA2 via DNMT1. Taken together, HOTARIM1 and HOXA2 exerted pivotal functions in hDFSCs, and the regulatory mechanism of HOTARIM1 within the HOXA cluster was uncovered.

Evidence suggests that short amyloid-forming peptides derived from bacterial proteomes have functional roles; however, the reported activities are diverse and the underlying mechanisms remain unclear. In this study, we simulated short amyloidforming peptides from the amyloid-forming truncated protein C123 of Streptococcus mutans (S. mutans), studied their biological functions in microbial proliferation and biofilm formation, and further investigated the underlying mechanism. Fourteen hexapeptides were simulated, 13 of which were successfully synthesized. We found that the amyloidforming hexapeptides (AFhPs) displayed efficient broad-spectrum antibiofilm activity against the Gram-positive bacteria S. mutans, Streptococcus sanguis and Staphylococcus aureus, Gram-negative bacteria Escherichia coli and fungus Candida albicans, by aggregating into rigid amyloid fibres agglutinating microbes, whereas the non-amyloid-forming hexapeptides (non-AFhPs) did not. The AFhPs did not kill microbes and showed little or no cytotoxicity. Furthermore, a set of AFhPs displayed broad-spectrum antibiofilm activity, regardless of its source. The microbial cell wall carbohydrates, peptidoglycan (PGN), lipoteichoic acid (LTA), glucan and zymosan A, mediated AFhP binding and triggered significant AFhP fibrillation. Although amyloid fibres agglutinated lipid membrane modellarge unilamellar vesicles (LUVs)and LUVs facilitated AFhP fibrillation, the roles of lipid membranes in AFhP antibiofilm activities remain to be elucidated. We highlight the potential use of AFhPs as novel antibiofilm agents.

Background Infiltration and sealing are micro-invasive treatments for arresting proximal non-cavitated caries lesions; however, their efficacies under different conditions remain unknown. This systematic review and meta-analysis aimed to evaluate the caries-arresting effectiveness of infiltration and sealing and to further analyse their efficacies across different dentition types and caries risk levels. Methods Six electronic databases were searched for published literature, and references were manually searched. Split-mouth randomised controlled trials (RCTs) to compare the effectiveness between infiltration/sealing and non-invasive treatments in proximal lesions were included. The primary outcome was obtained from radiographical readings. Results In total, 1033 citations were identified, and 17 RCTs (22 articles) were included. Infiltration and sealing reduced the odds of lesion progression (infiltration vs. non-invasive: OR = 0.21, 95% CI 0.15–0.30; sealing vs. placebo: OR = 0.27, 95% CI 0.18–0.42). For both the primary and permanent dentitions, infiltration and sealing were more effective than non-invasive treatments (primary dentition: OR = 0.30, 95% CI 0.20–0.45; permanent dentition: OR = 0.20, 95% CI 0.14–0.28). The overall effects of infiltration and sealing were significantly different from the control effects based on different caries risk levels (OR = 0.20, 95% CI 0.14–0.28). Except for caries risk at moderate levels (moderate risk: OR = 0.32, 95% CI 0.01–8.27), there were significant differences between micro-invasive and non-invasive treatments (low risk: OR = 0.24, 95% CI 0.08–0.72; low to moderate risk: OR = 0.38, 95% CI 0.18–0.81; moderate to high risk: OR = 0.17, 95% CI 0.10–0.29; and high risk: OR = 0.14, 95% CI 0.07–0.28). Except for caries risk at moderate levels (moderate risk: OR = 0.32, 95% CI 0.01–8.27), infiltration was superior (low risk: OR = 0.24, 95% CI 0.08–0.72; low to moderate risk: OR = 0.38, 95% CI 0.18–0.81; moderate to high risk: OR = 0.20, 95% CI 0.10–0.39; and high risk: OR = 0.14, 95% CI 0.05–0.37). Conclusion Infiltration and sealing were more efficacious than non-invasive treatments for halting non-cavitated proximal lesions.