Background Bio-root regeneration is a promising treatment for tooth loss. It has been reported that dental-derived stem cells are effective seed cells for bio-root construction, but further applications are limited by their few sources. Human adipose tissues have a wide range of sources and numerous studies have confirmed the ability of adipose-derived stromal/stem cells (ASCs) in regenerative medicine. In the current study, the odontogenic capacities of ASCs were compared with dental-derived stem cells including dental follicle cells (DFCs), and stem cells from human exfoliated deciduous teeth (SHEDs). Methods The biological characteristics of ASCs, DFCs, and SHEDs were explored in vitro. Two-dimensional (2D) and three-dimensional (3D) cultures were compared in vitro. Odontogenic characteristics of porcine-treated dentin matrix (pTDM) induced cells under a 3D microenvironment in vitro were compared. The complexes (cell/pTDM) were transplanted subcutaneously into nude mice to verify regenerative potential. RNA sequencing (RNA-seq) was used to explore molecular mechanisms of different seed cells in bio-root regeneration. Results 3D culture was more efficient in constructing bio-root complexes. ASCs exhibited good biological characteristics similar to dental-derived stem cells in vitro. Besides, pTDM induced ASCs presented odontogenic ability similar to dental-derived stem cells. Furthermore, 3D cultured ASCs/pTDM complex promoted regeneration of dentin-like, pulp-like, and periodontal fiber-like tissues in vivo. Analysis indicated that PI3K-Akt, VEGF signaling pathways may play key roles in the process of inducing ASCs odontogenic differentiation by pTDM. Conclusions ASCs are potential seed cells for pTDM-induced bio-root regeneration, providing a basis for further research and application. Graphical Abstract
The aim of this system review and meta-analysis was to explore the epidemiological characteristics of dental fluorosis in mainland China from 1995 to 2020. A comprehensive literature search was conducted through PubMed, Embase, CBM, CNKI, Chinese Wan Fang database, and VIP database. Subgroup analyses were done to explore epidemic tread of dental fluorosis (gender, location, survey year and geographical distribution) with the help of relative software. Forty-one publications were included in this study. The overall prevalence was 23.6%, and the prevalence of dental fluorosis increased from 18.8% during 1995–1999 to 34.3% during 2010–2014, while it decreased to 20.5% during 2015–2019. There was no significant difference in prevalence between boys (15.7%) and girls (15.2%) (RR = 1.05, 95% CI: 1.02–1.07); and the prevalence of dental fluorosis in rural areas (14.5%) was slightly higher than those in urban areas (12.7%) (RR = 0.93, 95% CI: 0.76–1.13). The prevalence before (63.3%) and after (34.7%) water improvement showed a great benefit of fluoride reduction policy. Result of this meta-analysis provides evidence enable governments taking effective measures to control dental fluorosis.
Background Periodontitis is a serious threat to oral quality of life and overall health. Although our previous studies confirmed that long intergenic non-coding RNA 01126 (LINC01126) is aberrantly expressed in periodontitis tissues, there are few reports on the pathogenesis of LINC01126 in periodontitis. Our study investigated the biological functions of LINC01126 in periodontitis and the potential mechanism. Results An inflammatory model of human gingival fibroblasts (HGFs) was successfully established. LINC01126 silencing can alleviate lipopolysaccharide (LPS) induced cell inflammation, reduce cell apoptosis, and promote cell migration. As a "sponge" for miR-655-3p, LINC01126 inhibits its binding to mRNA of IL-6, thereby promoting inflammation progression and JAK2/STAT3 pathway activation. qRT- PCR, WB, and IHC results of clinical tissue samples further confirmed that miR-655-3p expression was down-regulated and IL-6/JAK/STAT3 was abnormally activated in periodontitis tissues. Conclusions Our results indicate that LINC01126, as an endogenous competitive RNA (ceRNA) of miR-655-3p, can promote IL-6/JAK3/STAT3 pathway activation, thereby promoting periodontitis pathogenesis. And this is the first study of miR-655-3p in inflammatory periodontal diseases. Our study reveales a new pathogenesis of periodontitis, and provides a new strategy for preventing and treating periodontitis.
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