Objectives Mammalian palatogenesis is a highly regulated morphogenetic process to form the intact roof of the oral cavity. Long noncoding RNAs (lncRNAs) and mRNAs participate in numerous biological and pathological processes, but their roles in palatal development and causing orofacial clefts (OFC) remain to be clarified. Methods Palatal tissues were separated from ICR mouse embryos at four stages (E10.5, E13.5, E15, and E17). Then, RNA sequencing (RNA-seq) was used. Various analyses were performed to explore the results. Finally, hub genes were validated via qPCR and in situ hybridization. Results Starting from E10.5, the expression of cell adhesion genes escalated in the following stages. Cilium assembly and ossification genes were both upregulated at E15 compared with E13.5. Besides, the expression of cilium assembly genes was also increased at E17 compared with E15. Expression patterns of three lncRNAs (H19, Malat1, and Miat) and four mRNAs (Cdh1, Irf6, Grhl3, Efnb1) detected in RNA-seq were validated. Conclusions This study provides a time-series expression landscape of mRNAs and lncRNAs during palatogenesis, which highlights the importance of processes such as cell adhesion and ossification. Our results will facilitate a deeper understanding of the complexity of gene expression and regulation during palatogenesis.

Osteoporosis is a frequently occurring bone remodeling disorder worldwide with one characteristic being decreasing bone mineral density and a predisposition to bone fracture,which diminishes patients’quality of life

以大肠杆菌(E.coli)作为研究对象,通过标准平板计数法、活死菌染色法以及扫描电子显微镜镜下观察细菌表面结构来研究Ti_(3)C_(2)/Co纳米材料在近红外光照射下的抗菌性能,同时进一步通过溶血实验、脐静脉内皮细胞的cck8细胞毒性试验及迁

Osteoclastogenesis in alveolar bone induced by compression stress triggers orthodontic tooth movement.Compression stress also stimulates angiogenesis,which is essential for osteoclastogenesis.However,the effects of os

Osteoporosis is a frequently occurring bone remodeling disorder worldwide with one characteristic being decreasing bone mineral density and a predisposition to bone fracture, which diminishes patients' quality of life. Several studies showed that imbalance between the osteogenesis and adipogenesis of bone marrow mesenchymal stem cells (BMSCs) took part in the development of osteoporosis. In previous study, we found MIR22HG regulated the osteogenesis of human BMSCs positively. In this study, we found that MIR22HG was decreased during the adipogenesis of human BMSCs and exerted negative effects on adipogenesis with the involvement of Wnt/beta-catenin signaling pathway both in vitro and in vivo. Nitazoxanide could inhibit Wnt signaling and relieve MIR22HG's suppression on adipogenesis. These findings indicated that MIR22HG had great potential in clinical application for osteoporosis treatment and prevention.

Introduction: Patients with severe periodontitis typically present with pathologic tooth migration. To improve esthetics and masticatory function, orthodontic treatment is required. Research on periodontal orthodontic treatment has been sparse, particularly from the microbial perspective. Hence, we analyzed the microbial and clinical changes in patients with well-controlled periodontitis in the early stage of orthodontic treatment. Methods: Ten patients with well-controlled periodontitis were asked to collect saliva before and 1 and 3 months after appliance placement (T0, T1, and T2, respectively) and underwent clinical examinations before and 1, 3, and 6 months after appliance placement (T0, T1, T2, and T3, respectively). The microbial community of saliva was analyzed by 16S rRNA gene sequencing. Gingival index, the plaque index, and the probing pocket depth were clinically assessed. Results: The plaque index significantly increased from T0 to T1 and decreased at T2 and T3. The probing pocket depth and gingival index increased slightly at T2, but not significantly, in both the high-risk site and low-risk site. The alpha and beta diversity increased at T1. The microbial community structure was similar at T0 and T2. The relative abundance of core genera and periodontal pathogens was stable during the initial 3 months of orthodontic treatment. Conclusions: The orthodontic appliance promoted plaque accumulation and altered the microbial community of patients with well-controlled periodontitis during the first month of orthodontic treatment. The microbial community returned to the basal composition at 3 months after appliance placement, and the periodontal inflammation during the 6-months orthodontic treatment was under control.

Orthodontic tooth movement is triggered by orthodontic force loading on the periodontal ligament and is achieved by alveolar bone remodeling, which is regulated by intimate crosstalk between osteoclastogenesis and osteoblast differentiation. Whether the communication between osteoclasts and osteoblasts is influenced by orthodontic compression stress requires further clarification. In this study, osteoclasts were differentiated for 10 days. On day 4 of differentiation, the number of pre-osteoclasts peaked, as determined by the increased expression of RANK and the number of multinucleated cells. After 24 h of compression stress loading, on day 4, the number of osteoclasts increased, and the optimal magnitude of stress to promote osteoclastogenesis was determined as 1 g/cm(2). Moreover, the results of RNA-sequencing analysis showed that the miRNA expression profile changed markedly after compression loading and that many of the altered miRNAs were associated with cell communication functions. A series of indirect co-culture experiments showed an inhibitory effect of osteoclasts on osteoblast differentiation, especially after compression. Next, we added osteoclast-derived exosomes to hPDLSCs during osteoblast differentiation. Exosomes derived from osteoclasts under compression (cEXO) showed a greater inhibitory effect on osteoblast differentiation, compared to exosomes from osteoclasts without compression (EXO). Therefore, we analyzed differentially expressed miRNAs associated with bone development functions in exosomes: miR-223-5p and miR-181a-5p were downregulated, whereas miR-133a-3p, miR-203a-3p, miR-106a-5p, and miR-331-3p were upregulated; these altered expressions may explain the enhanced inhibitory effect of compression stress.

近年来,抗生素耐药菌在全球范围内得到迅速而广泛地传播,新型抗菌药物的开发刻不容缓。随着生物纳米技术的发展,二维层状纳米材料有望成为处理耐药菌的替代选择。本文综述了石墨烯及其衍生物（GMs）、过渡金属硫化物（TMDs）、层状双氢氧化物（LDHs）及MXenes二维层状纳米材料的结构特征及其抗菌应用的最新报道,讨论了材料的抗菌机制,例如物理/机械损伤、脂质提取、氧化应激和光热/光动力效应等。最后,本文针对二维层状纳米材料的抗菌应用前景进行了展望:（1）材料特有的空间结构及优异的生物相容性决定了其可以作为抗菌药物的理想载体;（2）优异的光动力和光热杀菌效应使它具有治疗局部皮肤感染的强大潜力;（3）拥有光催化抗菌特性的2D材料可制成抗菌涂层,实现简易的原位消毒,有望应用于无菌医疗设备中。

Microstructured titanium surface implants, such as typical sandblasted and acid-etched (SLA) titanium implants, are widely used to promote bone apposition in prosthetic treatment by dental implants following tooth loss. Although there are multiple factors associated with the superior osseointegration of an SLA titanium surface, the molecular mechanisms of long noncoding RNAs (lncRNAs) are still unclear. In this study, we characterized smooth (SMO) and SLA surfaces, and compared the osteoinduction of these surfaces using human bone marrow-derived mesenchymal stem cells (hBMSCs)in vitroand implants in a rat modelin vivo. Then, we used microarrays and bioinformatics analysis to investigate the differential expression profiles of mRNAs and lncRNAs on SMO and SLA titanium surfaces. An lncRNA-mRNA network was constructed, which showed an interaction between lncRNA HIF1A antisense RNA 1 (HIF1A-AS1) and vascular endothelial growth factor. We further found that knockdown of HIF1A-AS1 significantly decreased osteogenic differentiation of hBMSCs. This study screened SLA-induced lncRNAs using a systemic strategy and showed that lncRNA HIF1A-AS1 plays a role in promotion of new bone formation in the peri-implant area, providing a novel insight for future surface modifications of implants. © The Royal Society of Chemistry 2020.

Osteoporosis is a prevalent metabolic bone disease characterized by low bone mineral density and degenerative disorders of bone tissues. Previous studies showed the abnormal osteogenic differentiation of endogenous bone marrow mesenchymal stem cells (BMSCs) contributes to the development of osteoporosis. However, the underlying mechanisms by which BMSCs undergo osteogenic differentiation remain largely unexplored. Recently, long non-coding RNAs have been discovered to play important roles in regulating BMSC osteogenesis. In this study, we first showed MIR22HG, which has been demonstrated to be involved in the progression of several cancer types, played an important role in regulating BMSC osteogenesis. We found the expression of MIR22HG was significantly decreased in mouse BMSCs from the osteoporotic mice and it was upregulated during the osteogenic differentiation of human BMSCs. Overexpression of MIR22HG in human BMSCs enhanced osteogenic differentiation, whereas MIR22HG knockdown inhibited osteogenic differentiation both in vitro and in vivo. Mechanistically, MIR22HG promoted osteogenic differentiation by downregulating phosphatase and tensin homolog (PTEN) and therefore activating AKT signaling. Moreover, we found MIR22HG overexpression promoted osteoclastogenesis of RAW264.7 cells, which indicated that MIR22HG played a significant role in bone metabolism and could be a therapeutic target for osteoporosis and other bone-related diseases.