The mechanisms of inflammation in bone and joint tissue are complex and involve long non-coding RNAs (lncRNAs), which play an important role in this process. The aim of the present study was to screen out differentially expressed genes in human osteoblasts stimulated by inflammation, and to further explore the mechanisms underlying inflammatory responses and the functional activity of human osteoblasts through bioinformatics methods and in vitro experiments. For this purpose, MG63 cells were stimulated with various concentrations of lipopolysaccharide (LPS) for different periods of time to construct an optimal inflammatory model and RNA sequencing was then performed on these cells. The levels of nuclear enriched abundant transcript 1 (NEAT1), various inflammatory factors, Nod-like receptor protein 3 (NLRP3) protein and osteogenesis-related proteins, as well as the levels of cell apoptosis- and cell cycle-related markers were measured in MG63 cells stimulated with LPS, transfected with NEAT1 overexpression plasmid and treated with bexarotene by western blot analysis, RT-qPCR, immunofluorescence, FISH, TEM and flow cytometry. There were 427 differentially expressed genes in the LPS-stimulated MG63 cells, in which NEAT1 was significantly downregulated. LPS upregulated the expression of inflammatory cytokines and NLRP3, inhibited the expression of autophagy-related and osteogenesis-related proteins, promoted apoptosis and altered the cell cycle, which was partially inhibited by NEAT1 overexpression and promoted by bexarotene. LPS stimulated inflammation in the MG63 cells and inhibited the retinoid X receptor (RXR)-α to downregulate the expression of NEAT1 and decrease levels of autophagy, which promoted the activation of NLRP3 and the release of inflammatory factors, and impaired the functional activity of osteoblasts, thus promoting the development of inflammation.

Objective Measurement of the periodontal soft tissue dimension is crucial for clinical decision‐making and aesthetic prognosis. However, the effectiveness of different measuring methods remains unclear. This systematic review aimed to explore the diagnostic accuracy of two non‐invasive methods (namely CBCT and ultrasound) for gingival thickness measurement at different tooth positions. Materials and methods A systematic search was performed using PubMed (including Medline), PubMed Central, OVID, Cochrane Library, LILACS and OpenGrey. Studies focusing on comparisons between CBCT, ultrasound and direct transgingival probing were included. The means, SDs and correlation coefficients with 95% confidence intervals were extracted and analyzed using Review Manager and R software. Results Twelve studies were selected. No significant difference was found between CBCT measurement and transgingival probing in the anterior and posterior dentition, and a moderate correlation was observed between these two methods (r = 0.41). A weak correlation was found between ultrasound measurement and transgingival probing (r = 0.32), and a slight but statistically significant difference was found when comparing ultrasonic devices and transgingival probing in the posterior area. Conclusion CBCT can be considered a relatively reliable method for gingival thickness measurement in both the anterior and posterior areas compared with direct probing. Ultrasonic devices provide limited accuracy in the posterior area but are relatively comparable with direct clinical assessments in the anterior area. Clinical significance Measurement location may affect the diagnostic accuracy and repeatability of gingival thickness measurements. Appropriate method selection in different clinical scenarios is crucial to aesthetic outcome prediction and decision‐making.

Atherosclerosis is the underlying cause for cardiovascular disease. Current pharmacotherapies are limited by the inadequate targeting and insufficient treatment. Herein, inspired by the interaction of macro phage and lipoprotein as a typical hallmark of atherosclerosis, hybrid nano vesicles (MLPNVs) are designed by fusion of antiinflammatory M2phenotype macrophage membranes and lipidated peptide (DOPEpp HBSP) to mimic the binding manner of celllipoprotein for atherosclerotic treatment. Through hybridization of M2 macrophage membranes and lipidated peptide film, MLPNVs facilitate the inflammatory cell inter nalization at atherosclerotic site, and sequester the proinflammatory cytokines to suppress local inflammation. Moreover, MLPNVs exhibit a matrix metalloprotease 2 (MMP2)responsive release of the peptide HBSP in plaques, leading to the restoration of dysfunctional endothelial cells. In the ApoE −/− mice with atherosclerosis, simvastatinloaded MLPNVs provide comprehensive treatment by inherent inflammation suppression, endothelial repair, and cholesterol efflux capacities, resulting in athero sclerotic plaques regression. Through closely mimicking physiological cues, this biomimetic hybrid nano vesicle platform provides a potential strategy for antiatherosclerotic therapy.

Age-related bone loss and disease strongly affect the quality of life of the elderly population. Cellular circadian rhythms have been reported to regulate bone aging, and micro RNAs (miRNAs) play crucial posttranscriptional regulatory roles in the peripheral clock network. Proliferation capability, osteogenic lineage commitment, senescence-associated secreted phenotype (SASP) and circadian oscillation of clock genes under osteogenic condition were assessed in bone marrow mesenchymal stromal cells (BMSCs) from young adult and aged adult mice. miRNAs targeting the core clock gene brain and muscle arntl-like protein 1 (Bmal1) were screened and verified in young and old BMSCs with RT-qPCR and Western Blot analysis. ChIP-seq and RNA-seq datasets were mined to define the downstream mechanism and gain- and loss-of-function genetic experiments were performed to confirm the hypothesis. To compare the therapeutic effect of these clock-engineered BMSCs, SASP and osteogenic capability of Bmal1-overexpressing and miR-142-3p-inhibited BMSCs were investigated in vitro and transplanted into bone defects and femur cavities of aged mice. Aged BMSCs displayed an abolished circadian rhythm, impaired self-renewal capability and decreased osteoblast differentiation. miR-142-3p was elevated with aging, which downregulated Bmal1 and diminished the osteogenic potential of BMSCs. In addition, Bmal1 inhibited YAP expression to promote BMSCs osteogenesis, which was independent from the activation of Hippo signaling pathway. Overexpression of Bmal1 or inhibition of miR-142-3p rescued the molecular temporal rhythm and osteoblast differentiation ex vivo. Cell-based circadian therapy showed improved bone formation and higher turnover levels in vivo. This study demonstrates that transcriptional and post-transcriptional level clock-modified BMSCs rescued circadian oscillation and age-related bone loss via miR-142-3p/Bmal1/YAP signaling axis. These data provide promising clinical prospects of circadian-mediated stromal cell-based therapy and bone tissue regeneration.