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Background Nowadays, robotic computer-assisted implant surgery (r-CAIS) has drawn great attention in implant dentistry; however, the clinical application of r-CAIS for limited operating space such as the second molar region, has not been demonstrated. Thus, this study aimed to evaluate the accuracy of r-CAIS in second molars in combination with step drills and manual-automatic mode switching function. Methods Patients who lost second molars and underwent r-CAIS were enrolled in this study. The positioning marker was installed preoperatively, and a cone-beam computed tomography (CBCT) scan was subsequently performed. The CBCT data were subsequently transferred into the robotic software, and a preoperative surgical plan was generated. After marker registration and calibration, the implant osteotomy was completed by the robotic arm under the control of the surgeons. Owing to the limited operating space in the second molar region, the operation mode of r-CAIS was switched between manual and automatic modes, and step drills were used in combination. Patients underwent postoperative CBCT, and the accuracy was evaluated using the CBCT data between the planned and placed implants. Results A total of 16 patients were enrolled in this study, and no adverse events occurred during or after surgery. The mean global coronal, apical and angular deviations were 0.43 ± 0.10 mm (95%CI: 0.38 to 0.49 mm), 0.44 ± 0.10 mm (95%CI: 0.38 to 0.49 mm), and 0.88 ± 0.53°(0.60 to 1.16°), respectively. Conclusions r-CAIS can achieve high accuracy in the second molar region when combined with step drills and manual-automatic mode switching function. Further prospective studies are needed to validate the effects.

Chronic inflammatory diseases are widespread and often accompanied by comorbidities, making treatment challenging. Current immunosuppressive and anti-inflammatory therapies have limited efficacy and significant side effects, and are insufficient to address the complexity of coexisting conditions. This review explores recent advances in innate immune memory, also known as trained immunity, and its potential role in inflammatory diseases. We hypothesize that targeting the regulatory mechanisms of trained immunity may lead to novel therapeutic strategies that more effectively control inflammation and improve disease outcomes. Finally, we highlight that the interplay between trained immunity and inflammatory diseases remains incompletely understood, and further research is needed to elucidate its mechanisms and clinical translational potential.

Background The potential of the robotic system for transalveolar sinus floor elevation (TSFE) with simultaneous implant placement has not been verified. This study aimed to assess implant placement accuracy and membrane perforation in robotic computer-assisted implant surgery (r-CAIS) for TSFE. Methods Patients who underwent r-CAIS for TSFE were enrolled in this study. Positioning markers were placed in the patient’s oral cavity, and cone-beam computed tomography (CBCT) was performed. Subsequently, the surgical plan was generated using robotic software. After the markers were registered with the robotic arm, TSFE and implant placement were performed using the robotic arm and crestal approach sinus (CAS) kit drills under the control of the surgeons. Deviations between the planned and placed implants were assessed using preoperative and postoperative CBCT data. In addition, perforation of the Schneiderian membrane was evaluated intraoperatively using the Valsalva maneuver and postoperatively using CBCT images. Results Ten patients were enrolled, and no adverse events occurred during the surgery. The mean global coronal, global apical, and angular deviations were 0.55 ± 0.20 mm (95% confidence interval [CI]: 0.41 to 0.69 mm), 0.56 ± 0.23 mm ( 95%CI:0.40 to 0.73 mm), and 1.38 ± 0.83° ( 95%CI: 0.78 to 1.97°), respectively. No membrane perforation was observed during or after the surgery. Conclusions Within the limitations of this study, r-CAIS for TSFE showed high accuracy and a low membrane perforation rate.

Background Robotic computer-assisted implant surgery (r-CAIS) is a revolutionary innovation in oral implantation; however, the clinical feasibility of r-CAIS for immediate implant placement (IIP) in posterior teeth has not been verified. Thus, this study aimed to evaluate the accuracy of r-CAIS for IIP in posterior tooth regions. Methods Patients with posterior teeth to be extracted and indicated to undergo r-CAIS were evaluated. The patients had positioning markers installed in the oral cavity and underwent cone-beam computed tomography (CBCT). Subsequently, minimally invasive tooth extractions were performed, and an individualised surgical plan was generated in the robotic software. After marker registration, implantation surgery was performed by the robotic arm under the supervision and assistance of the surgeons. Finally, the deviations between the planned and placed implants were evaluated based on preoperative and postoperative CBCT data. Results A total of 12 patients were evaluated. No adverse events occurred during the surgery. The mean global coronal, global apical, and angular deviations were 0.46 ± 0.15 mm (95%CI:0.36 to 0.56 mm), 0.46 ± 0.14 mm (95%CI:0.37 to 0.54 mm), and 1.05 ± 0.55° (0.69 to 1.40°), respectively. Conclusions Under the limited conditions of this study, the r-CAIS exhibited high accuracy in posterior teeth IIP surgery. Further multicentre randomised controlled studies are required to confirm the feasibility of this technology.

Background. Exosomes from human dental pulp stem cells (hDPSCs) were indicated to play a positive role in vascular regeneration processes. But the angiogenic capabilities of exosomes from inflammatory hDPSCs and the underlying mechanism remain unknown. In this study, the inflammatory factor lipopolysaccharide (LPS) was used to stimulate hDPSCs, and exosomes were extracted from these hDPSCs. The proangiogenic potential of exosomes was examined, and the underlying mechanism was studied. Method. Exosomes were isolated from hDPSCs with or without LPS stimulation (N-EXO and LPS-EXO) and cocultured with human umbilical vein endothelial cells (HUVECs). The proangiogenic potential of exosomes was evaluated by endothelial cell proliferation, migration, and tube formation abilities in vitro. To investigate the proangiogenic mechanism of LPS-EXO, microRNA sequencing was performed to explore the microRNA profile of N-EXO and LPS-EXO. Gene Ontology (GO) analysis was used to study the functions of the predicted target genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was used to estimate the signaling pathways associated with the inflammation-induced angiogenesis process. Result. Compared to the uptake of N-EXO, uptake of LPS-EXO activated the angiogenic potential of HUVECs by promoting the proliferation, migration, and tube formation abilities in vitro. The mRNA expression levels of vascular endothelial growth factor (VEGF) and kinase-insert domain-containing receptor (KDR) in the LPS-EXO group were significantly higher than those in the N-EXO group. MicroRNA sequencing showed that 10 microRNAs were significantly changed in LPS-EXO. Pathway analysis showed that the genes targeted by differentially expressed microRNAs were involved in multiple angiogenesis-related pathways. Conclusion. This study revealed that exosomes derived from inflammatory hDPSCs possessed better proangiogenic potential in vitro. This is the first time to explore the role of exosomal microRNA from hDPSCs in inflammation-induced angiogenesis. This finding sheds new light on the effect of inflammation-stimulated hDPSCs on tissue regeneration.

The spatial and temporal differences influence the development of vertebrate teeth in specific cell types, as well as the precise regulation of signalling networks. During early embryogenesis, the odontogenic potential shifts from the dental epithelium to the mesenchyme, initiating subsequent morphogenetic processes. Across the bud, cap, and bell stages, incisors and molars undergo distinct morphological and functional transformations driven by dynamic mesenchymal subpopulations. These subpopulations exhibit temporally specific gene expression profiles and differentiation trajectories, which orchestrate crown-root patterning, odontoblast differentiation, and pulp-stroma interactions. Recent advances in single-cell RNA sequencing (scRNA-seq) have revolutionised our understanding of dental mesenchymal heterogeneity, unveiling previously unidentified progenitor populations and their regulatory networks. By mapping developmental trajectories and intercellular communication, scRNA-seq has elucidated the transition of mesenchymal cells between stat dental papilla precursors, follicle progenitors, and apical papilla stem cells. Furthermore, this technology highlights the functional divergence of mesenchymal stem cells (MSCs) in postnatal teeth, which balance mineralisation, immune modulation, and repair capacities. However, expansion of MSCs alters their native properties, underscoring the importance of niche-specific signaling. This review synthesises scRNA-seq findings to review the hierarchy of dental mesenchymal subpopulations, offering insights into their roles in developmental defects and regenerative strategies. These discoveries bridge developmental biology and clinical applications, paving the way for novel therapies in tooth regeneration and pulp repair.

The regulation of macrophage polarization by mesenchymal stem cells (MSCs) is a prominent area of research but faces challenges due to limited MSC sources and incomplete understanding of underlying mechanisms. We sought to identify an accessible MSC source and investigate how MSCs regulate macrophage polarization using high‐throughput sequencing. We isolated dental follicle MSCs from discarded human third molar dental follicles and cocultured them with THP‐1‐derived macrophages in the conditioned medium. Transcriptome sequencing identified differentially expressed genes (DEGs) in macrophages, integrating with multiomics database analysis to uncover polarization mechanisms. Our findings demonstrated successful MSC extraction from dental follicles, with the conditioned medium suppressing proinflammatory macrophage functions and influencing macrophage subtyping. MSCs, through paracrine signaling, activated the mitogen‐activated protein kinase (MAPK) pathway, leading to extracellular regulated protein kinases (ERK)1/2 phosphorylation and upregulation of early growth response 1 (EGR1) protein. Elevated EGR1 levels inhibited inflammatory gene expression, inhibiting the pro‐inflammatory immunoregulatory function of macrophages in inflammatory states. This study provides an efficient method for in vitro macrophage polarization identification. It offers insights into MSC‐regulated polarization mechanisms, with potential clinical implications for anti‐inflammatory therapy and immune regulation.

Human microbiome dysbiosis is related to various human diseases, and identifying robust and consistent biomarkers that apply in different populations is a key challenge. This challenge arises when identifying key microbial markers of childhood caries. We analyzed unstimulated saliva and supragingival plaque samples from children of different ages and sexes, performed 16S rRNA gene sequencing, and sought to identify whether consistent markers exist among subpopulations by using a multivariate linear regression model. We found that and bacterial taxa were associated with caries in plaque and saliva, respectively, while and were found in plaque isolated from children of different ages in preschool and school. These identified bacterial markers largely differ between different populations, leaving only as a significant caries-associated phylum in children. is a newly identified phylum, and our taxonomic assignment database could not be used to identify its specific genus. Our data indicated that, in a South China population, oral microbial signatures for dental caries show age and sex differences, but might be a consistent signal and worth further investigation, considering the lack of research on this microbe.

Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) belongs to the long non-coding RNA (LncRNA) family. LncRNA-MALAT1 is expressed in a variety of tissues and is involved in a variety of diseases and biological processes. Although LncRNA-MALAT1 is upregulated in a high-glucose microenvironment and may participate in odontogenic differentiation, the underlying mechanism is not yet well elucidated. Here, we show that MALAT1 was mainly expressed in the cytoplasm of dental pulp cells (DPCs) in situ hybridization. In addition, high levels of mineralization-related factors, namely, tumor growth factors β 1 and 2 (TGFβ-1 and TGFβ-2), bone morphogenetic proteins 2 and 4 (BMP2 and BMP4), bone morphogenetic protein receptor 1 (BMPR1), SMAD family member 2 (SMAD2), runt-related transcription factor 2 (RUNX2), Msh homeobox 2 (MSX2), transcription factor SP7 (SP7), alkaline phosphatase (ALP), dentin matrix acidic phosphoprotein 1 (DMP1), and dentin sialophosphoprotein (DSPP), were expressed, and MALAT1 was significantly overexpressed in DPCs 7 and 14 days after mineralization induction in a high-glucose microenvironment, but only TGFβ-1, BMP2, MSX2, SP7, ALP, and DSPP were significantly downregulated in DPCs after MALAT1 inhibition. MALAT1 may participate in the mineralization process of DPCs by regulating multiple factors (TGFβ-1, BMP2, MSX2, SP7, ALP, and DSPP).

Macrophages are the main mediators of the inflammatory response and play a major role in the onset and maintenance of periodontitis. Studies revealed that photobiomodulation (PBM) can change the polarization state of macrophages and inflammation reduction, although the cellular mechanisms are not fully elucidated. Here, the present study explored the effect of PBM (980 nm) on undifferentiated and M1-type macrophages and the underlying mechanism. RAW264.7 cells were exposed to laser irradiation under different laser parameters (0.5, 5.0, and 10.0 J/cm2) with or without LY294002 (an inhibitor of PI3K pathway). Then, confocal laser microscopy was used to observe cell differentiation; qPCR was performed to examine the gene expression and western blotting was used to detect the protein in the PI3K/AKT/mTOR pathway and activated macrophage markers. The obtained results revealed that 980 nm PBM increased the mRNA expression of iNOS, Il-10, Arg1, and Il-12 along with the inflammatory cytokines Tnfα, IL-1β, and Il-6 in M0-type macrophages in dose-dependent manner. More interestingly, PBM at 5 J/cm2 decreased the mRNA expression of iNOS, Il-12, Tnfα, IL-1β, and Il-6 and increased the expression of Arg1 and Il-10 by M1-type macrophages, along with the elevated expression of phosphorylation of AKT and mTOR. Moreover, PBM-induced M1-type macrophage polarization was significantly attenuated via LY294002 treatment. These suggest that 980 nm PBM could activate M0-type macrophages and increase M2/M1 ratio via the PI3K/AKT/mTOR pathway.