Objective. Accumulating evidence indicates that microRNAs (miRNAs) play crucial roles in osteogenic differentiation. However, the associated mechanisms remain elusive. This paper is aimed at exploring the role of miR-129-5p in regulating bone marrow mesenchymal stem cell (BMSC) differentiation and bone regeneration in vivo and in vitro. Methods. BMSCs were transduced by miR-129-5p mimic, miR-129-5p inhibitor, and negative control lentivirus. The ability of BMSC differentiation to osteoblast was tested by alkaline phosphatase (ALP) and alizarin red staining (ARS). The expression of osteogenic genes (Runx2, Bmp2, and OCN) was examined via quantitative RT-PCR and western blot. A mouse model of calvaria defect was investigated by Micro-CT, immunohistochemistry, and histological examination. The luciferase reporter gene assay was performed to confirm the binding between Dkk3 and miR-129-5p. For the transfection experiments, lipofectamine 3000 was used to transfect pcDNA-Dkk3 into BMSCs to overexpress Dkk3. Coimmunoprecipitation and immunofluorescent localization assay were included for exploring the role of Dkk3 and β-catenin. Results. miR-129-5p was induced in BMSCs and MSC cell line C3H10T1/2 cells under osteogenic medium. Overexpression of miR-129-5p significantly promoted osteogenic differentiation of BMSCs in vitro. Moreover, BMSCs transduced with miR-129-5p mimic exhibited better bone regeneration compared with BMSCs transduced with control counterpart in vivo. Luciferase and western blot data showed that Dickkopf3 (Dkk3) is a target gene of miR-129-5p and the expression of Dkk3 was inhibited in BMSCs transduced with miR-129-5p mimic but enhanced in BMSCs transduced with miR-129-5p inhibitor. In addition, Dkk3 interacted with β-catenin directly. Conclusions. miR-129-5p promotes osteogenic differentiation of BMSCs and bone regeneration, and miR-129-5p/Dkk3 axis may be new potential targets for the treatment of bone defect and bone loss.

Since the discovery of mesenchymal stem cells (MSCs) in the 1970s, they have been widely used in the treatment of a variety of diseases because of their wide sources, strong differentiation potential, rapid expansion in vitro, low immunogenicity, and so on. At present, most of the related research is on mesoderm-derived MSCs (M-MSCs) such as bone marrow MSCs and adipose-derived MSCs. As a type of MSC, ectoderm-derived MSCs (E-MSCs) have a stronger potential for self-renewal, multidirectional differentiation, and immunomodulation and have more advantages than M-MSCs in some specific conditions. This paper analyzes the relevant research development of E-MSCs compared with that of M-MSCs; summarizes the extraction, discrimination and culture, biological characteristics, and clinical application of E-MSCs; and discusses the application prospects of E-MSCs. This summary provides a theoretical basis for the better application of MSCs from both ectoderm and mesoderm in the future.

This study aimed to evaluate the limitations of large language models (LLMs) in orthodontics by comparing their performance on licensing exam questions categorized by knowledge domains and error types. Deepseek-R1(DS) and ChatGPT-4(GPT) were evaluated using 396 text-based questions from the Chinese National Orthodontic Specialist Licensing Examination. Questions were classified through dual taxonomies: (1) "knowledge domains" including foundational biomechanical principles, cross-disciplinary medical integration, specialized orthodontic theory, and clinical decision-making skills; (2) "error types" including factual inaccuracies, logical deficits, and semantic misinterpretations. DS demonstrated significantly higher overall accuracy than GPT (80.3% vs 52.3%, p < 0.001), with statistically significant differences in foundational knowledge (79.8% vs 43.4%) and cross-disciplinary domains (81.0% vs 53.0%). Factual errors were predominant in both models (DS:57.7%, GPT:69.3%), though DS exhibited higher logical error rates (24.4% vs 16.4%). While DS outperforms GPT in general orthodontic knowledge assessment, both models show limitations in specialized domains requiring clinical reasoning. The superior performance of DS in standardized exams suggests potential for AI-assisted decision support in orthodontic training and licensing evaluation. However, the persistent factual errors and domain-specific limitations highlight the necessity for clinician verification in real-world applications. Integrating domain-specific knowledge refinement with logical reasoning modules could enhance LLMs' clinical utility in orthodontic practice.

The regeneration and repair of maxillofacial bone defects remain a significant clinical challenge. Jaw marrow-derived mesenchymal stem cells (JMMSCs) have attracted considerable attention owing to their favourable biological properties; however, the low survival rate of transplanted MSCs in vivo has substantially limited their therapeutic application. In this study, we demonstrate that hypoxic preconditioning enhances both the osteogenic and angiogenic potential of JMMSCs in vitro and in vivo. In vitro, the expression levels of osteogenic and angiogenic-related genes were assessed via qRT-PCR and Western blot following hypoxic preconditioning. In vivo, the impact of hypoxic preconditioning on the bone defect repair capacity of JMMSCs was evaluated. Micro-CT scanning was employed to compare microstructural changes at the defect sites. Microarray analysis identified differentially expressed long noncoding RNAs (lncRNAs) in JMMSCs subjected to hypoxic preconditioning. Subsequent bioinformatics analysis was conducted to explore potential regulatory interactions and key signalling pathways among lncRNAs, miRNAs, and mRNAs, followed by experimental validation. Microarray analysis revealed a significant upregulation of lnc-4632427E13Rik in JMMSCs following hypoxic preconditioning. Mechanistic studies demonstrated that lnc-4632427E13Rik functions as a molecular 'sponge' by sequestering miR-34a-5p, leading to activation of the Aldoa/ERK/Hif-1α signalling axis and subsequent promotion of both angiogenesis and osteogenesis in JMMSCs. Our findings reveal hypoxic preconditioning as a highly effective strategy for enhancing the differentiation potential of JMMSCs, and further highlight the therapeutic potential of targeting the lnc-4632427E13Rik/miR-34a-5p/Aldoa axis to improve the bone repair capacity of JMMSCs. The lnc-4632427E13Rik/miR-34a-5p/Aldoa axis significantly enhances the efficiency and reliability of bone regeneration, representing a promising therapeutic target for clinical applications in the repair of maxillofacial bone defects.

The mandible is essential for facial structure and oral function. Jaw bone marrow mesenchymal stromal cells (JBMMSCs) exhibit self-renewal and multi-lineage potential for bone regeneration, but are compromised by post-injury inflammation, poor vascularization, and osteogenic microenvironment disruption. This study evaluated the effect of ultrashort wave (USW) therapy on enhancing JBMMSCs function and promoting mandibular repair. In a murine bone defect model, 3 min USW treatment significantly improved bone regeneration (35.2 ± 3.8% increase in BV/TV, P < 0.01) and induced a 42% reduction in fibrosis versus controls. In vitro, USW enhanced JBMMSCs proliferation (2.1-fold increase in Ki67 + cells) and osteogenesis (3.5-fold higher ALP activity; 4.2- and 3.8-fold upregulation of RUNX2 and OCN expression). RNA-seq identified 141 differentially expressed genes, with phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling as the most enriched pathway (FDR < 0.01). Functional annotation of these transcriptomic alterations highlighted significant enrichment in cytokine responses and GTPase activity, suggesting that USW drives JBMMSC osteogenesis through the transcriptional modulation of the PI3K/Akt and JAK-STAT signaling networks These findings demonstrate USW therapy possibly promotes mandibular repair through JBMMSCs activity increase by regulating the gene expressions involved in the PI3K/Akt signaling pathway, with 3 min exposure being optimal. This study offers both theoretical insights and clinical rationale for USW-based maxillofacial bone regeneration strategies.