Biogenic hydroxyapatite is known for its osteoinductive potential due to its similarity to human bone and biocompatibility, but insufficient vascularization compared to autogenous bone during early implantation limits bone integration and osteogenesis. Fluorine has been shown to improve hydroxyapatite’s mechanical properties and the coupling of osteogenic and angiogenic cells. In this study, fluorine-modified biogenic hydroxyapatite (FPHA) with varying fluorine concentrations was prepared and tested for its ability to promote vascularized osteogenesis. FPHA prepared in this study retained the natural porous structure of biological cancellous bone and released F⁻ ions when immersed in cell culture medium. The extraction solutions of FPHA0.25 and FPHA0.50 promoted the formation of capillary-like tubes by human umbilical vein endothelial cells (HUVECs), with FPHA0.25 significantly upregulating vegf mRNA and VEGF protein levels in co-cultured human bone marrow mesenchymal stem cells (HBMSCs). Additionally, FPHA0.25 and FPHA0.50 upregulated pdgf-bb mRNA and PDGF-BB protein levels in HUVECs. In vivo experiments using a rabbit cranial defect model demonstrated that FPHA0.25 promoted early bone formation and angiogenesis in the defect area, enhanced VEGF secretion, and increased PDGFR-β expression in endothelial and mesenchymal cells. These findings suggest that fluorine-modified biogenic hydroxyapatite with an optimal fluorine concentration (FPHA0.25) may offer a promising strategy to enhance the body’s innate bone-healing potential by accelerating vascularization.

Background: The reparative regeneration of jawbone defects poses a significant challenge within the field of dentistry. Despite being the gold standard, autogenous bone materials are not without drawbacks, including a heightened risk of postoperative infections. Consequently, the development of innovative materials that can surpass the osteogenic capabilities of autologous bone has emerged as a pivotal area of research. Methods: Mesenchymal stem cells (MSCs), known for their multilineage differentiation potential, were isolated from human umbilical cords and transfected with miR-181a. The osteogenic differentiation of miR-181a/MSC was investigated. Then, physicochemical properties of miR-181a/MSC-loaded nano-hydroxyapatite (nHAC) scaffolds were characterized, and their efficacy and underlying mechanism in rat calvarial defect repair were explored. Results: miR-181a overexpression in MSCs significantly promoted osteogenic differentiation, as evidenced by increased alkaline phosphatase activity and expression of osteogenic markers. The miR-181a/MSC-loaded nHAC scaffolds exhibited favorable bioactivity and accelerated bone tissue repair and collagen secretion in vivo. Mechanistic studies reveal that miR-181a directly targeted the TP53/SLC7A11 pathway, inhibiting ferroptosis and enhancing the osteogenic capacity of MSCs. Conclusions: The study demonstrates that miR-181a/MSC-loaded nHAC scaffolds significantly enhance the repair of bone defects by promoting osteogenic differentiation and inhibiting ferroptosis. These findings provide novel insights into the molecular mechanisms regulating MSC osteogenesis and offer a promising therapeutic strategy for bone defect repair.

This study aims to explore the effect of implant apex design, osteotomy preparation, intraosseous depth and bone quality on immediate implant placement insertion torque and establish a more sophisticated decision model with multi-factor analysis based on machine learning for improving the success rate of immediate implant placement. Six implant replicas of each of the three implant systems with different implant apex design were placed in polyurethane foam block with different densities(soft, medium and hard) via two osteotomy preparation protocols (normal preparation and undersized preparation) at different implant intraosseous depths (3 mm, 5 mm and 7 mm). The insertion torque for each implant was recorded and subsequently analyzed using one-way and four-way ANOVA. Prediction models of insertion torque were then constructed using multiple linear regression (MLR) and decision tree regression (DTR) analyses based on multi-factors. These machine learning models were evaluated and compared for their predictive accuracy and performance. The influencing factors of immedate implant placement insertion torque are ranked as follows: bone quality, intraosseous depth, osteotomy preparation protocol, and implant apex design. Both two machine learning preoperative prediction models (MLR and DTR) showed high accuracy in insertion torque prediction, with the latter’s R² reaching as high as 0.951. This research is of significant reference value for optimizing clinical decision-making, improving the success rate of immediate implant placement, and enhancing the efficiency of doctor-patient communication. In addition, this study further refined the evaluation framework for implant performance, rendering it more comprehensive and standardized.

Background: The regeneration of bone tissue is a critical challenge in oral and maxillofacial surgery, with the success of such procedures often depending on the ability to promote osteogenesis while managing the soft tissue environment. The role of gingival fibroblasts in modulating the osteogenic potential of mandible mesenchymal stem cells (MMSCs) mediated by bone substitute materials (BSMs) is not fully understood. This study aimed to investigate the impact of gingival fibroblasts on the osteogenic differentiation of MSCs in the presence of BSMs and to elucidate the underlying mechanisms, focusing on the WNT/β-catenin signaling pathway.Methods: Gingival fibroblasts and BSMs co-culture conditioned medium was used to culture MMSCs, and the expression and activity of alkaline phosphatase (ALP), as well as osteogenic and fibrogenic gene and protein expression, were evaluated. Additionally, the expression of key factors of WNT/β-catenin signaling pathway were investigated. In vivo animal experiments were conducted to assess the effect of gingival fibroblasts on BSM-mediated bone regeneration.Results: Gingival fibroblasts and BSMs co-culture environment did not affect MMSCs proliferation but significantly inhibited ALP expression and activity, as well as osteogenic gene and protein expression, while promoting expression of fibrogenic markers. This suppression was associated with the downregulation of key factors in the WNT/β-catenin signaling pathway. In vivo, increased suppression of bone defect repair was observed with higher amounts of gingival fibroblasts, confirming the in vitro findings.Conclusion: Our study demonstrates that gingival fibroblasts can suppress the osteogenic potential of BSMs by inhibiting the autocrine WNT expression and the activation of the WNT/β-catenin signaling pathway in MMSCs. These findings highlight the importance of considering the cellular microenvironment in tissue engineering and regenerative medicine and suggest potential targets for modulating MMSCs behavior to enhance bone regeneration.

Healing abutment dislodgement is a common clinical complication in dental implantology, yet its impact on peri-implant soft tissue immunity remains unclear. This exploratory pilot study aimed to investigate the immunological changes associated with different healing modes, which is essential for optimizing peri-implant tissue management. In this observational study, peri-implant soft tissues were collected from 12 patients and assigned to 4 groups: (A) sites with healing abutment dislodgement, (B) pre-implant recipient sites, (C) fully closed healing abutment sites, and (D) partially closed healing abutment sites. Histological and immunohistochemical analyses were performed to evaluate tissue morphology and the distribution of immune cell populations, including neutrophils, macrophages, T cells, B cells, and plasma cells. Dislodgement of the healing abutment resulted in disruption of the epithelial barrier and pronounced infiltration of both innate and adaptive immune cells in peri-implant soft tissue. Compared to the fully and partially closed groups, the dislodgement group exhibited significantly higher densities of MPO⁺ neutrophils, CD68⁺ macrophages, CD3⁺ T cells, CD20⁺ B cells, and CD138⁺ plasma cells within both epithelial + superficial connective tissue region and deep connective tissue region. In contrast, intact healing abutments were associated with minimal immune cell infiltration and preserved tissue architecture. Notably, partially closed sites displayed localized immune cell aggregation at the deep connective tissue region (abutment-soft tissue interface). Disruption of the soft tissue barrier following healing abutment dislodgement is associated with persistent inflammatory responses and long-lasting immune cell infiltration. These findings highlight the importance of maintaining healing abutment stability and prompt restoration of the mucosal barrier to minimize immune activation and protect peri-implant tissue health. Healing abutment dislodgement is a common but often under-recognized complication in implant dentistry. This study demonstrates that loss of the soft tissue seal following abutment dislodgement leads to persistent and pronounced immune cell infiltration and long-lasting inflammatory responses Clinically, these findings highlight the importance of maintaining healing abutment stability and prompt restoration of the mucosal barrier to minimize inflammation and protect peri-implant tissue health. Improved awareness and evidence-based management of abutment dislodgement may help prevent peri-implant complications and optimize long-term treatment outcomes.