Vascular calcification, characterized by the ectopic deposition of calcium and phosphate crystals or even bone-like tissue, is a major risk factor for cardiovascular diseases such as atherosclerosis. However, the explicit mechanism remains unsettled. Current research demonstrates that atherosclerotic vascular calcification is a form of extraskeletal ossification—an active, cell-mediated process that closely resembles bone from macroscopic features down to the nanoscale structure. The mechanism underlying atherosclerotic calcification may be remarkably similar to those regulating bone remodeling and biomaterials-induced heterotopic ossification. This similarity is notably evidenced by the presence of osteoclast-like cells within vascular plaques. Based on previous findings that osteoclasts play key roles in initiating biomaterial-induced heterotopic ossification, we hypothesize for the first time that osteoclasts formed within the vascular wall may act as an ‘initiating signal’ triggering the development of atherosclerotic vascular calcification. This perspective may open new avenues for research into atherosclerotic calcification and contribute to the future development of strategies for its prevention and treatment.

Osteoinductive calcium phosphate ceramics (CaPs) hold great promise for bone repair, yet the metabolic principles governing their efficacy are poorly defined. Here, we identify mitochondrial oxidative phosphorylation (OXPHOS) as an early and indispensable pathway activated specifically by an osteoinductive tricalcium phosphate (TCPS) in material-induced bone formation. Our findings demonstrate that OXPHOS critically governs the M2 macrophage-osteoclast axis for bone formation by regulating both cellular energy supply and reactive oxygen species (ROS) homeostasis. Disrupting either function-by inhibiting OXPHOS (reducing ATP production) or by disrupting ROS balance (including ROS scavenging or accumulation)-uncouples this metabolic-immunological cascade and abrogates bone formation. Our work establishes mitochondrial OXPHOS as a central metabolic hub that integrates bioenergetics with ROS balance to orchestrate material-induced bone formation via M2 macrophage polarization-osteoclastogenesis axis. Consequently, these insights provide a rational basis for therapeutic modulation of the immunometabolic cascade in bone regeneration, via strategies designed to co-activate OXPHOS and fine-tune ROS dynamics.

Background Plasma fluoride reflects fluoride exposure from multiple sources. Fluoride exposure and health outcome observational studies are susceptible to confounding. We estimated the systemic effects of plasma fluoride attributable to drinking-water fluoride exposure in U.S. children and adolescents using an instrumental variable (IV) approach. Methods We analyzed NHANES 2013–2016 data including participants aged ≤ 19 years with measurements of plasma fluoride and household tap-water fluoride. Household tap-water fluoride was used as an IV for plasma fluoride to reduce unmeasured confounding. Survey=weighted two-stage least squares (2SLS) regression was applied: (1) plasma fluoride modeled as a function of tap-water fluoride; (2) each systemic biomarker regressed on predicted plasma fluoride. Biomarkers represented cardiovascular, metabolic, electrolytes, hormones, renal, and hepatic function. Models were adjusted for age, sex, body mass index, race/ethnicity, household income, maternal age, health insurance status, food security, birthweight, and US citizenship. We evaluated effect modification by age, sex, race/ethnicity, and household income. Results Mean plasma fluoride was 0.40 µmol/L (95% CI: 0.38–0.43) and mean water fluoride was 0.50 mg/L (0.43–0.57). Each one-unit increase in plasma fluoride concentration derived from tap-water fluoride was associated with lower systolic blood pressure (− 7.82 mmHg; 95% CI: −14.37, − 1.26), higher serum uric acid (0.92 mg/dL; 95% CI: 0.02, 1.82), higher insulin levels (geometric mean ratio [GMR]: 1.26; 95% CI: 0.53, 2.98), increased serum sodium (3.41 mmol/L; 95% CI: 1.18, 5.64), lower testosterone (GMR: 0.49; 95% CI: 0.30, 0.80), and reduced estimated glomerular filtration rate (GMR: 0.94; 95% CI: 0.89, 0.99). Across biomarker domains, significant effect modification of plasma fluoride associations was observed primarily by age, sex, race/ethnicity, and household income(p-value < 0.05). Conclusions Plasma fluoride attributable to tap-water exposure was associated with lower systolic blood pressure, testosterone, and renal function, and with higher serum sodium and uric acid, alongside heterogeneity across demographic subgroups.

Periodontitis is characterized by a self-sustaining pathophysiological cycle in which bacterial infection propagates destructive inflammation and oxidative stress, compromises tissue repair capacities, and facilitates recurrent infection. Current monotherapeutic strategies exhibit limited efficacy against this multifactorial pathology. Although resveratrol (RSV) exhibits significant anti-inflammatory and antioxidant activities, its clinical application is limited by poor solubility and suboptimal bioavailability. Herein, we fabricate a kind of injectable composite microspheres (RSV@Lipo@PMS) that encapsulate RSV-loaded cationic liposomes into polydopamine-modified alginate microspheres. This design leverages the synergistic interplay among the therapeutic bioactivity of RSV, the inherent antibacterial function of cationic liposomes, and the sustained retention afforded by the adhesive microcarriers. The composite system demonstrates robust reactive oxygen species (ROS) scavenging capacity, effectively suppresses lipopolysaccharide-induced inflammation in macrophages, and potently enhances bactericidal efficacy against key periodontal pathogens in vitro. In an experimental rat model of periodontitis, local administration significantly inhibits alveolar bone resorption and promotes functional tissue regeneration. Furthermore, to elucidate the underlying mechanisms of the composite system in alleviating periodontitis, we apply integrated transcriptomic and metabolomic profiling, which indicates a coordinated restoration of lipid metabolic homeostasis and mitochondrial energy metabolism. This multi-targeted strategy not only presents a promising therapeutic platform but also provides a mechanistic framework for the management of complex inflammatory conditions.

Objective:Multinucleated osteoclasts are the principal specialised cells responsible for bone resorption, but osteoclastogenesis, the formation of osteoclasts, entails substantial nutrient and bioenergetic demands. Macropinocytosis is an efficient pathway for nutrient scavenging in metabolically active cells; however, the interplay among metabolic state, osteoclast differentiation and macropinocytosis in bone-related diseases remains poorly understood. Methods:In this study, osteoclast differentiation was induced using murine bone marrow-derived macrophages and RAW 264.7 cells to investigate the role of macropinocytosis in metabolic regulation. Lipopolysaccharide (LPS) was applied to mimic inflammatory conditions in vitro to assess the influence of macropinocytosis on both metabolic profiles and inflammation-associated osteoclastogenesis. Additionally, ligature-induced periodontitis and ovariectomy (OVX)-induced bone loss models in mice were employed to evaluate the in vivo impact of macropinocytosis on bone resorption. Results:Enhanced macropinocytosis promoted osteoclast formation, with LPS further accelerating differentiation and increasing macropinocytic activity. This upregulation helped to meet the energy requirements of osteoclastogenesis via oxidative phosphorylation and glycolysis. Inhibition of macropinocytosis with (N-ethyl-N-isopropyl) amiloride (EIPA) reduced energy production and suppressed osteoclast differentiation. Elevated macropinocytosis was also observed in the periodontitis and OVX models, and its inhibition led to early, dose-dependent restoration of bone mass. Conclusion:Macropinocytosis provides a critical energy source for osteoclast differentiation. Targeting this pathway with EIPA represents a promising therapeutic approach for bone-related diseases. The translational potential of this article:As a bulk endocytic process, macropinocytosis offers a novel therapeutic target for bone-related diseases. The efficacy of EIPA in suppressing osteoclastogenesis and bone resorption suggests its potential as a clinical intervention drug.

Aim or purpose: We explored a shell-core structured biomaterial coated with a metal phenolic network, which exhibited adaptive sensitivity to pH values, to conduct bone repair in periodontitis. Materials and methods: Materials: Tannic acid, Cerium sulfate, NaOH, h gelatin nanoparticle powder, BSA, RhodaMine labeled BSA (BSA/RBITC), Murine sRank-Ligand (Rankl), Recombinant Macrophage Colony Stimulating Factor 1 (M-CSF), Lipopolysaccharide (LPS), Recombinant Mouse BMP9, phosphate buffered saline (PBS). Method: The animal experiments were approved by the Animal Ethics Committee of Chongqing Medical University. SD rats were assigned to four groups to study the effects of periodontitis repair as group 1 (control), group 2 (periodontitis), group 3 (4-week treatment), group 4 (12-week treatment) randomly (n≥3) . Results: Extracellularly, it rapidly responded to lower pH, achieving specific release in an inflammatory microenvironment. Intracellularly, it impacted the formation, function, and differentiation of osteoclasts through the macrophage-osteoclast axis, thereby promoting bone defect repair. Conclusions: In vivo and in vitro studies showed the biomaterial regulated osteoclasts to optimize periodontitis treatment strategies, highlighting the potential of modified nanobiomaterials for clinical application.

Aim or purpose: To clarify whether Drp1 mediates mitochondrial homeostatic imbalance involved in regulating osteoclast differentiation and its specific mechanism in the periodontal inflammatory microenvironment. And to design effective strategies to target depletion of osteoclasts in the periodontitis microenvironment. Materials and methods: Using immunofluorescence co-localization analysis, siRNA combined with Ad-Dnm1l to regulate Dnm1l and analyze the effect of Drp1 on the differentiation of pOCs. And combined with untargeted metabolomics to detect differential metabolites and enrich metabolic pathways to explore the effect of Drp1 on pOCs metabolism. Synthesize spatiotemporally selective biomimetic nanoparticles of pOCs and probe the homologous targeting ability; analyze their mitochondrial protective effects by Trap staining and qPCR. Construct an experimental periodontitis model and evaluate the periodontal bone resorption; detect the depletion of osteoclasts in the periodontal tissues by immunological staining. Results: Mitochondrial dynamics imbalance occurs in pOCs under the inflammatory microenvironment, with increased expression of Drp1, which increases their mitochondrial division, triggers mitochondrial metabolic reprogramming, causes aggregation of the metabolite succinic acid, and activates the downstream inflammatory signaling pathway, promoting the differentiation of pOCs to mOCs. Biomimetic nanoparticles with spatio-temporal selectivity of pOCs alleviate periodontitis bone resorption by targeting recognition of pOCs, exerting mitochondrial protection of pOCs, and depleting osteoclasts. Conclusions: The present study elucidates the abnormal mitochondrial morphology and functional manifestation and its specific mechanism in pOCs cells under inflammatory microenvironment and targeted depletion of osteoclasts, which may provide a new strategy for precision treatment of periodontitis.

Osteomyelitis exhibits bone defects in an inflammatory and acid microenvironment. As a crucial factor in this inflammation responses, the macrophage-osteoclast axis is absolutely the core to regulate. The research explored a shell-core structured biomaterial, consisting of a gelatin nanoparticle (GNP) platform loaded with bone morphogenetic protein 9 (BMP9) and coated with a metal phenolic network (TA-Ce), which exhibited adaptive sensitivity to pH values. Extracellularly, it rapidly responded to lower pH, achieving specific release in an inflammatory microenvironment. Intracellularly, it impacted the formation, function, and differentiation of osteoclasts through the macrophage-osteoclast axis, thereby promoting bone defect repair. In vivo and in vitro studies showed GNPs-BMP9@TA-Ce regulated osteoclasts to optimize osteomyelitis treatment strategies, highlighting the potential of modified nanobiomaterials for clinical application.

Repairing bone defects in inflammatory conditions remains a significant clinical challenge. An ideal scaffold material for such situations should enable minimally invasive implantation and integrate capabilities for immunomodulation, anti-infection therapy, and enhanced bone regeneration. In this study, we developed injectable calcitriol@polydopamine@gelatin methacryloyl hydrogel microspheres (CAL@PDA@GMs) using microfluidic technology. This system facilitates the sustained release of calcitriol, which features excellent biocompatibility and biodegradability, promotes osteogenesis, scavenges excessive reactive oxygen species (ROS), and induces the polarization of macrophages from the M1 to M2 phenotype, thereby mitigating lipopolysaccharide (LPS)-induced inflammation. These mechanisms work synergistically to create an optimal immune microenvironment for bone regeneration in inflammatory conditions. RNA sequencing (RNA-Seq) analyses revealed that immunomodulation is achieved by regulating macrophage phenotypes, inhibiting the nuclear transcription factor-kappa B (NF-κB) and ROS signaling pathways, and reducing the secretion of pro-inflammatory cytokines. This study proposes a novel method to enhance tissue regeneration by remediating the damaged tissue microenvironment and presents a potential clinical therapeutic strategy for large-scale bone injuries.

Critical-size bone defects (CSDs), which are those that do not self-repair in a given period, are essential for evaluating bone-regeneration strategies. We established CSDs models in the rabbit cranium and ulna, and the bone-regeneration capacities of porous calcium phosphate (CaP) ceramics were assessed. A 12.6-mm cranial defect was confirmed as a CSDs after 12 weeks, with submicron surface-structured biphasic calcium-phosphate (BCP) implants [consisting of 20% hydroxyapatite and 80% tricalcium phosphate (TCP)] demonstrating significantly higher bone formation (32.2% ± 10.6%) than micron surface-structured TCP (TCP-B) implants (17.8% ± 4.6%, p = 0.0121). Ulna defects (15.0 mm in length) failed to heal spontaneously within 24 weeks when the periosteum was removed from both the ulna and radius, and the radius was covered with an expanded polytetrafluoroethylene (ePTFE) membrane. No bone bridging (i.e., union) was observed in the BCP implants at 12 weeks, whereas 80% of BCP implants (four out of five) achieved union by 24 weeks. Furthermore, the bone area within the available space of BCP implants increased significantly from 19.3% ± 7.3% at 12 weeks to 37.7% ± 8.5% at 24 weeks (p = 0.0063), accompanied by significant BCP resorption (14.8% at 12 weeks and 30.2% at 24 weeks). This study offers two rabbit CSDs models for evaluating bone-regeneration strategies (including bone substitution), and the overall data obtained in the current study indicate the possibility of repairing CSDs with CaP ceramics demonstrating improved bone-forming ability given adequate implantation time.

Tooth formation is a highly orchestrated process that precisely regulates the size and shape of the tooth. During typical tooth development, Hertwig's epithelial root sheath (HERS) interacts with mesenchymal cells to direct the elongation of the tooth root and the deposition of dentin and cementum, thereby contributing to the formation of a fully developed tooth root. BMP9, a member of the BMP family, plays a significant role in growth, development, and cell differentiation. However, the precise function of BMP9 in dental root development remains unclear, particularly regarding its influence on HERS and odontoblasts. In this study, we utilized a mouse molar model to investigate the role of BMP9 signaling in tooth root development. The tooth formation of Bmp9 knockout (Bmp9-KO) mice and wild-type (WT) littermates was compared. Our findings revealed that Bmp9-KO mice exhibited shorter mandibular first molar roots, wider apical foramina, and thinner dentin compared with WT mice by micro-CT and hematoxylin-eosin staining analysis. Additionally, the results of immunohistochemistry and quantitative PCR indicated that in the absence of Bmp9, odontoblast differentiation and secretory function were compromised. Furthermore, Bmp9 ablation resulted in reduced cell proliferation and increased intercellular junctions within HERS, subsequently impacting root dentin formation and apical foramen closure. This study offers new insights into the regulatory role of BMP9 signaling in odontoblast and HERS function, highlighting its significance in root development and providing potential avenues for future research in tooth root regeneration.

Ectopia lentis (EL), characterised by impaired zonular fibers originating from non-pigmented ciliary epithelial cells (NPCEC), presents formidable surgical complexities and potential risks of visual impairment. Cataract surgery is the only treatment method for EL, but it leads to the loss of accommodative power of the lens post-operatively. Furthermore, the challenge of repairing zonular ligaments in situ remains a significant global issue. Ocular tissue and aqueous humour samples from patients with EL were subjected to RNA sequencing and Olink high-throughput proteomic analysis, revealing the downregulation of pathogenic genes (FBN1, MFAP2) and upregulation of secretory proteins (IL-12, MMP-1). The high expression of FBN1 and MFAP2 in NPCECs suggests their potential as candidates for zonular fiber construction; however, the limited availability of donor sources restricts the feasibility of NPCEC transplantation therapy. The reprogramming and directional differentiation of induced pluripotent stem cells (iPSC) to NPCEC was successfully achieved using the developed biomimetic scaffolds that mimic the microstructures of natural radial zonular fibers. Excitingly, the single injection of induced NPCEC-like cells significantly contributed to restoring and enhancing mechanical properties in zonular fiber structures in a rabbit model with EL. This proposed in situ iPSC-based regeneration technique might serve as an innovative therapeutic strategy for clinical EL patients, reduce the cataract surgery rate, and retain the adjustment capacity of inherent lentis.

Periodontal tissue regeneration remains a major challenge in oral regenerative medicine, aiming to restore functional structures such as cementum, periodontal ligament, and alveolar bone. Animal models are essential for evaluating the biocompatibility and regenerative efficacy of biomaterials, elucidating repair mechanisms, and supporting clinical translation. This review systematically summarizes chronic and acute periodontal defect models, their establishment protocols, and applications, covering oral gavage, periodontal inoculation, ligature, fenestration, dehiscence, intrabony, and furcation defects. The advantages and limitations of each model are analyzed in relation to simulating pathological microenvironments, testing regenerative scaffolds, and assessing drug delivery systems, with attention to combined modeling strategies. Evaluation methods from histology and immunohistochemistry to molecular assays and omics technologies are outlined, forming a multilevel assessment framework. Integrative multiomics approaches reveal key signaling pathways and metabolic networks in regeneration, guiding biomaterial design and targeted therapy development. This review offers a comprehensive methodological reference to bridge basic research with clinical application and to optimize experimental systems.

Background: Periodontitis is a prevalent oral inflammatory disease that leads to alveolar bone resorption and tooth loss. It is hard to control and prone to recurrence. Current treatments often fall short due to deep, tortuous periodontal pockets and antibiotic-resistant bacteria, such as Fusobacterium nucleatum (F. nucleatum). Notably, current clinical therapies fail to simultaneously fulfill three critical objectives: robust antimicrobial efficacy, potent anti-inflammatory activity, and effective periodontal regenerative capacity. Methods: Inspired by the structure of the lotus flower, nano/micron-combined hydrogel microspheres (PDA/BBR@Gel@BMP9-PDLSC), encapsulating polydopamine (PDA) nanoparticles carrying berberine (PDA/BBR) and BMP9-infected PDLSCs (BMP9-PDLSC), were developed. Results: Microspheres exhibited excellent biocompatibility and sustained drug release, along with significant antibacterial, anti-inflammatory, and bone tissue regenerative effects. In vivo studies confirmed their efficacy in treating calvaria defects and periodontitis with persistent F. nucleatum infection, showing superior new bone formation and anti-inflammatory effects without organ toxicity. Notably, our study demonstrated that the anti-inflammation and osteogenesis effects were due to the synergistic effects of BBR and BMP9 released by PDA/BBR@Gel@BMP9-PDLSC microspheres. RNA-Seq and Western blot analysis showed that BBR and BMP9 synergistically reduced inflammation and promoted bone formation by regulating key genes involved in TNF, TGF-β, and PPAR signaling pathways. Conclusions: Our study provides a novel approach for comprehensively treating periodontitis with antibacterial, anti-inflammatory, and bone tissue regenerative effects.

Early patterning of DNA methylation (DNAm) may play an important role in later disease development. To better understand intergenerational epigenetic inheritance, we investigated the correlation between DNAm in blood in mother-newborn and in father-newborn pairs in the Isle of Wight (IoW) birth cohort. For parent-newborn pairs (n = 48), offspring DNAm was measured in cord blood and the parent’s DNAm in whole blood. Mothers’ DNAm was analyzed at birth (Guthrie card), age 18, early and late pregnancy respectively, and fathers’ DNAm was measured during the mother’s pregnancy. Linear regressions were applied to assess the intergenerational correlation of parental DNAm with that of offspring. Among various pairs of mother-newborn and father-newborn DNAm, the pairs where the mothers’ DNAm was measured at age 18 years exhibited the highest number of CpGs with significant intergenerational correlation in DNAm, with 1829 CpGs (0.54%) of the 338,526 CpGs studied (FDR < 0.05). Amongst these 1829 CpGs, 986 (54%) are known quantitative trait loci (QTL) for CpG methylation (methQTL). When the mother’s DNAm was assessed at early pregnancy, the number of CpGs showing intergenerational correlation was the smallest (384 CpGs, 0.11%). The second smallest number of such CpGs (559 CpGs, 0.17%) was found when investigating DNAm in offspring cord blood and father pairs. The low proportions of intergenerationally correlated CpGs suggest that epigenetic inheritance is limited.

Abstract Background Cadmium (Cd) is extremely toxic and non-essential for plants. Different soybean varieties differ greatly in their Cd accumulation ability, but little is known about the underlying molecular mechanisms. Results Here, we performed transcriptomic analysis using Illumina pair-end sequencing on root tissues from two soybean varieties (su8, high-Cd-accumulating (HAS) and su7, low Cd-accumulating (LAS)) grown with 0 or 50 μM CdSO4. A total of 18.76 million clean reads from the soybean root samples were obtained after quality assessment and data filtering. After Cd treatment, 739 differentially expressed genes (DEGs; 265 up and 474 down) were found in HAS; however, only 259 DEGs (88 up and 171 down) were found in LAS, and 64 genes were same between the two varieties. Pathway enrichment analysis suggested that after cadmium treatment, the DEGs between LAS and HAS were mainly enriched in glutathione metabolism and plant-pathogen interaction pathways. KEGG analysis showed that phenylalanine metabolism responding to cadmium stress in LAS, while ABC transporters responding to cadmium stress in HAS. Besides we found more differential expressed heavy metal transporters such as ABC transporters and zinc transporters in HAS than LAS, and there were more transcription factors differently expressed in HAS than LAS after cadmium treatment in two soybean varieties, eg. bHLH transcription factor, WRKY transcription factor and ZIP transcription factor. Conclusions Findings from this study will shed new insights on the underlying molecular mechanisms behind the Cd accumulation in soybean.

Because its long, tender pods supply essential proteins, vitamins, and fibers to humans, yardlong bean (Vigna unguiculata ssp. sesquipedalis) is a commonly consumed vegetable, especially in Southeast Asia. To provide insights into the genetic bases of key agricultural traits in yardlong bean, we here created a high-density bin-map with 2084 bin markers using 514 227 SNPs from a recombinant-inbred line (RIL) population. Quantitative trait loci (QTL) mapping was carried out to identify loci associated with anthocyanin content (ANT), vitamin E content (VE), total soluble protein content (TSP), pod length (PL), hundred-seed weight (HSW), seed length and width (SL and SW, respectively), and seed coat color (SCC). In total, 20 related QTLs were isolated, explaining 7.58-56.03% of the phenotypic variation. Of these, five major QTLs (qANT5, qTSP11, qVE7, qPL3, and qSCC9) were detected in 2020, 2021, and the combined environment, explaining 11.96-56.03% of the phenotypic variation. VuANT1 was identified as a causal gene for the QTL qANT5, which regulated anthocyanin content; VuANT1 was highly expressed in immature purple pods but barely detectable in white pods. VuANT1 overexpression in tobacco leaves and yardlong bean hairy roots resulted in purple coloration as a result of anthocyanin accumulation. These findings suggested that VuANT1 was a key regulator of anthocyanin accumulation in yardlong bean. Our results lay a firm foundation for target agricultural trait improvement and clarification of the genetic mechanisms underlying agricultural traits in yardlong bean.

Background DNA methylation is a biochemical process in which a methyl group is added to the cytosine-phosphate-guanine (CpG) site on DNA molecules without altering the DNA sequence. Multiple CpG sites in a certain genome region can be differentially methylated across phenotypes. Identifying these differentially methylated CpG regions (DMRs) associated with the phenotypes contributes to disease prediction and precision medicine development. Results We propose a novel DMR detection algorithm, gbdmr. In contrast to existing methods under a linear regression framework, gbdmr assumes that DNA methylation levels follow a generalized beta distribution. We compare gbdmr to alternative approaches via simulations and real data analyses, including dmrff, a new DMR detection approach that shows promising performance among competitors, and the traditional EWAS that focuses on single CpG sites. Our simulations demonstrate that gbdmr is superior to the other two when the correlation between neighboring CpG sites is strong, while dmrff shows a higher power when the correlation is weak. We provide an explanation of these phenomena from a theoretical perspective. We further applied the three methods to multiple real DNA methylation datasets. One is from a birth cohort study undertaken on the Isle of Wight, United Kingdom, and the other two are from the Gene Expression Omnibus database repository. Overall, gbdmr identifies more DMR CpGs linked to phenotypes than dmrff, and the simulated results support the findings. Conclusions Gbdmr is an innovative method for detecting DMRs based on generalized beta regression. It demonstrated notable advantages over dmrff and traditional EWAS, particularly when adjacent CpGs exhibited moderate to strong correlations. Our real data analyses and simulated findings highlight the reliability of gbdmr as a robust DMR detection tool. The gbdmr approach is accessible and implemented by R on GitHub: https://github.com/chengzhouwu/gbdmr .

Vertical bone augmentation remains a significant challenge in implant dentistry and orofacial surgery, which is aimed at regenerating bone extraskeletal. This study conducts a proof-of-concept investigation into the effects of additively manufactured bioceramic scaffolds featuring bioinspired 3D architectures (trabecular, open channel, and layered) on vertical bone augmentation from the perspectives of osteogenesis and biomechanics. The experimental scaffold design was categorized into 4 Groups. Compression tests and finite element analysis (FEA) were conducted to assess the mechanical properties of scaffolds, Computational Fluid Dynamics (CFD) was employed to evaluate permeability and wall shear stress in scaffolds. Subsequently, the osteogenesis and biomechanical properties of these scaffolds were systematically evaluated in vivo using a rabbit calvarium model. The results illustrated that compression strength for all groups was within the typical range of trabecular bone. Remarkable bone neoformation was observed around the lower half of the scaffold, establishing a strong osseointegration effect with both the calvaria bone and scaffolds, and the highest osteogenic growth (approximately 4 mm) was observed at the interface between the titanium screw and the scaffold. This study scientifically proves that DLP-based bioceramic scaffolds effectively fulfill the osteogenic and biomechanical prerequisites for vertical bone augmentation, thereby providing preliminary validation of this concept.

Diabetes mellitus (DM) is regarded as one of the most critical public health challenges of the 21st century. It has evolved into a burgeoning epidemic since the last century, and today ranks among the major causes of mortality worldwide. Diabetes specialist nurses (DSNs) are central to good patient care and outcomes including confident self-care management. Evidence shows that DSNs are cost-effective, improve clinical outcomes, and reduce length of stay in hospital. In this brief narrative review, we aim to describe the roles of DSNs and their contribution in the treatment and management of patients with DM. This narrative review describes the importance of DSNs in healthcare practice, in the inpatient and outpatient departments, in the pediatrics department, in managing diabetic foot ulcers, in the treatment and management of gestational diabetes, in prescribing medications for DM and in diabetes self-management education on glycosylated hemoglobin, and cardiovascular risk factors. To conclude, DSNs have a crucial role in the treatment and management of patients with DM and its complications. DSNs have a great impact on diabetes therapy, and hence implementation of DSNs and nurse-led diabetic clinics might be beneficial for the health care system. Finally, having DSNs might significantly contribute to good healthcare practice and support. Even though DSNs are not available in several regions around the globe, and even though this post is still new to several health care institutions, the presence of DSNs recognized and certified by the various healthcare systems would be very useful.