Journal of dental research最新文献

Traumatic life events may shape how individuals utilize health care, yet their impact on medical and dental service utilization is underexplored. This study investigates how such events influence subsequent health care use. We analyzed data from the Mexican Health and Aging Study, the first longitudinal cohort in Mexico of middle-aged and older adults. The analytic sample comprised 17,424 unique individuals across 39,875 total observations. Three traumatic events were examined in relation to their effects on medical and dental service use: (1) experience of a natural disaster, (2) experience of the death of a child, and (3) experience of a crime or accident. We combined propensity score weighting with multivariable mixed-effects logistic regression to account for both confounding and correlation arising from repeated measures. We estimated the effect of exposure to each traumatic event by parametric g-computation, calculating risk differences with 95% confidence intervals (CIs). Exposure to a natural disaster increased medical service use by 4.2% (95% CI, 2.2 to 6.2) while reducing utilization of dental care by 4.8% (95% CI, -7.0 to -2.5). The death of a child increased medical service use by 4.9% (95% CI, 2.7 to 7.2) while reducing utilization of dental care by 6.0% (95% CI, -8.6 to -3.4). Crime or accidents increased utilization of medical services by 12.7% (95% CI, 11.1 to 14.2) while having no clear effect on utilization of dental care. Traumatic events have substantial and differential impacts on health care utilization. In particular, among middle-aged and older adults in Mexico, natural disasters and the death of a child have divergent effects on the utilization of medical versus dental care, while crime and accidents only affect medical care. Future research into this underdeveloped area may help to develop a more precise understanding of the underlying mechanisms.

To reduce secondary caries-related restoration failure, ion-releasing fillers are being incorporated into resin-based composites (RBCs). However, a comprehensive investigation into the cytocompatibility of these materials, particularly concerning transcriptomic responses to monomer and ion release, has yet to be conducted. This study investigated model RBCs (80:20 UDMA:HEMA matrix, 62 vol% filler), including a fluorapatite (FA) containing composite (FA+, 9 vol%), to assess the effect of fluoride ion-releasing filler content on degree of conversion (DC%) and monomer release. Apparent water sorption and fluoride release were evaluated after 28 d of storage in artificial saliva (pH 7 and pH 4) and distilled deionized water. Cytocompatibility was assessed using an XTT assay on human gingival fibroblasts (HGFs), and the expression of genes encoding DNA-repair and stress-response markers following composite exposure was analyzed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). RNA sequencing (RNA-seq) identified differentially expressed genes in response to FA+ and fluorapatite-free RBCs (FA-). Unfilled specimens exhibited lower DC% and higher monomer release compared to the RBCs. FA+ specimens had the highest apparent water sorption, particularly after pH 7 artificial saliva storage. Fluoride release was most significant in acidic environments. UDMA reduced HGF viability compared to HEMA at all concentrations up to 5 mM, but the polymerized RBCs caused no reduction compared to control HGFs. However, expression analysis by RT-qPCR of DNA-repair and stress-response markers following composite exposure revealed that UDMA reduced repair gene expression, whereas HEMA stimulated it. RNA-seq analysis revealed significant changes in gene expression profiles upon composite exposure, with enriched pathways related to ferroptosis and protein digestion. These findings highlight, for the first time, the potential for significant cellular responses even with limited composite component release from ion-releasing RBCs, underscoring the need for further research into the long-term biocompatibility of these materials.

Organs and tissues develop in close association with the vasculature, which transports blood and nutrients and helps to remove waste. The vasculature is composed primarily of endothelial cells, which provide structure, form barriers, and are a source of developmental signals. We recently found that Mediator, a multiprotein complex that regulates transcription, was essential for proper vascular development. Here, we investigated the specific role of the Mediator tail subunit Med23 in endothelial cells. Endothelial cell-specific knockout of Med23 in mouse embryos using Tek-Cre resulted in vascular anomalies, including edema, hemorrhage, and mispatterned vasculature, alongside craniofacial defects such as micrognathia and cleft palate. Spatial transcriptomics revealed the downregulated expression of key vascular and osteogenic genes in Med23 mutants, including Vegfr1 and Col1a1, with altered signaling dynamics between endothelial and osteoblast populations. Elevated hypoxia-inducible factor 1-alpha (HIF1α) expression and reduced vascular endothelial growth factor (VEGF) signaling were observed in Med23 mutants, suggesting a hypoxia-driven suppression of neural crest cell-derived osteoblast maturation. Consistent with this model, the pharmacologic inhibition of HIF1α, combined with VEGFA supplementation, rescued craniofacial ossification and extended embryonic viability. These findings reveal a critical role for Med23 in coordinating vascular patterning and intramembranous ossification and highlight distinct hypoxic and angiogenic requirements in craniofacial dermal bone versus axial and appendicular endochondral bone development. Thus, the cranial vasculature, and more specifically endothelial cells, plays an instructive role in neural crest cell and osteogenic differentiation during cranioskeletal development.

Salivary gland (SG) fibrosis represents a critical pathological feature of exocrine hypofunction driven by the persistent activation of myofibroblasts (MFs). However, the translational gap between the convoluted in vivo regulatory networks governing these cells and the deployment of precise, disease-modifying interventions remains a formidable challenge. This review systematically examines current mechanistic evidence undergirding MF activation, survival, and its phenotypic reversal, focusing on restoring glandular function. We synthesize recent literature mapping in vivo canonical profibrotic signaling cascades, noncanonical crosstalks, and cellular heterogeneity within the injured exocrine stroma. Evidence underscores that the pathological tilt between profibrotic Smad3 and inhibitory Smad7 acts as a critical rheostat for MF differentiation across diverse etiologies. Beyond classical pathways, emerging mechanisms-such as mitochondrial metabolic reprogramming, store-operated calcium entry (SOCE) collapse, and persistent cGAS-STING innate immune sensing-are mechanically reinforced by extracellular matrix rigidity via a YAP/TAZ mechanotransduction loop. These events, coupled with aberrant epigenetic imprinting, structurally lock the persistent MF phenotype and restrict cellular plasticity. Consequently, we evaluate targetable interventions-ranging from small-molecule inhibitors (SB431542, decitabine) and biologics (rituximab) to traditional botanical formulations (Shengmai San) and stem cell-derived extracellular vesicles-that effectively attenuate scar formation and improve salivary flow rates in preclinical or clinical models. Ultimately, this review establishes a novel, etiology-driven "etiology-origin-pathway-target" matrix that shifts the paradigm from empirical anti-inflammatory management toward origin-specific precision therapeutics capable of reversing established salivary gland fibrosis.

Molar root-incisor malformation (MRIM) is characterized by abnormalities in the root and pulpal floor, which may lead to dental complications. However, research on MRIM remains limited and is largely confined to case-based observations. Therefore, this study aimed to characterize the morphology and proteomic profile of the cervical mineralized diaphragm (CMD) in MRIM. Extracted MRIM-affected teeth (n = 11) from 6 patients and extracted third molars as controls (n = 11) were collected. Two MRIM-affected teeth and two control teeth were subjected to micro-computed tomography and scanning electron microscopy. CMD tissues adjacent to the pulpal floor and control pulpal-floor dentin were harvested for protein extraction and analyzed by liquid chromatography-tandem mass spectrometry. Label-free quantification and bioinformatics analyses (gene set enrichment and protein-protein interaction network analysis) were performed, and proteins with >2-fold change were considered differentially expressed. Micro-computed tomography demonstrated a highly radiopaque CMD at the pulpal floor that occluded pulp-root canal communication, with a radiodensity between that of the enamel and dentin and a dense/porous internal architecture. Scanning electron microscopy revealed columnar and crystal-like structures. Proteomic profiles differed between MRIM and controls, with reduced epithelial-mesenchymal transition signaling in MRIM (normalized enrichment score = 1.47, false discovery rate = 0.116; control vs. MRIM). A total of 116 proteins showed >2-fold change (62 upregulated and 54 downregulated). Upregulated proteins included keratinization-associated proteins (KRT75, KRT82, EVPL, and KRT6B) with enrichment of keratinization- and epidermis-related terms, whereas downregulated proteins included SPP1, AMBN, and ECM1, which were associated with biomineral tissue development. Within the limits of this study, the CMD in MRIM exhibits a distinctive mineralized microarchitecture and a proteomic signature implicating altered epithelial-associated and extracellular matrix/mineralization processes. These findings provide candidate targets for tissue-level validation and mechanistic studies of MRIM.

Additive manufacturing (AM) has expanded in dentistry, yet the color and translucency stability of 3-dimensional-printed resin-based materials remain insufficiently understood. This study investigated the main and interaction effects of printing orientation, specimen thickness, and surface treatments on the color and translucency stability of a 3-dimensional printed resin-ceramic hybrid material. Ninety AM specimens were fabricated using a factorial design combining 3 printing orientations, 3 specimen thicknesses, and 2 surface treatments (3 × 3 × 2, n = 5 per condition) and compared with 30 subtractively manufactured control specimens (Vita Enamic). Aging was simulated by thermocycling (5000 cycles, 5-55 °C). Color coordinates were measured via the Commission Internationale de l'Éclairage L*a*b* color system, and color change and translucency change were calculated. Degree of conversion, water sorption, and surface roughness were also evaluated. Printing orientation and specimen thickness significantly affected color change and translucency change (P < 0.05), with the 90° orientation showing lower changes than 0° and 45°. Surface treatment had a limited influence on color and translucency stability, although glazing resulted in higher water sorption as compared with polishing (P < 0.05). No significant effects of printing orientation were observed for degree of conversion or surface roughness, whereas surface treatment significantly influenced surface roughness (P < 0.05). Despite these variations, all groups remained within clinically acceptable thresholds for color and translucency changes. Overall, the findings suggest that AM resin-ceramic restorations have potential for use in definitive restorations. Optimizing printing orientation and material thickness may enhance the color and translucency stability of AM resin-ceramic restorations, supporting their clinical applicability.