Integration of metabolomics and transcriptomics provides insights into the molecular mechanism of temporomandibular joint osteoarthritis.

The deficiency of clinically specific biomarkers has made it difficult to achieve an accurate diagnosis of temporomandibular joint osteoarthritis (TMJ-OA) and the insufficient comprehension of the pathogenesis of the pathogenesis of TMJ-OA has posed challenges in advancing therapeutic measures. The combined use of metabolomics and transcriptomics technologies presents a highly effective method for identifying vital metabolic pathways and key genes in TMJ-OA patients. In this study, an analysis of synovial fluid untargeted metabolomics of 6 TMJ-OA groups and 6 temporomandibular joint reducible anterior disc displacement (TMJ-DD) groups was conducted using liquid and gas chromatography mass spectrometry (LC/GC-MS). The differential metabolites (DMs) between TMJ-OA and TMJ-DD groups were analyzed through multivariate analysis. Meanwhile, a transcriptomic dataset (GSE205389) was obtained from the GEO database to analyze the differential metabolism-related genes (DE-MTGs) between TMJ-OA and TMJ-DD groups. Finally, an integrated analysis of DMs and DE-MTGs was carried out to investigate the molecular mechanisms associated with TMJ-OA. The analysis revealed significant differences in the levels of 46 DMs between TMJ-OA and TMJ-DD groups, of which 3 metabolites (L-carnitine, taurine, and adenosine) were identified as potential biomarkers for TMJ-OA. Collectively, differential expression analysis identified 20 DE-MTGs. Furthermore, the integration of metabolomics and transcriptomics analysis revealed that the tricarboxylic acid (TCA) cycle, alanine, aspartate and glutamate metabolism, ferroptosis were significantly enriched. This study provides valuable insights into the metabolic abnormalities and associated pathogenic mechanisms, improving our understanding of TMJOA etiopathogenesis and facilitating potential target screening for therapeutic intervention.

Enhancing angiogenesis in peri-implant soft tissue with bioactive silk fibroin microgroove coatings on zirconia surfaces.

Zirconia abutments and restorations have improved the aesthetic appeal of implant restoration, yet peri-implantitis poses a significant threat to long-term success. The soft tissue surrounding implants is a crucial biological barrier against inflammation and subsequent bone loss. Peri-implantitis, akin to periodontitis, progresses rapidly and causes extensive tissue damage. Variations in tissue structure significantly influence disease progression, particularly the lower vascular density in peri-implant connective tissue, compromising its ability to combat infection and provide essential nutrients. Blood vessels within this tissue are vital for healing, with angiogenesis playing a key role in immune defense and tissue repair. Enhancing peri-implant soft tissue angiogenesis holds promise for tissue integration and inflammation control. Microgroove surfaces have shown potential in guiding vessel growth, but using subtractive technologies to carve microgrooves on zirconia surfaces may compromise mechanical integrity. In this study, we utilized inkjet printing to prepare bioactive silk fibroin microgrooves (SFMG) coating with different sizes on zirconia surfaces. SFMG coating, particularly with 90 µm width and 10 µm depth, effectively directed human umbilical vein endothelial cells (HUVECs) along microgrooves, promoting their proliferation, migration, and tube formation. The expression of vascular endothelial growth factor A and fibroblast growth factor in HUVECs growing on SFMG coating was upregulated. Additionally, the SFMG coating activated the PI3K-AKT pathway and increased glycolytic enzyme gene expression in HUVECs. In conclusion, SFMG coating enhances HUVEC growth and angiogenesis potential by activating the PI3K-AKT pathway and glycolysis, showing promise for improving tissue integration and mitigating inflammation in zirconia abutments and restorations.

The influence of hygroscopic expansion of resin supporting dies on the fracture resistance of ceramic restorations during thermal cycling.

OBJECTIVES: To evaluate the hygroscopic expansion characterization of resin composite dies during thermal cycling, and their influence on the fracture resistance of dental ceramic materials as well as the effect of pre-immersion on these measurements. METHODS: Disc-shaped specimens (φ = 15.0 mm, h = 1.2 mm) and anatomical crown dies of four resin composites (epoxy, Z350, P60, G10) were fabricated. Disc-shaped samples were continuously soaked in distilled water and the volume expansion was measured at different time point by Archimedes method. Disc-shaped samples were pre-immersed for 0, 7, or 30 days, elastic modulus and hardness were measured using Nanoindentation test; thermal cycling (TC) test was performed (5 °C-55 °C, 104 cycles), and volume expansion during TC was measured. Four kinds of resin die with pre-immersion for 0, 7, or 30 days were cemented to 5Y-Z crown, or epoxy dies without pre-immersion were cemented to 5Y-Z, 3Y-Z and lithium disilicate glass (LDG) crowns, and load-to-failure testing was performed before and after TC. Finite element analysis (FEA) and fractography analysis were also conducted. RESULTS: The hygroscopic expansion was in the order: epoxy > Z350 > P60 > G10. Except for G10, the other three resin composites exhibited different degrees of hygroscopic expansion during TC. Only the elastic modulus and hardness of epoxy decreased after water storage. However, only the fracture loads of 5Y-Z and LDG crowns supported by epoxy dies were significantly decreased after TC. FEA showed a stress concentration at the cervical region of the crown after volume expansion of the die, leading to the increase of the peak stress at the crown during loading. SIGNIFICANCE: Only the hygroscopic expansion of epoxy dies caused by TC led to the decrease in the fracture resistance of the 5Y-Z and LDG crown, which may be related to the decrease in the elastic modulus of the epoxy die and the tensile stress caused by it.