Artificial intelligence (AI) has been increasingly applied in the diagnosis and treatment of endodontic conditions. This narrative review summarizes the cu

Overexpression of urokinase‑type plasminogen activator receptor (uPAR) has been implicated in promoting tumor invasion in various cancer types, including oral tongue squamous cell carcinoma (OTSCC); therefore, the effect of suppressing uPAR expression on the invasive and metastatic potential of OTSCC was investigated. A total of 65 paraffin‑embedded tissues were obtained from patients with OTSCC. Immunohistochemistry was used to determine the expression level of uPAR. The Ts cells transfected with short hairpin RNA targeting uPAR were constructed and validated. The cells were used in a number of in vitro analyses, including migration, invasion and western blot analysis assays. Furthermore, a mouse lung metastatic model was used to detect the metastatic ability of OTSCC cells in the lungs. OTSCC cell metastasis and relapse were determined to be associated with uPAR immunopositivity. Inhibition of uPAR expression in Ts cells demonstrated a 40% decrease in migration and a 60% decrease in invasion in vitro, with an associated downregulation of matrix metalloprotease (MMP)‑2, MMP‑9 and phosphorylated extracellular signal‑regulated kinase. In vivo analysis indicated a 90% decrease in the number of mice bearing macroscopic lung metastases. In conclusion, the present study demonstrated that the targeting of uPAR‑inhibited cellular proliferation and invasion would provide a potential treatment for OTSCC in the future.

Retaining a lubricating, drug-delivering hydrogel on a load-supporting implant requires coordinated scaffold and interface design. We developed an osteochondral-inspired poly(ether ether ketone) (PEEK)/hydrogel bilayer by continuous 3D printing and surface modification. A dense PEEK base supports a porous upper region containing a poly(vinyl alcohol)/poly(acrylic acid) (PVA/PAA) composite hydrogel. Sulfonation and ultraviolet-assisted acrylic acid (AA) treatment prepare the substrate for hydrogel attachment. At a 4:1 PVA:AA feed mass ratio, the drug-free composite construct (gPCH) exhibited a maximum detachment force per unit width of 304.60 ± 7.20 N m⁻¹, 2.39 times that of PVA on sulfonated PEEK without AA/UV treatment. Its friction coefficient was 0.073 ± 0.005 during a 10 min screening test under 2 N in 25% fetal bovine serum at room temperature. The diclofenac sodium (DFN)-loaded counterpart (gPCHD) released 73.92 ± 3.24% of DFN over 72 h in PBS at 37 °C. In lipopolysaccharide-stimulated rabbit bone marrow-derived mesenchymal stem cells, gPCHD showed lower COX-1, COX-2, and IL-6 mRNA expression than composition-matched, drug-free gPCH. Twelve-week rabbit histology (n = 3 per group) provided descriptive observations of tissue contact and a retained hydrogel-bearing layer. This architecture–interface design integrates structural support, interfacial retention, short-duration lubrication, and drug delivery; long-term tribological performance and component-specific in vivo effects remain to be established.

Objective Wnt5a is involved inflammation, including pulpitis, by upregulating cytokine/chemokine expression. Odontoblasts are the first layer cells in dental pulp and respond to inflammatory stimuli. However, whether Wnt5a is involved in odontoblast inflammation is unclear. This study aimed to investigate the role of Wnt5a in odontoblast inflammation. Methods We measured and compared Wnt5a- or TNF-α-induced cytokine/chemokine expression in mouse odontoblast-like (17IIA11) cells by real-time PCR and Western blotting. Transwell assays were used to examine the effect of Wnt5a on RAW264.7 macrophage migration. We examined whether the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways were involved in the molecular mechanism of TNF-α or Wnt5a in 17IIA11 cells by Western blotting. Results TNF-α upregulated Wnt5a in odontoblasts. Wnt5a upregulated CCL2 expression in odontoblasts and enhanced RAW264.7 cell migration. We also found that TNF-α-induced Wnt5a expression was abrogated by inhibiting the MAPK pathway or NF-κB activity and that inhibiting MAPK activity could lead to decreased NF-κB activity. Conclusions Wnt5a is involved in the TNF-α-induced inflammatory response in odontoblasts. TNF-α upregulates Wnt5a expression via MAPK-dependent NF-κB activation in odontoblasts. Wnt5a upregulates CCL2 expression in odontoblasts and enhances RAW264.7 macrophage migration.

Manual dexterity is fundamental to preclinical dental training, yet opportunities for standardized early psychomotor practice remain limited. This study evaluated changes in simulator-based manual dexterity task performance following a curriculum-embedded virtual simulation course for second-year undergraduate dental students. Ninety-nine students completed identical pre- and post-training assessments using the man001 three-dimensional tunnel module over a six-week course; during the intervening training period, students practiced other, more advanced manual dexterity modules. Ninety-eight students completed an anonymous post-course questionnaire. The mean total score increased from 79.94 ± 4.54 to 86.26 ± 3.60, with a mean paired difference of 6.32 points (95% CI, 5.29–7.36; p < 0.001; Cohen’s d_z = 1.22). Leeway decreased from 10.92 ± 4.53 to 4.96 ± 2.79 (p < 0.001), and container values also decreased (p < 0.001), whereas target performance did not change significantly (p = 0.169). Overall, 92.93% of students improved their total score. Most respondents reported active engagement (94.90%), considered the course helpful (96.94%), and perceived it as clinically relevant and supportive of theory–practice integration (98.98%). The six-week course was associated with short-term changes in man001 simulator-task performance and predominantly favorable student perceptions; further research is needed to explore the retention of these changes and their transfer to broader manual dexterity and physical preclinical procedures.