Oral cancer (OC), characterized by malignant tumors in the mouth, is one of the most prevalent malignancies worldwide. Chemotherapy is a commonly used treatment for OC; however, it often leads to severe side effects on human bodies. In recent years, nanotechnology has emerged as a promising solution for managing OC using nanomaterials and nanoparticles (NPs). Nano-drug delivery systems (nano-DDSs) that employ various NPs as nanocarriers have been extensively developed to enhance current OC therapies by achieving controlled drug release and targeted drug delivery. Through searching and analyzing relevant research literature, it was found that certain nano-DDSs can improve the therapeutic effect of drugs by enhancing drug accumulation in tumor tissues. Furthermore, they can achieve targeted delivery and controlled release of drugs through adjustments in particle size, surface functionalization, and drug encapsulation technology of nano-DDSs. The application of nano-DDSs provides a new tool and strategy for OC therapy, offering personalized treatment options for OC patients by enhancing drug delivery, reducing toxic side effects, and improving therapeutic outcomes. However, the use of nano-DDSs in OC therapy still faces challenges such as toxicity, precise targeting, biodegradability, and satisfying drug-release kinetics. Overall, this review evaluates the potential and limitations of different nano-DDSs in OC therapy, focusing on their components, mechanisms of action, and laboratory therapeutic effects, aiming to provide insights into understanding, designing, and developing more effective and safer nano-DDSs. Future studies should focus on addressing these issues to further advance the application and development of nano-DDSs in OC therapy.

Background: Primary failure of eruption (PFE) is a rare disorder characterized by a posterior open bite. While mutations in the parathyroid hormone 1 receptor (PTH1R) gene have been demonstrated to cause PFE, the underlying mechanisms remain largely unknown. Methods: Whole exome sequencing was conducted to identify PTH1R variants in a PFE family. MG63 cells that stably expressed the corresponding mutant PTH1R were established using lentiviruses. Next, osteogenesis was assessed by measuring cell alkaline phosphatase activity, conducting alizarin red staining, and evaluating osteoblast-specific gene expression. Then, computational analysis of binding affinity and RNA sequencing were carried out. Lastly, rescue experiments were performed to validate the mechanism underlying the pathogenesis of PFE. Results: A novel PTH1R missense mutation (c.904G > A, p.E302K) was identified in a Chinese family affected by PFE. Moreover, the E302K mutation inhibited the expression of osteogenic-specific genes and proteins in MG63 cells. Computational analysis revealed the E302K mutation decreased the binding affinity of Gα_s to the PTH1R protein. Consistently, cAMP accumulation assays demonstrated that the E302K mutation impaired the intracellular PTH_1-34 -induced accumulation of cAMP. Further RNA sequencing analysis and validation experiments revealed that the PI3K-AKT signaling pathway was predominantly down-regulated in response to the E302K mutation. Finally, forskolin partially restored the effects of the E302K mutation on osteogenesis. Conclusions: This study indicated that the E302K mutation in PTH1R decreased the binding affinity of PTH1R protein for Gα_s, down-regulated the cAMP-PI3K/AKT signaling pathway, and inhibited osteogenesis, eventually leading to PFE. This study not only expands the genotypic spectrum of PTH1R mutations but also elucidates the underlying pathogenic mechanism of PTH1R-associated PFE.

Objective: Emerging evidence suggests that oral squamous cell carcinoma (OSCC) harbors distinct microbial communities, yet their influence on tumor immunobiology remains unclear. This study investigated the prognostic value of intratumoral microbiota and their role in modulating CD8⁺ T-cell function. Materials and methods: Using TCGA datasets, a 19-microorganism prognostic signature was constructed via Cox and LASSO regression and validated with Kaplan–Meier survival analysis. Comprehensive bioinformatics analyses, including GSEA/GSVA, CIBERSORT, ESTIMATE, pharmacogenomics, and mutational profiling, were performed to explore underlying mechanisms. Results: The microbial signature demonstrated strong predictive performance, with higher risk scores significantly associated with reduced overall survival (p < 0.001). High-risk tumors exhibited enrichment of PI3K/AKT/mTOR signaling, metabolic reprogramming, and epithelial–mesenchymal transition, alongside an immunosuppressive microenvironment characterized by CD8⁺ T-cell depletion, M0 macrophage infiltration, and upregulation of immunosuppressive markers including CD276 and TGF-β1. Conversely, immune-activating checkpoints such as PD-1 and CTLA-4 were elevated in low-risk tumors. Notably, periodontal pathogens negatively correlated with immune effector activity, and TP53 mutations were more frequent in high-risk cases (82% vs. 67%). Conclusions: This study identified intratumoral microbial signatures as independent prognostic biomarkers and validated their reproducibility in an external cohort. Our findings support a microbiota–immune axis contributing to immune evasion in OSCC, offering novel avenues for prognostic stratification and therapeutic intervention.

Cleidocranial dysplasia (CCD) is an uncommon autosomal dominant disease, characterized by hypoplasia of clavicles, delayed fontanelle closure, dental anomalies, and short stature. It has been reported in the literature that the pathogenic variants of Runt-related transcription factor 2 (RUNX2) gene are correlated with CCD patients. Here, we report a consanguineous Chinese family with 2 patients suffering from CCD, presenting similar skeleton and dentition malformation. Upon whole-exome sequencing, 52863 variants were detected in the propositus. Based on the genotype phenotype correlation, a frameshift deletion c.1554delG p.(Trp518Cysfs∗61), located in exon 8 of RUNX2, remained after filtration. For Sanger sequencing, all exons of the RUNX2 gene in members of this Chinese family were amplified by polymerase chain reaction. Mutation mentioned above was confirmed in the propositus and his mother, which has not been reported previously and cannot be found in the publicly available databases. The present study expands the pathogenic variant spectrum of RUNX2 gene and contributes to molecular diagnosis.