With the development of nanomaterials and nanotechnology, nanomedicine possesses the vast application prospects in the field of cancer therapy. Although the proportion of radiotherapy in cancer comprehensive therapy is rising, the radiotherapy resistance of cancer cells and the side effects of radiotherapy are the existing problems. Compared with the traditional radiotherapy sensitization, it will present a higher treatment efficiency and lower toxicity to introduce nanomaterials and nanotechnology to cancer radiotherapy. This review elaborates the research of nanomaterials and nanotechnology on cancer radiotherapy sensitization.

The abuse of antibiotics has been increasing bacterial resistance, which means there is a need to develop methods for the efficient detection and effective treatment of multiresistant bacterial infections. As one of graphene-based materials, graphene quantum dots (GQDs) have distinct mechanical, electrical, and optical properties, including a small size, a large surface area-to-volume ratio, biocompatibility, antimicrobial activity and tunable photoluminescence. Therefore, GQDs are expected to be widely used as antimicrobial materials, drug delivery carriers and photosensitizers in antibacterial applications. In this review, we focus on their synthesis, characteristics and antimicrobial applications in oral medicine.

During tumor progression, the mechanical properties of the tumor microenvironment play a pivotal regulatory role. As core mechanical indicators, cellular stiffness and extracellular matrix stiffness profoundly influence tumor development through multiple pathways, including cytoskeletal remodeling, activation of signaling pathways, and metabolic regulation. Studies have demonstrated that the tissue stiffness of various solid tumors is significantly higher than that of corresponding normal tissues, while their cellular stiffness exhibits the opposite trend. This mechanical characteristic is also observed in oral squamous cell carcinoma and exerts crucial regulatory effects during tumor progression. This review systematically summarizes the molecular composition and regulatory mechanisms underlying the stiffness of tumor cells and extracellular matrix (ECM). Mainstream stiffness detection technologies such as atomic force microscopy, microfluidic deformation, and real-time deformability cytometry are outlined, with particular emphasis on their applications and limitations in oncology research. This review comprehensively analyzes how mechanical properties regulate key processes in tumor progression, including growth, proliferation, invasion, metastasis, angiogenesis, lymphangiogenesis, drug resistance, and immune escape. This review synthesizes biomechanics-based therapeutic strategies, including: ① targeting the regulation of tumor cell stiffness through cytoskeletal modulators and cholesterol-depleting agents to enhance immune responses; ② reducing ECM stiffness by matrix remodeling enzyme inhibitors, ECM component modulators, or receptor antagonists to improve drug delivery efficiency, and combining with immunotherapy or photothermal therapy for enhanced therapeutic effects; ③ enhancing the mechanical adaptability and anti-tumor activity of immune cells through pharmacological or genetic approaches. This review establishes a robust conceptual framework for developing novel anti-tumor therapeutic strategies and provides insights for future clinical management of oral squamous cell carcinoma.

Circular RNAs (circRNAs) are RNAs with a covalently closed loop structure, characterized by its conservation, stability, tissue specific and ubiquity. CircRNAs can serve as miRNA ‘sponges’ to modulate the mRNA targets of miRNAs. CircRNAs can bind with RNA binding proteins and regulate the expression of some genes. The differential expression of circRNAs between pathogenic and normal tissues makes circRNAs possibly promising biomarkers for diagnosis and targets for treatment. In this article, we reviewed the research progress of circRNA and discussed its research prospects in oral diseases.

Periodontitis, a chronic inflammatory disease caused by plaque biofilm, is characterized by the irreversible pathological destruction of periodontal supporting tissues, including gums, periodontal membranes, alveolar bone, and cementum, resulting in tooth loosening and dislocation in severe cases. Currently, research on the pathogenesis, early diagnosis, and treatment of periodontitis is limited. Circular RNAs (circRNAs), previously considered “splicing noise”, have gained increasing research attention with the development of high-throughput sequencing technologies and bioinformatics. CircRNAs are non-coding RNAs lacking a 5' cap and 3' poly(A) tail, with a unique covalently closed ring structure, high expression, long half-life, and resistance to nuclease degradation, which can regulate splicing, encode proteins, and act as microRNA and RNA-binding protein sponges. In recent years, circRNAs have been reported to be involved in the occurrence and development of periodontitis, suggesting its potential role as a therapeutic target for periodontitis treatment. In this study, we described the biological function of circRNAs and their role in the development of periodontitis and the regulation of periodontal homeostasis and immune microenvironment. We found that circRNAs affect periodontal homeostasis and immune microenvironment by regulating the apoptosis of periodontal tissue cells (such as periodontal ligament stem cells and gingival fibroblasts) and regulating immune cells or cytokines, respectively. This review article summarizes the latest research progress on the association between circRNAs and periodontitis to provide a scientific basis for the development of novel diagnostic, therapeutic, and prognostic strategies for periodontitis.

Periodontitis is a chronic inflammatory disease caused by plaque microorganisms, which is the main cause of tooth loss in adults in China. Due to the complexity of periodontitis, their pathogenesis is still unclear. Ferroptosis is a form of iron-dependent regulation of cell death, which affects the function of glutathione peroxidase (GPX4) in the cell through different signaling pathways, thus decreasing antioxidant capacity, accumulation of reactive oxygen species and lipid peroxidation, eventually causing cell and tissue damage. Recent studies have found that iron overload, oxidative stress and lipid peroxidation are closely related to the occurrence and development of periodontitis. This article reviews the characteristics of ferroptosis and the relationship between ferroptosis and inflammatory diseases, especially periodontitis, to provide new ideas for the diagnosis, treatment, and prognosis evaluation of periodontitis. ferroptosis is mainly manifested as the disruption of the body’s redox homeostasis, decreased antioxidant capacity, activation of damage related molecular patterns, release of pro-inflammatory mediators, and induction or exacerbation of inflammation. Iron dependent oxidative stress and lipid peroxidation are simultaneously involved in the regulation of ferroptosis and inflammatory diseases. Pathogenic bacteria of periodontitis can induce ferroptosis of periodontal ligament stem cells, thereby activating the release of inflammatory factors such as interleukin-17, tumor necrosis factor alpha, and hypoxia inducible factor-1 alpha, exacerbating periodontitis;In addition, inflammatory factors activated by ferroptosis play an important role in alveolar bone homeostasis, and ferroptosis is involved in the process of lipopolysaccharide induced inflammation of gingival fibroblasts. Future research can focus on exploring the molecular mechanisms and therapeutic targets of ferroptosis in periodontitis, providing new strategies for the prevention and treatment of periodontal disease.

Epigenetic modification plays an important role in the biological regulatory process of eukaryotic cells. Tumor immunotherapy is an important means and clinical strategy for the treatment of some cancers. 5-Methylcytosine (m5C) is an important component of the epigenetic regulatory network discovered after m6A and has become a new topic for life science research in recent years. The m5C methylation of RNA can affect the fate of the modified RNA molecules and play an important role in various biological processes, including RNA stability, protein synthesis and transcriptional regulation. Recent studies have shown that m5C writers, erasers and readers are related to a variety of cellular biological processes and systemic diseases, including the occurrence, metastasis and tumor immune microenvironment. m5C methylation can widely affect gene expression and the biological process of tumorigenesis and development at multiple levels, but its specific mechanism and potential interaction with other epigenetic modifications in tumor immunotherapy are still unclear, and its regulatory mechanism, risk assessment and role in targeted therapy for malignant tumors need to be further studied. This article will review the dynamic regulatory network of m5C, the biological role of m5C modification in solid tumors and potential targets in tumor immunotherapy.