Burn wounds present significant challenges for traditional dressings due to excessive exudate secretion and persistent inflammation. To address these, the study developed a multifunctional high-exudate-absorption patch (SPC@C) loaded with bioactive curcumin nanoparticles for enhanced burn wound healing. A biomimetic three-dimensional nanoflower hybrid was synthesized through a mild one-pot self-assembly process. It was loaded into an acrylamide-sodium alginate hydrogel and dried, producing the SPC@C patch. The exudate absorption capacity, drug release characteristics, as well as anti-inflammatory and antioxidant properties of the patch were systematically studied. Additionally, the pro-healing performance and potential mechanisms in vivo were evaluated using a rat burn model. SPC@C absorbs wound exudate rapidly, transforming its initially dense internal network to a macroporous structure, thereby facilitating the release of the bioactive curcumin. In vitro, SPC@C exhibited a significant capacity to scavenge reactive oxygen species (ROS) and mitigate the loss of mitochondrial membrane potential. Furthermore, it suppressed the expression of pivotal pro-inflammatory cytokines (tumor necrosis factor-α and interleukin-1β) and modulated macrophage M1-to-M2 polarization. In vivo, SPC@C significantly improved epidermal regeneration, angiogenesis, and collagen deposition in burn tissues. RNA sequencing analysis showed that in burn tissues, SPC@C releases curcumin to modulate antioxidant and anti-inflammatory immunomodulation by regulating the AMPK/Sirt3/NF-κB signaling axis. This work provides a theoretical foundation for developing materials aimed at managing burn wound exudate and modulating the immune responses.

Bone is a hierarchically structured and highly mineralized hard tissue composed of an organic phase (type I collagen and noncollagenous proteins) and an inorganic phase (nanohydroxyapatite). Intrafibrillar mineralized collagen is the basic structural unit of bone tissue and is of high significance due to its superior mechanical and biological properties. Thus, to truly understand the unique properties of bone, it is necessary to review the most basic structural level of bone. In this article, we review the recent advances in understanding the development of intrafibrillar mineralization and the prevailing theories in the formation of such intrafibrillar minerals. Understanding the mechanisms of intrafibrillar mineralization may facilitate the development of engineered bone for clinical applications and provide deeper insight into the nature of biomineralization.

In recent years, due to precise control of the amorphous mineral precursor in the demineralization of dentine collagen fibers in orderly deposition, forming apatite crystals similar to the natural mineralized dentin, the bottom-up remineralization approach which does not depend on the existence of seed crystallites, dentin biomimetic mineralization techniques gradually become a hotspot in the research field of restoration of demineralized dentin caused by dental caries. This paper reviews the changing concepts and practices of the remineralization of demineralized dentin, emphasizing biomimetic remineralization studies. The results of the literature review show that the traditional dentin remineralization method is usually a disordered mixture of demineralized dentin and minerals, so mineralized dentin is not comparable to natural mineralized dentin in terms of the morphological characteristics and mechanical properties. With its gradual increase in recent years, dentine biomimetic mineralization technology perfectly resembles the minerals in the dentin overlapping sequence arranged with the dentine collagen fiber structure characteristics, leading to greatly improved microstructural, physical and chemical properties. As a result, dentine biomimetic mineralization technology is expected to achieve new breakthroughs in the fields of resin-dentin bonding mixing layers and the decay of dentin. At present, the technical obstacles that need to be overcome in the clinical application of the biomimetic remineralization of dentin are how to continuously supplement all the active ingredients needed for mineralization in the process of remineralization and how to keep the mechanical properties of the parent material unchanged while slowly releasing all ingredients. Researchers have successively proposed three-step transportation of the biomimetic remineralization of raw materials, as well as the preparation of mineralization precursors stabilized by polymers in advance and the reuse of mesoporous silicon nanomaterials for the transportation of the mineralized ingredient system. The concept described above provides the preliminary in vitro experimental basis for the transformation of the biomimetic remineralization strategy of dentin in clinical applications.

The colonization of microorganisms planted on the surface of teeth and restoration materials is the main cause of oral disease and treatment failure. How to improve the antibacterial properties of dental materials is a hot topic in dentistry. Nano - sized antibacterial materials have attracted much attention. Among them, metal and metal oxide nanoparticles are prominent due to their strong and broad-spectrum antibacterial activity. Thus, in recent years, many studies have used metal and metal oxide nanoparticles to develop antimicrobial dental materials for resin restoration, root canal therapy, orthodontic treatment, and implant surface and removable denture repair and have found that the antibacterial properties of nano-sized materials are significantly enhanced. However, the mechanical properties and esthetic properties of the modified materials are affected, so it is still necessary to explore appropriate modification methods. In addition, most of the experiments are carried out in vitro, which cannot accurately simulate the oral environment. Therefore, the antibacterial effect, cytotoxicity and immune response of these materials in vivo still need further research and exploration. This paper reviewed the potential antibacterial mechanisms and the safety of those nanoparticles and their applications in dentistry.

Oral squamous cell carcinoma (OSCC) is a common malignant tumor of the head and neck. In recent years, the incidence rate has been increasing. Mitochondria are dynamic organelles involved in various cell behaviors in eukaryotic cells. Mitochondrial dysfunction is closely related to tumor development. As a switch that determines cancer cell death, targeting mitochondria has become the focus of OSCC treatment. This article reviews the relationship between mitochondria and tumorigenesis and development, OSCC treatment, and cisplatin resistant OSCC. Current studies have found that mitochondrial dysfunction promotes cell carcinogenesis, and the mitochondrial morphology and function of cancer cells are significantly changed. The increase of mitochondrial fission improves the invasiveness of cancer cells, and mitophagy dysfunction can induce cancer cell apoptosis. The emergence of drugs and the development of nanotechnology in targeted drug delivery systems have opened up new methods for targeting mitochondria to treat OSCC, reducing the side effects of systemic medication. The cisplatin resistance of OSCC is generated through the mitochondrial pathway, and the mitochondrial function and mutation mechanism of mitochondrial DNA are clarified in order to provide new ideas for targeting mitochondria to treat cisplatin resistant OSCC.

Patients with impaired quality of life associated with xerostomia need long-term treatment, and a nerve stimulator has the advantage of providing natural saliva and long-term management for patients with xerostomia by electrically stimulating the relevant secretory nerves to promote saliva production. A number of clinical trials have preliminarily demonstrated the efficacy of nerve electrical stimulation in the treatment of xerostomia. However, electrical stimulation has not yet become the mainstream treatment for xerostomia. Large prospective randomized controlled clinical trials are still needed to confirm its long-term effectiveness and safety. In addition, the design of nerve stimulators is of great significance for clinical application. The large volume and inconvenient treatment associated with the extra oral nerve stimulator and the first generation intraoral nerve stimulator hinder their clinical application and popularization. The second- and third-generation intraoral nerve stimulator devices are small, convenient to use and have great application prospects. Research on electrical nerve stimulators for xerostomia treatment is mainly concentrated in European and American countries, while there is very little domestic research. It is urgent to master the core technology for the research and development of electrical nerve stimulators. The innovation of miniaturization, efficient power supply, data feedback and packaging will be the key issues of electrical nerve stimulators in the future. In this paper, the treatment and research of electrical nerve stimulation for xerostomia are reviewed to provide a reference for related basic research and the clinical application of electrical stimulators treating xerostomia in China.

X-linked hypophosphatemia (XLH) is a hereditary disorder caused by dysregulation of the FGF23-kidney-bone/teeth axis, leading to chronic hypophosphatemia and impaired mineralization. As target organs highly sensitive to phosphate homeostasis, the teeth and jaw often exhibit pathological changes that precede skeletal deformities, offering early diagnostic value. This article elucidates the damaging effects of hypophosphatemia on dental hard tissues and craniofacial development. Hypophosphatemia-induced impaired dentin mineralization results in interglobular dentin retention and abnormal pulp morphology, which, together with enamel microcracks, constitute the pathological basis for spontaneous pulp infections and periapical lesions. Craniofacial manifestations also include jaw abnormalities, periodontal bone loss, and craniosynostosis. A diagnostic framework for XLH-related oral manifestations integrating imaging, biochemical markers, and genetic testing is proposed, with key differential diagnoses clarified. The article emphasizes the paradigm shift in managing XLH-associated oral complications from conventional phosphate/vitamin D supplementation to anti-FGF23 targeted therapy. It advocates for life-cycle oral management coordinated with systemic homeostatic reconstruction for XLH encompassing prevention, infection control, and multidisciplinary care. By integrating systemic etiological intervention with local precision therapy, this review aims to provide a basis for early identification and standardized management of XLH.

Periodontitis is a widespread disease worldwide, with the primary cause of tissue loss being an immune inflammatory response mediated by bacteria. Increasing evidence has revealed a significant correlation between mitochondrial dysfunction and the occurrence and progression of periodontitis. This paper provides a review of current research on the role of mitochondrial dysfunction in the occurrence and development of periodontitis and related therapies from the perspectives of oxidative stress, inflammatory responses, and the regulation of mitochondrial homeostasis. Mitochondria are the main source and target of cellular reactive oxygen species. Mitochondrial dysfunction can generate large amounts of reactive oxygen species, exacerbating local oxidative stress in periodontal tissues and causing cell toxicity and tissue damage. Mitochondria are also the center of cellular inflammatory responses, and the positive feedback loop of inflammation induced by mitochondrial dysfunction may explain the persistent and unresolved nature of periodontitis. Biomaterials loaded with pharmacological agents show potential in restoring mitochondrial function, controlling the development of periodontitis, and promoting periodontal tissue regeneration. However, the key sites of mitochondrial dysfunction in the occurrence and development of periodontitis are not yet fully understood, and the improvement of mitochondrial function in periodontal therapy is still in the experimental stage. Future research efforts should focus on the effect of mitochondrial dysfunction on periodontal cells and explore its specific mechanism in the occurrence and progression of periodontitis in order to provide new insights into the treatment of periodontitis.