Background: Head and Neck Squamous Cell Carcinoma is a malignant tumor with high morbidity and mortality. The MMP family plays an important role in tumor invasion and metastasis. However, the mechanistic value of the MMP family as a therapeutic target and prognostic biomarker in HNSC has not been fully elucidated. Methods: Oncomine, UALCAN, GEPIA, cBioportal, GeneMANIA, STRING, DAVID6.8, TRRUST, TIMER and Linkedomics were used for analysis. Results: The mRNA expression levels of MMP1, MMP3, ILF3, MMP7, MMP9, MMP10, MMP11, MMP12, MMP13 and MMP16 were higher in HNSC than those in normal tissues, while the mRNA expression level of MMP15 was reduced. The relative expression levels of MMP1 and MMP14 were the highest in HNSC tissues. A significant correlation was found between the expression of MMP3, MMP11, MMP25 and the pathological stage of HNSC patients. There was no significant associations between all the MMP family members expression levels and DFS. Increased mRNA levels of MMP1, MMP8 and MMP25 were significantly associated with OS. In addition, we investigated the genetic changes of the MMP family in HNSC and found that all the MMP family members had genetic changes, most of which were amplification and depth loss. In the analysis of neighbor gene network and protein interaction, we found that the MMP family interacted with 25 neighboring genes, except for ILF3, MMP19, MMP20, MMP21, MMP23B, MMP27 and MMP28, other MMP proteins interacted with each other. Functional enrichment analysis showed that the MMP family could be present in the extracellular matrix, regulate peptidase activity, and participate in the catabolism of collagen. Meanwhile, we identified the transcription factor targets and kinase targets of the MMP family and found that ATM and ATR were the two most common kinase targets in the MMP family. We also found a significant correlation between the MMP family expression and immune cell infiltration. Cox proportional risk model analysis showed that macrophages, MMP14, MMP16, and MMP19 were significantly associated with clinical outcomes in HNSC patients. Conclusion: The MMP family might serve as therapeutic target and prognostic biomarker in HNSC.

Establishing animal models with critical size defects (CSDs) is critical for conducting experimental investigations engineering of bone tissue regeneration. Currently, a standardised protocol for establishing an animal CSDs model has not been developed. Furthermore, a consensus has not been reached regarding the critical values of CSDs. Successful establishment of animal models for CSDs is a complex process that requires researchers to meticulously consider a variety of factors such as age, species, bone defect size and anatomic location. The specific numerical values for CSDs in small animal models vary, and a clear definition of the critical value for large animal CSDs models in the literature is still lacking. This review consolidates the advancements in critical bone defects animal models by outlining the research landscape across variables, including animal species, age groups, bone defect sites, and sizes, to offer valuable guidance and a theoretical framework for the establishment of pertinent experimental animal models.

Decellularized vascular matrix is a natural polymeric biomaterial that comes from arteries or veins which are removed the cellular contents by physical, chemical and enzymatic means, leaving only the cytoskeletal structure and extracellular matrix to achieve cell adhesion, proliferation and differentiation and creating a suitable microenvironment for their growth. In recent years, the decellularized vascular matrix has attracted much attention in the field of tissue repair and regenerative medicine due to its remarkable cytocompatibility, biodegradability and ability to induce tissue regeneration. Firstly, this review introduces its basic properties and preparation methods; then, it focuses on the application and research of composite scaffold materials based on decellularized vascular matrix in vascular tissue engineering in terms of current in vitro and in vivo studies, and briefly outlines its applications in other tissue engineering fields; finally, it looks into the advantages and drawbacks to be overcome in the application of decellularized vascular matrix materials. In conclusion, as a new bioactive material for building engineered tissue and repairing tissue defects, decellularized vascular matrix will be widely applied in prospect.

Oxidative stress (OS) inhibits the osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs). Equol (Eq), a phytoestrogen, exhibits notable antioxidant properties and potential for preventing osteoporosis. However, the research on the regulatory effects of Eq on stem cell osteogenesis remains limited. This investigation aimed to identify whether Eq could protect the osteogenic potential of hPDLSCs under H₂O₂-induced oxidative microenvironment. We employed a series of assays, including CCK-8, DCFH-DA, ALP staining, ARS, RT-qPCR, and Western Blotting, to assess the changes in cell viability, antioxidant capacity, and osteogenic potential following H₂O₂ and Eq treatments. Our findings indicated that low concentrations of Eq had no cytotoxic effects on hPDLSCs and promoted their proliferation. Eq pre-treatment (0.5 μmol/L) partially counteracted the inhibitory effect of H₂O₂, reduced the generation of reactive oxygen species, and increased glutathione levels, thereby inhibiting oxidative damage. Eq suppressed the H₂O₂-induced inhibition of osteogenic differentiation, presenting as restoring the alkaline phosphatase levels and calcium nodule formation, as well as by upregulating the expression of BMP2 and RUNX2. Furthermore, bioinformatics analysis in this study suggested that the IL1B/NF-κB/CXCL1 signaling pathway might be a key pathway for Eq's enhancement of osteogenic differentiation potential of hPDLSCs under OS conditions. The activation of this axis by H₂O₂, which Eq can alleviate, was confirmed by validation experiments. This study provides new insights into the potential therapeutic application of Eq in alveolar bone resorption and bone regeneration research.

Oral squamous cell carcinoma (OSCC) severely affects facial aesthetics and the quality of life of patients. Although clinicians continue to improve diagnostic and treatment methods, they still cannot effectively improve the survival rate. Previous studies have found that Matrix Metalloproteinases (MMP2 \MMP9) can promote the formation of vascular mimicry (VM) in tumor tissues, but the relationship between MMP3 and VM in tumors tissues has not been clarified. In this study, we investigated the relationship between MMP3 and VM in OSCC tissues. Lasso regression analysis identified VM formation as an independent risk factor for patient prognosis. Subsequent survival analysis revealed a significant difference in prognosis between the VM-positive group and the VM-negative group (P = 0.00054). The constructed nomogram demonstrated that higher MMP3 expression levels were associated with increased risk scores and decreased 1- and 3-year expected survival rates. ROC curve analysis indicated excellent predictive performance of the model, with 1-year AUC = 0.906 and 2-year AUC = 0.970. Decision curve analysis (DCA) further confirmed the clinical utility of the model. Collectively, these findings suggest that MMP3 is a negative prognostic biomarker in OSCC. Research into MMP3 as a therapeutic target could represent a new and valuable treatment option.

Research on prognostic factors for oral squamous cell carcinoma (OSCC) has revealed new therapeutic targets, with angiogenesis playing a key role in tumor development, invasion, and prognosis. However, reports on OSCC prognostic prediction construction based on angiogenesis factors are limited. Through bioinformatics analysis, we aimed to identify angiogenesis factors whose expression changes may be linked to OSCC prognosis. RNA sequencing, clinical data, and angiogenesis factor data were obtained from The Cancer Genome Atlas and Molecular Signatures Database. The characterized gene was selected and analyzed for correlations with clinicopathological features, prognosis, and cancer-associated fibroblasts infiltration using various databases. Further analyses included gene mutation, functional enrichment, and validation using clinical OSCC samples and tumor-bearing nude mice. Gene expression was assessed by western blotting, immunohistochemistry, immunofluorescence, and quantitative reverse transcription polymerase chain reaction. Epidermal growth factor (EGF) emerged as a key gene, showing significant upregulation in OSCC tissues compared to normal oral mucosa. Univariate and multivariate Cox regression analyses confirmed that high EGF expression correlates with poor overall survival and serves as an independent prognostic factor. EGF was also linked to cancer-associated fibroblast infiltration and can influence angiogenesis pathways. Our findings indicate that EGF may serve as a prognostic biomarker and potential therapeutic target for OSCC.