Squamous cell carcinomas are the most common head and neck malignancies. Significant progress has been made in standard therapeutic methods combining surgery, radiation, and chemotherapy. Nevertheless, the 5-year survival rate remains at 40–50%. Immune checkpoint inhibitors (ICIs) are a new strategy for treating head and neck squamous cell carcinomas (HNSCCs). Still, the overall response and effective rates are poor, as HNSCCs are ‘cold’ tumors with an immunosuppressive tumor microenvironment (TME), limiting ICI’s beneficial effects. In this case, transforming the tumor suppression microenvironment before using ICIs could be helpful. Oncolytic viruses (OVs) can transform cold tumors into hot tumors, improving the situation. Talimogene laherparepvec (T-VEC), oncolytic immunotherapy authorized for advanced melanoma, also showed good safety and antitumor activity in treating head and neck cancer and pancreatic cancer. In combination with pembrolizumab, T-Vec may have more anticancer efficacy than either drug alone. Therefore, understanding the mechanisms underpinning OVs and their potential synergism with ICIs could benefit patients with HNSCC.

This study evaluated the use of bone ring technique with xenogeneic bone grafts in treating horizontal alveolar bone defects. In total, 11 patients in need of horizontal bone augmentation treatment before implant placement were included in this retrospective study. All patients received simultaneous bone augmentation surgery and implant placement with xenogeneic bone ring grafts. We evaluated the postoperative efficacy of the bone ring technique with xenogeneic bone grafts using radiographical and clinical parameters. Survival rates of implants were 100%. Cone-beam computed tomography revealed that the xenogeneic bone ring graft had significantly sufficient horizontal bone augmentation below the implant neck platform to 0 mm, 1 mm, 2 mm, and 3 mm. It could also provide an excellent peri-implant tissue condition during the 1-year follow-up after loading. The bone ring technique with xenogeneic bone ring graft could increase and maintain horizontal bone mass in the region of the implant neck platforms in serious horizontal bone defects.

Background: The oral cavity harbors a dynamic microbial ecosystem that interacts with epithelial barriers, host immunity, and local tissue environments. Disruption of this balance is increasingly recognized as a key driver of major oral diseases, including periodontitis, dental caries, and oral squamous cell carcinoma (OSCC). However, the biological links between microbial ecology, immune regulation, and disease progression are insufficiently integrated, limiting mechanistic understanding and translational progress. Methods: This structured narrative review searched PubMed/MEDLINE, Web of Science, Embase, and Scopus for relevant studies on oral microbiome ecology, mucosal immunity, dysbiosis, oral diseases, and emerging therapies. Evidence was narratively synthesized across microbiome ecology, mucosal immunology, disease pathogenesis, and translational research, with consideration of study type, mechanistic relevance, and translational significance. Results: Current evidence supports that oral homeostasis relies on coordinated interactions among commensal microbial communities (CMC), epithelial and salivary barriers, and immune surveillance. Dysbiosis disrupts this equilibrium by promoting the expansion of pathobionts, amplifying inflammatory responses, and contributing to tissue injury. This systems-level perspective helps explain the persistence and heterogeneity of oral diseases beyond pathogen-centered models. Emerging technologies are reshaping this field. These include microbiome-modulating therapies, host-directed interventions, multi-omics approaches, and artificial intelligence (AI). These approaches are advancing disease stratification, biomarker discovery, and precision therapeutic development. Conclusion: Oral diseases should be understood as disorders of host-microbiome-immune disequilibrium rather than as isolated infections. This perspective highlights the need for integrated strategies that consider microbial ecology, immune regulation, epithelial barrier function, and clinical context to improve prevention, diagnosis, and treatment in precision oral medicine.

This study examined the potential mechanism of zoledronate on interleukin (IL)-1β-induced temporomandibular joint osteoarthritis (TMJOA) chondrocytes, using IL-1β-induced rabbit immortalized mandibular condylar chondrocytes cultured with zoledronate. Cell viability, apoptosis, mRNA, and protein expression of relevant genes involved in extracellular matrix (ECM) degradation, apoptosis, and Wnt/β-catenin signaling were examined. The involvement of the Wnt/β-catenin signaling was examined using Wnt/β-catenin inhibitor (2-(4-(trifluoromethyl)phenyl)-7,8-dihydro-5H-thiopyrano[4,3-d]pyrimidin-4-ol (XAV-939)) and activator lithium chloride (LiCl). Aggrecan and type II collagen were downregulated by zoledronate, especially with 100 nM for 48 h (p < 0.01), consistently with the upregulation of A disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4) (p < 0.001), matrix metalloprotease-9 (MMP-9) (p < 0.01), caspase-3 (p < 0.001) and downregulation of proliferating cell nuclear antigen (PCNA) (p < 0.01). The apoptotic rate increased from 34.1% to 45.7% with 100 nM zoledronate for 48 h (p < 0.01). The effects of zoledronate on ADAMTs4 (p < 0.001), MMP-9 (p < 0.001), caspase-3 (p < 0.001), and PCNA (p < 0.01) were reversed by XAV-939, while LiCl increased caspase-3 expression (p < 0.01). In conclusion, zoledronate enhances IL-1β-induced ECM degradation and cell apoptosis in TMJOA chondrocytes. Wnt/β-catenin signaling might be involved in this process, but additional studies are necessary to determine the exact involvement of Wnt/β-catenin signaling in chondrocytes after zoledronate treatment.