Xinyi Huang, Yu Han, Shuangyan Yang. Korean J Orthod 2022;52:334-44. https://doi.org/10.4041/kjod21.324

Cellular senescence is a unique cellular state. Senescent cells enter a non-proliferative phase, and the cell cycle is arrested. However, senescence is essentially an active cellular phenotype, with senescent cells affecting themselves and neighboring cells via autocrine and paracrine patterns. A growing body of research suggests that the dysregulation of senescent stromal cells in the microenvironment is tightly associated with the development of a variety of complex cancers. The role of senescent stromal cells in impacting the cancer cell and tumor microenvironment has also attracted the attention of researchers. In this review, we summarize the generation of senescent stromal cells in the tumor microenvironment and their specific biological functions. By concluding the signaling pathways and regulatory mechanisms by which senescent stromal cells promote tumor progression, distant metastasis, immune infiltration, and therapy resistance, this paper suggests that senescent stromal cells may serve as potential targets for drug therapy, thus providing new clues for future related research.

Periodontitis and inflammatory bowel disease (IBD) are both chronic inflammatory diseases that are characterized by abnormal host immune responses and microbiota dysbiosis. Emerging evidence implies potential associations between periodontitis and IBD. Porphyromonas gingivalis (P. gingivalis), a primary cause of periodontitis, is thought to play a role in the development of IBD through the oral–gut disease axis. However, the precise mechanisms of its involvement remain enigmatic. In this narrative review, we begin with a discussion of the bidirectional relationship between periodontitis and IBD and the involvement of P. gingivalis in each of the two diseases. Further, we summarize the possible routes by which P. gingivalis links periodontitis and IBD through the oral–gut axis, as well as the underlying mechanisms of its involvement in the pathogenesis of IBD. Collectively, P. gingivalis participates in the progression of IBD through gut dysbiosis, impairment of the intestinal barrier, release of inflammatory mediators, and disturbance of the immune response. The above findings may provide new insights for exploring novel biomarkers and potential therapeutic approaches for IBD.

After oral carcinoma resection, postoperative cancer recurrence, bacterial infection, and craniomaxillofacial bone defect threaten patients’ health. Current treatment is mainly to repair bone defects by bone substitute implantation, but that ignores the side effects caused by residual tumor cells and oral bacteria. To reach a better therapeutic effect, this paper develops a novel self‐supplied catalytic nanocomposite (MX@Ca‐Ti) that mainly consists of Ti ₃ C ₂ MXene nanosheets and CaO ₂ nanoparticles with the purpose of synergistically promoting osteogenesis, inhibiting tumor cell growth, and preventing bacterial infection. Herein, the CaO ₂ activation creates TiO _2‐x with Ti ³⁺ and Ti ⁴⁺ on MX@Ca‐Ti, which is structurally composed of porous, monolayer nanosheet and TiO _2‐x nanodots. The self‐supplied catalytic effects of sonodynamic therapy by Ti ⁴⁺ and chemodynamic therapy by Ti ³⁺ , enhance the therapeutic efficiency of tumor recurrence and bacterial infection. More importantly, this nanocomposite is demonstrated to have good cytocompatibility and osteogenesis‐promoting capability because of the release of O ₂ and Ca ²⁺ . In conclusion, MX@Ca‐Ti not only defeats tumor cells and bacteria but also strengthens osteogenesis, which is an ideal treatment for avoiding postoperative complications and promoting bone defect repair from an oral carcinoma excision.

Purpose: Sleep apnea (SA), associated with absent neural output, is characterised by recurrent episodes of hypoxemia and repeated arousals during sleep, resulting in decreased sleep quality and various health complications. Mitochondrial DNA copy number (mtDNA-CN), an easily accessible biomarker in blood, reflects mitochondrial function. However, the causal relationship between mtDNA-CN and SA remains unclear. This study aimed to investigate the causality between mtDNA-CN and SA while identifying potential mediating brain imaging phenotypes (BIPs). Methods: Two-sample bidirectional Mendelian randomisation (MR) analysis was performed to estimate the causal relationship between mtDNA-CN and SA, with further validation using Bayesian framework-based MR analysis. A two-step approach was employed to evaluate causal relationships between BIPs, mtDNA-CN and SA, utilising the “product of coefficients” method to assess the mediating effects of BIPs. Multiple testing errors were corrected using the Benjamini–Hochberg method. Results: Genetically predicted mtDNA-CN had a negative causal effect on SA (OR = 0.859, 95% CI = 0.785– 0.939, P = 3.20× 10^{− 4}), whereas SA did not have a causal effect on mtDNA-CN (OR = 1.0056, 95% CI = 0.9954– 1.0159, P = 0.2825). Among 3935 BIPs, two features related to white matter microstructure served as partial mediators: the second eigenvalue from diffusion MRI data analysed by tract-based spatial statistics in the right posterior thalamic radiation, with a mediation proportion of 11.37% (P = 0.0450), and fractional anisotropy in the right sagittal stratum, with a mediation proportion of 12.79% (P = 0.0323). Conclusion: This study demonstrated a causal relationship between mtDNA-CN and SA, with specific brain white matter microstructure phenotypes potentially acting as mediators. These findings highlight the potential of mtDNA-CN as a biomarker for SA and underscore its relevance in guiding future therapeutic strategies targeting mitochondrial health and brain white matter microstructure.