Maxillomandibular advancement surgery is useful for treatment of sleep apnea. However, preoperative analysis and evaluation to facilitate decision-making regarding the direction and distance of maxillomandibular movement has primarily consisted of morphological analysis; physiological function is not evaluated. To improve preoperative prediction, this study used fluid simulation to investigate the characteristics and effects of airway changes associated with maxillomandibular movement. A one-dimensional model with general applicability was thus developed. Actual measurements of flow in patients were used in this fluid simulation, thus achieving an analysis closer to clinical conditions. The simulation results were qualitatively consistent with the actual measurements, which confirmed the usefulness of the simulation. In addition, the results of the one-dimensional model were within the error ranges of the actual measurements. The present results establish a foundation for using accumulating preoperative measurement data for more-precise prediction of postoperative outcomes.

This study evaluated the effect of maxillary advancement surgery on the size of the pharyngeal airway space (PAS). Lateral cephalometric radiographs were collected for 90 patients (29 men and 61 women; average age, 27.2 ± 8.1 years) before (T1) and 1 year after (T2) maxillary advancement surgery. Horizontal and vertical changes in the maxilla and PAS were measured and classified by distance. The maxilla was advanced horizontally by 2.9 ± 1.7 mm and vertically by 2.7 ± 1.4 mm. Upward maxillary movement of ≥4 mm significantly increased PAS (mean change in PAS, 2.6 mm), and upward maxillary movement significantly decreased the posterior nasal spine to the P-point. Only patients with vertical advancement ≥4 mm and horizontal advancement of 3 mm had significant increases in all three PAS parameters. Although forward maxillary movement is believed to have a large effect on PAS, it is suggest that upward vertical movement is more effective for improving PAS. Both the extent and direction of maxillar movement should be considered. Future studies should use cone-beam computed tomography to evaluate the effect of axial direction and differences in PAS.

Purpose: The present study aimed to identify dysregulated exosomal miRNAs associated with diagnostic and therapeutic biomarkers in oral squamous cell carcinoma (OSCC).Methods: Microarray analysis was used to compare expression profiles of exosomal miRNAs in the OSCC-derived cell lines HSC-2, HSC-3, Ca9-22, and HO-1-N1 with those in human normal keratinocytes (HNOKs). The identified OSCC-related miRNAs and their potential target genes were analyzed with bioinformatic analyses, and the data were subjected to Ingenuity Pathway Analysis (IPA) to clarify functional networks and gene ontologies of the identified exosomal miRNAs secreted by OSCC cells.Results: Comparison with HNOKs detected 8 upregulated and 12 downregulated miRNAs in OSCC-secreted exosomes. The potential target mRNAs of these dysregulated miRNAs were suggested by IPA, and 6 significant genetic networks were indicated by genetic network analysis. Furthermore, 4 crucial upstream miRNAs—miR-125b-5p, miR-17-5p, miR-200b-3p, and miR-23a-3p—were identified. miR-125b-5p was a central node in the most significant network. Gene ontology analysis showed significant enrichment of genes with cancer-related functions, such as molecular mechanisms of cancer, cell cycle, and regulation of the epithelial-mesenchymal transition.Conclusion: These results provide a comprehensive view of the functions of dysregulated exosomal miRNAs in OSCC, thus illuminating OSCC tumorigenesis and development.

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Purpose: Bacterial cells in mature dental plaque produce a high concentration of short-chain fatty acids (SCFAs) such as butyrate and propionate. SCFA-treatment on human gingival epithelial Ca9-22 cells induced cell death. However, the exact mechanism underlying cell death remains unclear. In this study, the relationship between reactive oxygen species (ROS) and autophagy induction during SCFA-induced cell death was examined.Methods: Human gingival epithelial Ca9-22 cells were treated with butyrate or propionate to induce cell death and the number of dead cells were measured using SYTOX-green dye. A siRNA for ATG5 and N-acetylcysteine (NAC) were used for autophagy reduction and ROS-scavenging, respectively. Release of damage-associated molecular patterns (DAMPs) such as Sin3A-associated protein 130 (SAP130) and high-mobility group box 1 (HMGB1) were detected using western blot.Results: Reducing autophagy significantly suppressed SCFA-induced Ca9-22 cell death. ROS generation was observed upon SCFA treatment, and scavenging ROS with NAC decreased cell death. NAC also reduced the SCFA-induced increase in microtubule-associated protein 1 light chain 3B (LC3B)-I and LC3B-II, and mitigated the release of DAMPs.Conclusion: The findings suggest that ROS generation is necessary for autophagy, which is required for SCFA-induced cell death and accompanying DAMP release.