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Objective This study aimed to explore the root length of maxillary and mandibular anterior teeth and central incisor crown-root morphology in patients with high-angle skeletal Class Ⅱ open bite, aiming to provide a reference for clinical treatment. Methods This study was reviewed and approved by the Ethics Committee, and informed consent was obtained from the patients. CBCT images of eighty-one untreated patients (40 anterior open bite patients and 41 normal overbite patients) with high-angle skeletal Class Ⅱ malocclusion were selected before treatment. Dolphin software was used to study the root length of maxillary and mandibular anterior teeth and central incisor crown-root morphology, and the differences between the two groups were analyzed. Results There was no statistical significance in the root length of maxillary lateral incisor and canine between the open bite group and the normal overbite group, significant differences were found in the root length of maxillary central incisor （11.12 ± 1.37） mm、mandibular central incisor（10.15 ± 1.09）mm, mandibular lateral incisor（11.27 ± 1.15）mm and mandibular canine（12.81 ± 1.48）mm between the open bite group and the normal overbite group（P

Background: Inducible nitric oxide synthase (iNOS) is associated with inflammation and osteoclastic differentiation in periodontal disease. This study was conducted to compare the time‐dependent variation in iNOS production between the gingiva and other periodontal tissues and to explore the potential association with C‐reactive protein (CRP) in early periodontal disease. Methods: Ligature‐induced periodontal disease models (0–14 days) were established in wild‐type and CRP knockout rats. Changes in CRP, iNOS, and autophagy levels were examined in the gingiva and other periodontal tissues. Macrophages were treated with lipopolysaccharide and chloroquine to explore the role of autophagy in iNOS production. iNOS, CRP, and autophagy‐related proteins were analyzed using Western blotting, immunostaining, and enzyme‐linked immunosorbent assays. mRNA expression was detected by quantitative real‐time polymerase chain reaction. Hematoxylin and eosin staining was used for histological analysis. Cathepsin K immunostaining and microcomputed tomography of the maxillae were performed to compare alveolar bone resorption. Results: iNOS and CRP levels increased rapidly in periodontal tissues, as observed on Day 2 of ligature, then decreased more rapidly in the gingiva than in other periodontal tissues. CRP deficiency did not prevent iNOS generation, but effectively accelerated iNOS reduction and delayed alveolar bone loss. The CRP effect on iNOS was accompanied by a change in autophagy, which was reduced by CRP knockout. Conclusions: The regulation of iNOS by CRP shows temporospatial variation in early periodontal disease and is potentially associated with autophagy. These findings may contribute to the early detection and targeted treatment of periodontal disease. [ABSTRACT FROM AUTHOR]

Background: Diabetes mellitus (DM) and periodontitis are two prevalent diseases with mutual influence. Accumulation of advanced glycation end products (AGEs) in hyperglycemia may impair cell function and worsen periodontal conditions. N6-methyladenosine (m6A) is an important post-transcriptional modification in RNAs that regulates cell fate determinant and progression of diseases. However, whether m6A methylation participates in the process of periodontitis with diabetes is unclear. Thus, we aimed to investigate the effects of AGEs on bone marrow mesenchymal stem cells (BMSCs), elucidate the m6A modification mechanism in diabetes-associated periodontitis. Methods: Periodontitis with diabetes were established by high-fat diet/streptozotocin injection and silk ligation. M6A modifications in alveolar bone were demonstrated by RNA immunoprecipitation sequence. BMSCs treated with AGEs, fat mass and obesity associated (FTO) protein knockdown and sclerostin (SOST) interference were evaluated by quantitative polymerase chain reaction, western blot, immunofluorescence, alkaline phosphatase and Alizarin red S staining. Results: Diabetes damaged alveolar bone regeneration was validated in vivo. In vitro experiments showed AGEs inhibited BMSCs osteogenesis and influenced the FTO expression and m6A level in total RNA. FTO knockdown increased the m6A levels and reversed the AGE-induced inhibition of BMSCs differentiation. Mechanically, FTO regulated m6A modification on SOST transcripts, and AGEs affected the binding of FTO to SOST transcripts. FTO knockdown accelerated the degradation of SOST mRNA in presence of AGEs. Interference with SOST expression in AGE-treated BMSCs partially rescued the osteogenesis by activating Wnt Signaling. Conclusions: AGEs impaired BMSCs osteogenesis by regulating SOST in an m6A-dependent manner, presenting a promising method for bone regeneration treatment of periodontitis with diabetes. [ABSTRACT FROM AUTHOR]

Introduction: Postoperative myocardial injury after noncardiac surgery is common and is associated with short- and long-term morbidity and mortality. However, the incidence and risk factors for postoperative acute myocardial injury (POAMI) are currently unknown due to inconsistent definitions. Methods: We systematically searched PubMed and Web of Science to identify studies that applied the change value of preoperative and postoperative cardiac troponins to define cardiac injury. We estimated the pooled incidence, risk factors, and 30-day and long-term mortality of POAMI in noncardiac patients. The study protocol was registered with PROSPERO, CRD42023401607. Results: Ten cohorts containing 11,494 patients were included for analysis. The pooled incidence of POAMI was 20% (95% CI: 16% to 23%). Preoperative hypertension (OR: 1.47; 95% CI: 1.30 to 1.66), cardiac failure (OR: 2.63; 95% CI: 2.01 to 3.44), renal impairment (OR: 1.66; 95% CI: 1.48 to 1.86), diabetes (OR: 1.43; 95% CI: 1.27 to 1.61), and preoperative beta-blocker intake (OR: 1.65; 95% CI: 1.10 to 2.49) were the risk factors for POAMI. Age (mean difference: 2.08 years; 95% CI: -0.47 to 4.62), sex (male, OR: 1.16; 95% CI: 0.77 to 1.76), body mass index (mean difference: 0.35; 95% CI: -0.86 to 1.57), preoperative coronary artery disease (OR: 2.10; 95% CI: 0.85 to 5.21), stroke (OR: 0.90; 95% CI: 0.50 to 1.59) and preoperative statins intake (OR: 0.65; 95% CI: 0.21 to 2.02) were not associated with POAMI. Patients with POAMI had higher preoperative hsTnT levels (mean difference: 5.92 ng/L; 95% CI: 4.17 to 7.67) and lower preoperative hemoglobin levels (mean difference: -1.29 g/dL; 95% CI: -1.43 to -1.15) than patients without. Conclusion: Based on this meta-analysis, approximately 1 in 5 of noncardiac patients develop POAMI. However, the lack of a universally recognized definition for POAMI, which incorporates diverse cardiac biomarkers and patient groups, poses a challenge in accurately characterizing its incidence, risk factors, and clinical outcomes. [ABSTRACT FROM AUTHOR]