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1.
STOMATOLOGY ; (12): 135-140, 2023.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-979287

ABSTRACT

Objective@#To explore the effect of miniscrew-assisted rapid palatal expansion (MARPE) on mandible position in the treatment of adult skeletal Class Ⅰ malocclusion with maxillary transverse deficiency. @*Methods@#In this retrospective study, 20 cases of adult skeletal Class Ⅰ malocclusion with maxillary transverse deficiency treated with MARPE in our hospital from July 2019 to March 2022 were selected as research objects. CBCT data of three time points before treatment (T0), immediately after expansion (T1) and six months after retention (T2) were collected. The head position was standardized and calibrated by Dolphin software, and then mandible landmarks (left and right Condylion, left and right Gonion, Menton) were positioned. The linear distance changes of each landmark relative to the reference plane of coronal plane, axial plane and sagittal plane were measured, which represented the sagittal, vertical and horizontal displacement of mandible respectively. Repeated measurement ANOVA and LSD multiple comparison were used to evaluate the position change of each landmark.@*Results @#The Menton and right Gonion rotated clockwise at T1, and relapsed to the initial position at T2. No lateral displacement of Menton was found.@*Conclusion@#When MARPE is used to treat skeletal Class Ⅰ malocclusion with maxillary transverse deficiency, it causes a transient clockwise rotation of the mandiblar. The mandible does not show sagittal, vertical and horizontal position changes in long-term evaluation.

2.
BMC Oral Health ; 22(1): 269, 2022 07 03.
Article in English | MEDLINE | ID: mdl-35786385

ABSTRACT

BACKGROUND: Pulpitis often are characterized as sustained inflammation and impaired pulp self-repair. Circular RNAs (circRNAs) have been reported to be involved in the development of inflammation, but their influence in pulpitis is still unidentified, which was examined in our research. METHODS: In this study, TNF-α (20 ng/mL) was used to treat DPSCs, then MTS identified cell proliferation. The circRNAs profile in DPSCs with or without TNF-α treatment was evaluated using RNA sequencing and subsequently by bioinformatics analysis. After that, the circular structure was assessed using agarose gel electrophoresis, followed by Sanger sequencing. And the circRNAs expression was ratified using quantitative real-time polymerase chain reaction in cell and tissues samples. Additionally, the plausible mechanism of circRNAs was envisaged, and the circRNA-miRNA-mRNA linkage was plotted using Cytoscape. RESULTS: The treatment of TNF-α inhibited cell proliferation capabilities in DPSCs, which also made 1195 circRNA expressions undergo significant alterations. Among these changes, 11 circRNAs associated with inflammation were chosen for circular structure verification, and only seven circRNAs (hsa_circ_0001658, hsa_circ_0001978, hsa_circ_0003910, hsa_circ_0004314, hsa_circ_0004417, hsa_circ_0035915, and hsa_circ_0002545) had circular structure. Additionally, five circRNAs expressions (hsa_circ_0001978, hsa_circ_0003910, hsa_circ_0004314, hsa_circ_0004417, and hsa_circ_0035915) had significantly altered between with or without TNF-α treated DPSCs. Furthermore, hsa_circ_0001978 and hsa_circ_0004417 were increased in patients suffering from pulpitis. Furthermore, their ceRNA linkage and Kyoto Encyclopedia of Genes and Genomes analysis suggested that these two circRNAs may participate in the inflammation development of pulpitis via mitogen-activated protein kinase and the Wnt signaling pathway. CONCLUSION: This study revealed that the circRNAs profile was altered in TNF-α treated DPSCs. Also, hsa_circ_0001978 and hsa_circ_0004417 may be involved in the inflammation progress of pulpitis. These outcomes provided the latest information for additional research on pulpitis.


Subject(s)
MicroRNAs , Pulpitis , Humans , Inflammation , MicroRNAs/genetics , MicroRNAs/metabolism , RNA, Circular/genetics , Tumor Necrosis Factor-alpha/pharmacology
3.
Nan Fang Yi Ke Da Xue Xue Bao ; 39(1): 106-112, 2019 Jan 30.
Article in Chinese | MEDLINE | ID: mdl-30692075

ABSTRACT

OBJECTIVE: To investigate the effects of autophagy on osteogenic differentiation of stem cells from the apical papilla (SCAPs) in the presence of tumor necrosis factor-α (TNF-α) stimulation in vitro. METHODS: SCAPs treated with TNF-α (0, 5, and 10 ng/mL) with or without 5 mmol/L 3-MA were examined for the expression of autophagy marker LC3-Ⅱ using Western blotting. The cells were transfected with GFP-LC3 plasmid and fluorescence microscopy was used for quantitative analysis of intracellular GFP-LC3; AO staining was used to detect the acidic vesicles in the cells. The cell viability was assessed with CCK-8 assays and the cell apoptosis rate was analyzed using flow cytometry. The cells treated with TNF-α or with TNF-α and 3-MA were cultured in osteogenic differentiation medium for 3 to 14 days, and real- time PCR was used to detect the mRNA expressions of osteogenesis-related genes (ALP, BSP, and OCN) for evaluating the cell differentiation. RESULTS: TNF-α induced activation of autophagy in cultured SCAPs. Pharmacological inhibition of TNF-α-induced autophagy by 3-MA significantly decreased the cell viability and increased the apoptosis rate of SCAPs (P < 0.05). Compared with the cells treated with TNF-α alone, the cells treated with both TNF-α and 3-MA exhibited decreased expressions of the ALP and BSP mRNA on days 3, 7 and 14 during osteogenic induction (P < 0.05) and decreased expression of OCN mRNA on days 3 and 7 during the induction (P < 0.05). CONCLUSIONS: Autophagy may play an important role during the osteogenic differentiation of SCAPs in the presence of TNF-α stimulation.


Subject(s)
Autophagy/drug effects , Cell Differentiation/physiology , Dental Papilla/cytology , Osteogenesis/physiology , Stem Cells/physiology , Tumor Necrosis Factor-alpha/pharmacology , Autophagy/physiology , Cell Differentiation/drug effects , Cell Survival/drug effects , Cells, Cultured , Green Fluorescent Proteins , Humans , Stem Cells/drug effects , Transfection , Tumor Necrosis Factor-alpha/administration & dosage , Tumor Necrosis Factor-alpha/antagonists & inhibitors
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