Study on the correlation parameters of Class II malocclusion in child tooth dentition early stage by using 3D technique.

OBJECTIVE: To record the dentition, jaw and facial growth and development of children with class II malocclusion at the age of 7-8 years old in the early dental transitional stage with 3D technology and to provide the study basis for the growth and development parameters of normal children and children with class II malocclusion. METHODS: Twenty-four children who were suffering class-II malocclusion in the early dental transitional stage and received treatment between July 2016 and July 2017 in our hospital were selected as the study group, and 20 healthy children were selected as the control group in the same period. SIRONA CEREC dentition scanning, 3D reconstruction of the lower mandible and 3d MD face scanning were performed on the children. Relevant data were recorded and compared. RESULTS: The dentition scanning results suggested that the study group had significantly larger anterior overbite and anterior overjet and smaller width of the upper arch than the control group; there was a significant difference between the two groups (P<0.05). The 3D reconstruction of the lower mandible suggested that the study group had smaller Go angle and SNB angle and shorter ANS-Me distance, Go-Me distance and N-Me distance compared to the control group; the differences had statistical significance (P<0.05). The face scanning results demonstrated that the nasolabial angle and facial convexity angle of the study group were significantly larger than those in the control group, and the difference was statistically significant (P<0.05). CONCLUSION: The dentition scanning results suggested that the study group had significantly larger anterior overbite and anterior overjet and smaller width of the upper arch than the control group; there was a significant difference between the two groups (P<0.05). The 3D reconstruction of the lower mandible suggested that the study group had smaller Go angle and SNB angle and shorter ANS-Me distance, Go-Me distance and N-Me distance compared to the control group; the differences had statistical significance (P<0.05). The face scanning results demonstrated that the nasolabial angle and facial convexity angle of the study group were significantly larger than those in the control group, and the difference was statistically significant (P<0.05).

Gingipain from Porphyromonas gingivalis causes insulin resistance by degrading insulin receptors through direct proteolytic effects.

Periodontitis is a critical risk factor for the occurrence and development of diabetes. Porphyromonas gingivalis may participate in insulin resistance (IR) caused by periodontal inflammation, but the functional role and specific mechanisms of P. gingivalis in IR remain unclear. In the present study, clinical samples were analysed to determine the statistical correlation between P. gingivalis and IR occurrence. Through culturing of hepatocytes, myocytes, and adipocytes, and feeding mice P. gingivalis orally, the functional correlation between P. gingivalis and IR occurrence was further studied both in vitro and in vivo. Clinical data suggested that the amount of P. gingivalis isolated was correlated with the Homeostatic Model Assessment for IR score. In vitro studies suggested that coculture with P. gingivalis decreased glucose uptake and insulin receptor (INSR) protein expression in hepatocytes, myocytes, and adipocytes. Mice fed P. gingivalis tended to undergo IR. P. gingivalis was detectable in the liver, skeletal muscle, and adipose tissue of experimental mice. The distribution sites of gingipain coincided with the downregulation of INSR. Gingipain proteolysed the functional insulin-binding region of INSR. Coculture with P. gingivalis significantly decreased the INSR-insulin binding ability. Knocking out gingipain from P. gingivalis alleviated the negative effects of P. gingivalis on IR in vivo. Taken together, these findings indicate that distantly migrated P. gingivalis may directly proteolytically degrade INSR through gingipain, thereby leading to IR. The results provide a new strategy for preventing diabetes by targeting periodontal pathogens and provide new ideas for exploring novel mechanisms by which periodontal inflammation affects the systemic metabolic state.

Downregulated microRNA-149-3p triggers malignant development and predicts worse prognosis in oral squamous cell carcinoma.

OBJECTIVE: Accumulating evidence reveals that aberrant expression of microRNAs contributes to the tumorigenesis and development of diverse human cancers. In the current study, we aimed to evaluate the functional role and prognostic value of miR-149-3p in oral squamous cell carcinoma (OSCC). METHODS: Real-time polymerase chain reaction (PCR) analysis was performed to detect the expression of miR-149-3p in 70 OSCC patients (64.10 ± 11.97 years; 31 males and 39 females). The prognostic ability of miR-149-3p in OSCC patients was assessed by Kaplan-Meier survival analysis. Transwell assays and cell adhesion assays were used to investigate the impact of miR-149-3p on cell migration and invasion. The regulation of MMP2 expression by miR-149-3p was determined by real-time PCR, western blotting and dual luciferase reporter assay. RESULTS: Our results revealed a lower level of miR-149-3p in OSCC tissues than in adjacent normal tissues. Downregulation of miR-149-3p was correlated with malignant development and poor outcomes in patients with OSCC. MiR-149-3p repressed the migratory and invasive abilities of OSCC cells. We confirmed that miR-149-3p targeted the 3'-untranslated region of MMP2 mRNA to suppress MMP2 expression. Moreover, the miR-149-3p-mediated decrease in metastasis was reversed by overexpression of MMP2 in OSCC cells. CONCLUSION: Our findings provide an important molecular mechanism by which miR-149-3p inhibits OSCC cell migration and invasion via negative regulation of MMP2 and implicate miR-149-3p as a prospective biomarker and therapeutic target for OSCC.

[Effect of continuously compressive pressure on the expression of RANKL mRNA in human periodontal ligament cells in vitro].

OBJECTIVE: To determine the effect of continuously compressive pressure (CCP) on the expression of receptor activator of nuclear factor kappa B ligand (RANKL) in human periodontal ligament cells (HPDLCs) and to investigate the role of RANKL in alveolar bone rebuilding during orthodontic tooth movement. METHODS: The primary HPDLCs were isolated from human periodontal ligament by explanting enzymatic digestion with trypsin and collagenase to establish a pressure model. Top-bottom axial pressures (1, 2, and 3 g/cm(2)) were laid on HPDLCs for 0.5, 1.5, 6, 12, 24, and 48 h, respectively. The RANKL expression was identified by the reverse transcription-polymerase chain reaction (RT-PCR) at the mRNA level. RESULTS: The expression of RANKL mRNA significantly increased in a time-dependent manner (P<0.01), so did the value of pressure, especially in the 2 g/cm(2) group (P<0.05). CONCLUSION: CCP can up-regulate the expression of RANKL mRNA in human periodontal ligament cells.

[Tension-force induced cyclooxygenase-2 expression mediated by microfilament in human periodontal ligament fibroblast].

OBJECTIVE: To study the role of microfilament polymerization in menchanotransduction by human periodontal ligament fibroblast (hPDLFs). METHODS: In tension-force group, hPDLFs were treated by tension-force values of 18% for 8 h, 16 h, 24 h. In tension-force and inhibitor group, the sample was treated with 5 microg/mL cytochalasin B before using tension-forece. Each sample was collected and the expression of cyclooxygenase-2 was measured by using immunohistoche staining. RESULTS: In tension-force group, the expression of cyclooxygenase-2 enhanced with the extension of loading time. In tension-force and inhibitor group, cyclooxygenase-2 expression was depressed and had no relation with loading time. CONCLUSION: Tension-force induced cyclooxygenase-2 expression is mediated by microfilament, disruption of the microfilament polymerization will destroy mechanotransduction in hPDLFs.