The purpose of this study was mainly to explore the role and mechanism of microRNA-18a-5p (miR-18a-5p) in oral squamous cell carcinoma (OSCC). The expression of miR-18a-5p in OSCC cells and normal cells was firstly detected using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The cell viability, apoptosis, migration and invasion abilities of OSCC cells were determined by MTT, cell apoptosis, wound healing and Transwell assays respectively. Additionally, bioinformatics software analysis and luciferase reporter assays were performed to predict and confirm the candidate target of miR-18a-5p. Western blot analysis was used to assess protein expression. It was revealed that the expression of miR-18a-5p in OSCC cells was higher than that in normal cells. In vitro studies revealed that the cell viability, migration and invasion abilities of OSCC cells were promoted and cell apoptosis was inhibited by miR-18a-5p overexpression. In addition, Smad2 was identified as a target of miR-18a-5p. It was also revealed that miR-18a-5p overexpression significantly inhibited the expression of Smad2, Smad4 and E-cadherin, and the levels of Smad7, collagen I, transforming growth factor-β (TGF-β), α-smooth muscle actin (α-SMA), vimentin were enhanced. While miR-18a-5p downregulation presented the opposite effects. In conclusion, the results indicated that miR-18a-5p can regulate the biological process of OSCC by targeting Smad2 and miR-18a-5p/Smad2 may be potential therapeutic targets for OSCC.

Background: Intra-articular disorders (ID) or anterior and/or medial displacement of the temporomandibular joint disorder (TMJ) disc are the most common form of TMJ dysfunction (TMD). TMD causes changes in the friction coefficient during TMJ movement. Herein, we provided a three-dimensional (3D) finite-elements model (FEM) including the maxilla, disc, and mandible and evaluated the stress distribution with different friction coefficient. Methods: Fourteen volunteers without TMD and 20 patients with MRI-diagnosed TMD were selected. CT and MRI data were collected to build the 3D FEA model of the mandible and TMJ disc. Stress distribution with different friction coefficient was measured. Result: In the normal model, stress distribution on the TMJ disc was 2.07 ± 0.17, 1.49 ± 0.14, and 1.41 ± 0.14 MPa with 0.001, 0.3, and 0.4 friction coefficient, respectively. In the TMD model, stress distribution was 3.87 ± 0.15, 7.23 ± 0.22, and 7.77 ± 0.19 MPa respectively. Conclusion: When the friction coefficient of the side with anterior displacement increased, stress on the disc, condyle and mandible of the opposite side increased. Simultaneously, stress values of the disc, condyle and mandible were higher than those of the normal lateral joint.

Oral squamous cell carcinoma (OSCC) is one of the most prevalent malignancies worldwide. MicroRNAs (miRNAs or miRs) serve crucial roles in the development of OSCC. miR-196a is upregulated in various tumors; however, the role of miR-196a in OSCC remains unclear. This present study aimed to determine the role and underlying mechanism of miR-196a in OSCC cells. Reverse transcription-quantitative PCR (RT-qPCR) was used to measure miR-196a levels in OSCC cells. MTT assays were also performed to determine cell proliferation. Cell migration was detected using wound healing assays and transwell assays, and cell apoptosis was analyzed via flow cytometry. The results indicated that the expression of miR-196a was increased in OSCC cells compared with normal oral squamous cells. TargetScan and luciferase reporter assays also confirmed that forkhead box O1 (FOXO1) was a target gene of miR-196a. It was demonstrated that FOXO1 small interfering RNA significantly promoted SCC9 cell proliferation and migration, and inhibited cell apoptosis. Furthermore, inhibition of miR-196a suppressed SCC9 cell proliferation and migration, and induced cell apoptosis. However, all effects of the miR-196a inhibitor were reversed following FOXO1 inhibition. Western blotting and RT-qPCR were subsequently performed to determine the effect of miR-196a on the PI3K/Akt signaling pathway. In the present study, transfection of miR-196a inhibitor suppressed the expression of phosphorylated (p)-PI3K and p-Akt, and enhanced the levels of FOXO1, while inhibition of FOXO1 exerted the opposite effects. Furthermore, it was demonstrated that miR-196a mimic significantly enhanced SCC9 cell proliferation and migration, and inhibited cell apoptosis. In conclusion, the results indicated that miR-196a serve as an oncogene in OSCCs. Downregulation of miR-196a inhibited the malignant biological processes of OSCC cells by targeting FOXO1. The current results may provide a novel therapeutic strategy for the treatment of patients with OSCC.

Background：Anterior and/or medial displacement of the temporomandibular joint disorder(TMJ) disc or intra-articular disorders( ID) is the most common form of TMJ dysfunction(TMD).TMD cause change of friction coefficient during TMJ movement. In the present study, We provided a 3D finite elements models(FEM) including the maxilla, disc and mandible and evaluated the stress distribution with different friction coefficient.Methods: 14 volunteers without TMD and 20 TMD patients,who were diagnosed by MRI, were selected.CT and MRI data were collected to build 3D FEA model of mandibular and TMJ disc.Stress distribution with different friction coefficient was measured.Result: In the normal model, stress distribution on TMJ disc was 2.07±0.17,1.49±0.14,1.41±0.14MPa with 0.001 0.3 and 0.4 friction coefficient.In TMD model,stress distribution is 3.87±0.15,7.23±0.22,7.77±0.19MPa respectively. Conclusion:When the friction coefficient of the side with anterior displacement increased, stress on the disc, condyle and mandible of the opposite side increased. Simultaneously, stress values of the disc, condyle and mandible were higher than those of the normal lateral joint.