Finite element analysis (FEA) has always been an important tool in studying the influences of stress and deformation due to various loads on implants to the surrounding jaws. This study assessed the influence of two different types of dental implant model on stress dissipation in adjoining jaws and on the implant itself by utilizing FEA. This analysis aimed to examine the effects of increasing the number of fences along the implant and to compare the resulting stress distribution and deformation with surrounding bones. When a vertical force of 100 N was applied, the largest displacements found in the three-fenced and single-fenced models were 1.7469 and 2.5267, respectively, showing a drop of 30.8623%. The maximum stress found in the three-fenced and one-fenced models was 13.518 and 22.365 MPa, respectively, showing a drop of 39.557%. Moreover, when an oblique force at 35° was applied, a significant increase in deformation and stress was observed. However, the three-fenced model still had less stress and deformation compared with the single-fenced model. The FEA results suggested that as the number of fences increases, the stress dissipation increases, whereas deformation decreases considerably.
Background: Previous studies have shown that many cruciferous vegetables have anticancer effects, which can be connected with the presence of allyl isothiocyanate (AITC). Histone demethylase KDM8 and cyclin A1 (CCNA1) were required for cell cycle G2/M progression. AITC could induce G2/M arrest of various types of human cancer cells. We aimed to validate KDM8 as a target of the antitumor effects of AITC in patient-derived tumor xenograft (PDTX) models of oral squamous cell carcinoma (OSCC).
Methods: The expression of KDM8 was assessed through tissue microarray (TMA) immunohistochemistry (IHC) assay. The effects of AITC on the expression of KDM8 and cell proliferation were investigated in OSCC cell lines, in PDTX models, and SAS subcutaneous xenograft tumors.
Results: KDM8 was overexpressed in OSCC. AITC repressed the tumor growth of OSCC PDTX and SAS subcutaneous xenograft. Furthermore, AITC downregulated the expression of KDM8 and CCNA1 and induced histone H3K36me2 expression in oral cancer cells.
Conclusions: AITC exerts anticancer effects on oral cancer by inducing cell cycle arrest via inhibiting the KDM8-CCNA1 axis.
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