应用锥形束CT对种植区牙槽骨质量分类方法的改良研究

目的    应用锥形束CT（cone beam CT，CBCT）测量种植区牙槽骨质量并结合Lekholm和Zarb分类法对骨质量分类方法进行改良，以期为提高牙槽骨质量分类的准确性提供指导。方法    选择2015年10月至2017年10月在呼和浩特市口腔医院种植科进行种植修复的196例患者术前CBCT影像资料，应用 Invivo5诊断设计软件测量306个种植位点的牙槽骨皮质骨厚度和松质骨密度（皮质骨与松质骨的CT值差值），以Lekholm和Zarb分类法为基础结合测量数据对骨质量进行改良后的量化分类。结果    牙槽骨皮质骨厚度为0.18 ~ 2.89 mm，中位数为0.92 mm。皮质骨与松质骨的CT值差值为88.5 ~ 667.8 HU，应用百分位数法找到33.3%和66.6%对应的数值分别为297.8 HU和356.1 HU。依据此数据结合Lekholm和Zarb分类法将196例患者的306个种植位点骨质量分为4类，其中Ⅰ类骨种植位点46个（占15.0%），Ⅱ类骨104个（占34.0%），Ⅲ类骨114个（占37.3%），Ⅳ类骨42个（占13.7%）。结论    结合Lekholm和Zarb分类法，应用CBCT测量种植区牙槽骨质量并进行分类方法的改良，可为临床医生术前评估牙槽骨质量提供一定参考。     

SMYD3 promotes implant metastasis of ovarian cancer via H3K4 trimethylation of integrin promoters

Detachment of cancer cells from the primary tumor and formation of spheroids in ascites is required for implantation metastasis in epithelial ovarian cancer (EOC), but the underlying mechanism of this process has not been thoroughly elucidated. To mimic this process, ovarian cancer cells were grown in 3D and 2D culture. Hey and OVCA433 spheroids exhibited decreased cell proliferation and enhanced adhesion and invasion. SMYD3 expression was elevated in ovarian carcinoma spheroids in association with increased H3K4 methylation. Depletion of SMYD3 by transient siRNA, stable shRNA knockdown and the SMYD3 inhibitor BCI-121 all decreased spheroid invasion and adhesion. Gene expression arrays revealed downregulation of integrin family members. Inhibition assays confirmed that invasion and adhesion of spheroids are mediated by ITGB6 and ITGAM. SMYD3-deficient cells regained the ability to invade and adhere after forced overexpression of SMYD3, ITGB6 and ITGAM. However, this biological ability was not restored by forced overexpression of SMYD3 in ITGB6- and/or ITGAM-deficient cancer cells. SMYD3 and H3K4me3 binding at the ITGB6 and ITGAM promoters was increased in spheroids compared to that in monolayer cells, and the binding was decreased when SMYD3 expression was inhibited, consistent with the expression changes in integrins. SMYD3 expression and integrin-mediated adhesion were also activated in an intraperitoneal xenograft model and in EOC patient spheroids. In vivo, SMYD3 knockdown inhibited tumor metastasis and reduced ascites volume in both the intraperitoneal xenograft model and a PDX model. Overall, our results suggest that the SMYD3-H3K4me3-integrin pathway plays a crucial role in ovarian cancer metastasis to the peritoneal surface.