糖尿病是一类以糖代谢异常为特征的慢性全身代谢性疾病,伴有神经病变、大血管疾病、炎症、创伤、骨愈合受损及对牙周疾病易感性增加等特点﹝1﹞.糖尿病可分为胰岛素分泌缺陷型(1型)和胰岛素作用障碍型(2型) ,其中约90％的患者都是以2型为主.其中,体内持续性的高血糖是糖尿病性骨病最重要的致病因素之一,可能造成钙( Ca )、磷( P)代谢障碍而导致骨量减少、骨质疏松等.

背景:随着口腔纳米材料不断的进步与发展,大量研究发现碳纳米材料在口腔种植领域有着广泛的应用.目的:文章就碳纳米材料主要分类、结构特征、成骨、抗菌、蛋白/药物载体作用以及在口腔种植方面的相关应用作一综述.方法:明确碳纳米材料的分类后,以"石墨烯/碳纳米管/碳纳米纤维/碳纳米材料,口腔种植/成骨AND口腔/抗菌AND口腔/载药AND口腔"为中文检索词检索,以"Graphene/carbon?nanotubes/Carbon?Nanofibers/carbon?nanomaterials,dental?implant/osteogenesis AND oral/antibacterial?AND?oral/drug?loaded?AND?oral"为英文检索词检索,由第一作者通过计算机在中国知网、万方、维普及PubMed等数据库检索1998年1月至2021年8月已发表的相关文献,部分经典文献延长检索时间限制.最终选取符合纳入标准的英文文献64篇、中文文献9篇.结果 与结论:①碳纳米材料主要分为3类,即零维、一维和二维碳纳米材料,因其具有独特的空间结构和良好的理化性质,在种植体表面涂层、支架材料改性、载药和制备屏障膜等方面具有较大应用潜力.②此外材料的成骨和抗菌作用还有利于形成稳定的骨整合和良好的软组织封闭作用,在种植体周围炎的预防与治疗中也有一定的研究意义.③碳纳米材料种类繁多,许多研究还将碳纳米材料与其他生物分子材料功能化组合成复合材料,从而可以获得某种特性.此外,碳纳米材料本身也具备抗菌作用,石墨烯也常与其他抗菌剂(如银纳米粒子)功能化来增强抗菌性能.④综合来看,碳纳米材料中石墨烯作为典型的二维碳纳米材料,一直是口腔种植及其他领域研究的热点,其中氧化石墨烯是应用较为广泛的一类石墨烯衍生物材料.有研究发现将其应用于种植体表面改性时,对种植体周围炎的治疗及预防方面具有一定的研究意义.⑤但关于碳纳米材料诱导干细胞分化/成骨相关信号通路以及免疫调节机制的研究还不太明确,材料的细胞毒性、降解和不良反应也仍需进一步研究.⑥目前也有待研究出一种具有成本效益、可扩展性和可重复制备碳纳米材料的工艺方法和材料生物相容性的评价指标,此外也需进一步深入研究当碳纳米材料应用于植体表面涂层时,对种植体周围炎的预防与治疗意义.

背景:富血小板纤维蛋白是第二代血小板浓缩物,近年来广泛应用于口腔医学领域.但目前仍无确凿的证据解释其对促进软硬组织愈合保存的影响.目的:针对当前富血小板纤维蛋白在口腔医学的研究概况做一综述.方法:设计综述的撰写结构,检索中国知网和PubMed数据库2001-2021年相关文献,检索词为"Platelet-rich fibrin,Stomatology""富血小板纤维蛋白,口腔医学",部分经典文献延长检索时间限制,分析所得文献的摘要及内容,通过纳入和排除得到相关文献,对53篇符合标准的文献进行综述.结果 与结论:尽管有文献证实,富血小板纤维蛋白在口腔疾病中对于软硬组织的修复重建有着良好的效果,但是目前的证据并不能明确解释其相关机制.加之富血小板纤维蛋白的制备方法目前还不尽相同,有着种类繁多的富血小板纤维蛋白衍生物以及不同离心方式,因此仍需要大量实验做进一步研究.

背景:研究种植体表面处理时更看重是否能提高种植体骨结合的效率,而有关口腔种植体骨感知功能的研究则相对较少.目的:探讨纯钛表面硅烷偶联剂共价连接氧化石墨烯涂层对体外施万细胞生物学行为的影响.方法:在TA4钛片表面通过硅烷偶联剂的氨基基团共价连接制备不同质量浓度的氧化石墨烯涂层(0.25,0.5,0.75,1.0 mg/mL,分别命名为0.25-Ti-APTES-GO组、0.5-Ti-APTES-GO组、0.75-Ti-APTES-GO、1.0-Ti-APTES-GO组),通过扫描电镜、拉曼光谱和接触仪对涂层的微观结构、成分及接触角进行表征.分别在光滑钛片、硅烷偶联改性钛片及不同质量浓度氧化石墨烯涂层改性钛片上培养大鼠施万细胞,采用CCK-8法检测各组施万细胞的增殖活性,RT-qPCR和Western blot检测钛片上施万细胞分泌神经生长因子、胶质细胞源性神经营养因子的能力.结果 与结论:①扫描电镜下可见,不同质量浓度的氧化石墨烯涂层呈云雾状,高质量浓度氧化石墨烯涂层呈现的云雾状突起更加致密;②与光滑钛片组相比,硅烷偶联改性组钛片表面接触角较小(P<0.05);随氧化石墨烯质量浓度的增加,钛片表面接触角逐渐变小,其中0.75-Ti-APTES-GO组、1.0-Ti-APTES-GO组组接触角小于光滑钛片组(P<0.05);③CCK-8实验显示,与光滑钛片组比较,硅烷偶联剂改性组、0.25-Ti-APTES-GO组、0.5-Ti-APTES-GO组细胞增殖无明显变化(P>0.05),0.75-Ti-APTES-GO组、1.0-Ti-APTES-GO组细胞增殖受到抑制(P<0.05),所以后续实验选择0.25-Ti-APTES-GO组、0.5-Ti-APTES-GO组;④RT-qPCR检测显示,0.5-Ti-APTES-GO组神经生长因子mRNA表达量高于其他3组(P<0.05);0.25-Ti-APTES-GO组胶质细胞源性神经营养因子mRNA表达量低于其他3组(P<0.05),0.5-Ti-APTES-GO组胶质细胞源性神经营养因子mRNA表达量高于光滑钛片组、硅烷偶联剂改性组(P<0.05);⑤Western blot检测显示,0.5-Ti-APTES-GO组神经生长因子蛋白表达量高于光滑钛片组、0.25-Ti-APTES-GO组(P<0.05),胶质细胞源性神经营养因子蛋白表达量高于其他3组(P<0.05);⑥结果表明,硅烷偶联剂复合0.5 mg/mL氧化石墨烯涂层有良好的生物相容性,能较好地促进纯钛表面施万细胞神经生长因子及胶质细胞源性神经营养因子的表达.

To study the effect of miR-153-3p on the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) in a high glucose environment and its potential mechanism. The results showed that high glucose inhibited the osteogenic differentiation of BMSCs, and the expression of miR-153-3p increased during osteogenic differentiation. Further experiments found that in BMSCs induced by high glucose, overexpression of miR-1533p inhibited the osteogenic differentiation of BMSCs, and the expressions of osteogenesis-related genes bone sialoprotein, Collagen I and alkaline phosphatase were down-regulated, while silencing of miR-153-3p alleviated the inhibition effect. The dual-luciferase reporter gene assay confirmed that the 3'-untranslated region (3'-UTR) of runt related transcription factor 2 (RUNX2) had a targeted binding site with miR-153-3p and a negative regulatory effect. Molecular studies further confirmed that miR-153-3p inhibited the osteogenic differentiation of BMSCs by targeting the 3'-UTR of RUNX2. In conclusion, our study found that as one key regulator of high glucose affecting the osteogenic differentiation of BMSCs, miR-153-3p may play a negative regulatory role by inhibiting the expression of RUNX2.

目的:探讨高糖微环境中釉基质衍生物(EMD)对喷砂酸蚀(SLA)钛表面上骨髓间充质干细胞(BMSCs)成骨分化与黏附的影响及机制.方法:BMSCs分别培养于正常糖(NG)和高糖(HG)微环境中,Transwell观察BMSCs的迁移情况;SLA钛表面培养BMSCs,使用ALP活性、茜素红染色半定量、扫描电镜、WB和RT-qPCR检测成骨和黏附的性能.结果:HG组细胞迁移、ALP活性、茜素红半定量和扫描电镜成骨分化能力减弱,WB和RT-qPCR检测成骨和黏附的蛋白和基因表达量均降低,添加EMD后改善.XAV-939处理后,Wnt/β-catenin信号通路下游的蛋白表达降低,EMD诱导后均增加.结论:高糖微环境下,EMD促进SLA钛表面BMSCs成骨分化和黏附,可能通过激活Wnt/β-catenin信号通路实现.

The influence of enamel matrix derivative (EMD) on proliferation and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) was explored in high glucose (HG) microenvironment with interaction of Wnt/β-catenin pathway. Extraction of BMSCs from Sprague–Dawley rats, culture, and identification were manifested. The cells were treated with different concentration of EMD in HG to figure out the most available concentration for proliferation and osteogenic differentiation. Then, observation of cell growth curve and cell cycle changes, and detection of Osterix, runt-related transcription factor 2 (Runx2), COL-I, early osteogenic indexes, Calcium salt deposition, and β-catenin protein in Wnt/β-catenin pathway were assured. After adding Wnt/β-catenin pathway inhibitor (XAV-939) in the cells with osteogenesis induction, detection of binding of β-catenin to Osterix was clarified. Via identification BMSCs cultured in vitro was qualified. Different concentrations of EMD could accelerate cell proliferation in HG and osteogenesis induction, and 75 μg/mL EMD had the best effect. The HG augmented BMSCs proliferation and the propidium iodide index of flow cytometry cycle was elevated in HG, which were strengthened via the EMD. After BMSCs’ osteogenesis induction, Osterix, Runx2, CoL-1, early osteogenic indexes, and calcium salt deposition were reduced, but elevated via EMD. β-Catenin was the lowest in the HG, but elevated after EMD. After addition of XAV-939, reduction of β-catenin and the downstream (Osterix and Runx2) were manifested. Detection of binding protein bands was in β-catenin and Osterix of the HG after EMD treatment. EMD may facilitate the osteogenic differentiation of BMSCs via activating the Wnt/β-catenin pathway in HG.