Department of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, VA, USA.
Department of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, VA, USA.
Dent Mater. 2019 Jan;35(1):176-184. doi: 10.1016/j.dental.2018.11.011. Epub 2018 Nov 30.
Roughened dental implants promote mesenchymal stem cell (MSCs) osteoblastic differentiation, and hydrophilic modifications induce anti-inflammatory macrophages activation. While the effect of different surface modifications on osseointegration of commercial dental implants have been compared in vivo and clinically, the initial cellular response to these modifications often overlooked. We aimed to characterize the macrophage inflammatory response and MSC osteogenesis across different commercially available implants in vitro.
Six commercially available rough implants [OsseoSpeed™ (Astra-Tech™, Implant A); Osseotite (Biomet 3i™, Implant B); TiUnite™ (Nobel-Biocare, Implant C); Ti-SLA, (Implant D), Roxolid (RXD-SLA, Implant E), RXD-SLActive (Implant F) (Straumann)] were examined. Macrophages and MSCs were seeded directly on implants and cultured in custom vials. mRNA and protein levels of pro- (IL1B, IL6, IL17A, CXCL10, TNFa) and anti- (IL4, IL10, TGFB1) inflammatory markers were measured after 24 and 48h in macrophages. Osteoblastic differentiation of MSCs was assessed after seven days by alkaline phosphatase activity, osteocalcin, and angiogenic, osteogenic, and inflammatory markers by ELISA and qPCR (n=6/variable, ANOVA, post hoc Tukey HSD with α=0.05).
Hydrophilic implant F induced the highest level of osteogenic factor released from MSCs and anti-inflammatory factors from macrophages with the lowest level of pro-inflammatory factors. Alternatively, implants A and C supported lower levels of osteogenesis and increased secretion of pro-inflammatory factors.
In this study, we successfully evaluated differences in cell response to commercially available clinical implants using an in vitro model. Data from this model suggest that not all surface modification procedures generate the same cell response.
粗糙化的牙种植体促进间充质干细胞（MSCs）成骨分化，而亲水改性则诱导抗炎巨噬细胞的激活。虽然已经在体内和临床上比较了不同表面改性对商业牙种植体的骨整合效果，但通常忽略了这些改性对初始细胞反应的影响。我们旨在体外研究不同商业可用种植体的巨噬细胞炎症反应和 MSC 成骨作用。
研究了六种商业上可用的粗糙种植体[OsseoSpeed™（Astra-Tech™，植入物 A）；Osseotite（Biomet 3i™，植入物 B）；TiUnite™（Nobel-Biocare，植入物 C）；Ti-SLA（植入物 D），Roxolid（RXD-SLA，植入物 E），RXD-SLActive（植入物 F）（Straumann）]。巨噬细胞和 MSC 直接接种在植入物上，并在定制小瓶中培养。在巨噬细胞中培养 24 和 48 小时后，测量促炎（IL1B、IL6、IL17A、CXCL10、TNFa）和抗炎（IL4、IL10、TGFB1）标志物的 mRNA 和蛋白水平。在第 7 天通过碱性磷酸酶活性、骨钙素以及通过 ELISA 和 qPCR 测量血管生成、成骨和炎症标志物来评估 MSC 的成骨分化（n=6/变量，ANOVA，事后 Tukey HSD，α=0.05）。
亲水植入物 F 诱导 MSC 释放的成骨因子水平最高，从巨噬细胞中释放的抗炎因子水平最低，促炎因子水平最低。相反，植入物 A 和 C 支持较低水平的成骨作用和增加促炎因子的分泌。
在这项研究中，我们使用体外模型成功评估了商业临床植入物对细胞反应的差异。该模型的数据表明，并非所有表面改性程序都会产生相同的细胞反应。
