Abstract：
OBJECTIVE: Silicon-releasing biomaterials are widely used in the field of dentistry. However, unlike bone, very little is known about the role of silicon on dental tissue formation and repair. This study investigates the influence of silicic acid on the survival, differentiation and mineralizing ability of human dental pulp stem cells (hDPSCs) in 3D pulp-like environments METHODS: Dense type I collagen hydrogels seeded with hDPSCs were cultured over 4 weeks in the presence of silicic acid at physiological (10 μM) and supraphysiological (100 μM) concentrations. Cell viability and proliferation were studied by Alamar Blue and live/dead staining. The collagen network was investigated using second harmonic generation imaging. Mineral deposition was monitored by histology and scanning electron microscopy. Gene expression of mineralization- and matrix remodeling-associated proteins was studied by qPCR.
RESULTS: Presence of silicic acid did not show any significant influence on cell survival, metabolic activity and gene expression of key mineralization-related proteins (ALP, OCN, BSP). However, it induced enhanced cell clustering and delayed expression of matrix remodeling-associated proteins (MMP13, Col I). OPN expression and mineral deposition were inhibited at 100 μM. It could be inferred that silicic acid has no direct cellular effect but rather interacts with the collagen network, leading to a modification of the cell-matrix interface.
CONCLUSIONS: Our results offer advanced insights on the possible role of silicic acid, as released by pulp capping calcium silicates biomaterials, in reparative dentine formation. More globally, these results interrogate the possible role of Si in pulp pathophysiology.
RESULTS: Presence of silicic acid did not show any significant influence on cell survival, metabolic activity and gene expression of key mineralization-related proteins (ALP, OCN, BSP). However, it induced enhanced cell clustering and delayed expression of matrix remodeling-associated proteins (MMP13, Col I). OPN expression and mineral deposition were inhibited at 100 μM. It could be inferred that silicic acid has no direct cellular effect but rather interacts with the collagen network, leading to a modification of the cell-matrix interface.
CONCLUSIONS: Our results offer advanced insights on the possible role of silicic acid, as released by pulp capping calcium silicates biomaterials, in reparative dentine formation. More globally, these results interrogate the possible role of Si in pulp pathophysiology.
摘要：
目的：硅释放生物材料广泛应用于牙科领域。然而,不像骨头,关于硅在牙齿组织形成和修复中的作用知之甚少。这项研究调查了硅酸对生存的影响，人牙髓干细胞(hDPSC)在3D牙髓样环境中的分化和矿化能力方法:在生理(10μM)和超生理(100μM)浓度的硅酸存在下,将接种有hDPSC的致密I型胶原水凝胶培养4周。通过AlamarBlue和活/死染色研究细胞活力和增殖。使用二次谐波生成成像研究胶原网络。通过组织学和扫描电子显微镜监测矿物质沉积。通过qPCR研究矿化和基质重塑相关蛋白的基因表达。
结果：硅酸的存在对细胞存活没有任何显著影响，关键矿化相关蛋白的代谢活性和基因表达(ALP，OCN,BSP）。然而,它诱导增强的细胞聚集和基质重塑相关蛋白（MMP13，ColI）的延迟表达。OPN表达和矿物质沉积在100μM时被抑制。可以推断，硅酸没有直接的细胞效应，而是与胶原蛋白网络相互作用。导致细胞-矩阵界面的修改。
结论：我们的结果为硅酸的可能作用提供了更深入的见解，由纸浆覆盖硅酸钙生物材料释放，修复性牙本质的形成。更全球,这些结果询问了硅在牙髓病理生理学中的可能作用。
结果：硅酸的存在对细胞存活没有任何显著影响，关键矿化相关蛋白的代谢活性和基因表达(ALP，OCN,BSP）。然而,它诱导增强的细胞聚集和基质重塑相关蛋白（MMP13，ColI）的延迟表达。OPN表达和矿物质沉积在100μM时被抑制。可以推断，硅酸没有直接的细胞效应，而是与胶原蛋白网络相互作用。导致细胞-矩阵界面的修改。
结论：我们的结果为硅酸的可能作用提供了更深入的见解，由纸浆覆盖硅酸钙生物材料释放，修复性牙本质的形成。更全球,这些结果询问了硅在牙髓病理生理学中的可能作用。
