{Reference Type}: Journal Article
{Title}: Silicon impacts collagen remodelling and mineralization by human dental pulp stem cells in 3D pulp-like matrices.
{Author}: Akoa DM;Hélary C;Foda A;Chaussain C;Poliard A;Coradin T;
{Journal}: Dent Mater
{Volume}: 40
{Issue}: 9
{Year}: 2024 Sep 21
{Factor}: 5.687
{DOI}: 10.1016/j.dental.2024.06.021
{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.