Enhanced Odontogenesis of Inflammation-Exposed DPSCs by Soluble Silicon

Objective:In carious lesions and dental injuries, inflammation occurs as inflammatory cells accumulate and release cytokines (tumor necrosis factor –α (TNF-α), interleukin – 1β (IL-1β)) that can interrupt DPSC odontogenesis and biomineralization during dental pulp repair. Recently, treatments involving the use of amorphous silica-based biomaterials have shown that the release of Si4+ from their matrices can stimulate biomineralization during osteogenesis and could be applied here. Therefore, the objective of this study is to determine the temporal effects of silicon on DPSC odontoblastic differentiation and collagen matrix formation under conditions of inflammation.

Methods:  Human DPSCs (p1-4) were exposed to control and treatment conditions. Control media was a-MEM with 10% FBS, 1% pen-strep, 50 ppm ascorbic acid, and 10mM β-glycerophosphate supplementation. IL-1β (0.5-20ng/ml) and TNF-α (1-40ng/ml) were added to media to mimic inflammatory conditions, and 0.1 mM sodium metasilicate was used to create Si4+ treatment. Treatments were added to cells for analysis of gene expression (days 1, 3, 7, 12) and extracellular matrix (ECM) formation (day 12). Genes studied included collagen type 1, Runx2, dentin sialophosphoprotein (DSPP), and osteocalcin (OCN) while ECM was stained for collagen matrix formation using Picrosirius staining. One-way analysis of variance was used for statistical comparison relative to control treated cells with p<0.05 reported for statistical significance.

Results:At Day 1, silicon enhanced the gene expression of odontoblastic marker DSPP and collagen in DPSCs with inflammation compared to Silicon-only. By day 7, silicon reduced the expression of osteoblastic genes Runx2 and OCN. ECM staining illustrated an increased density of collagen fibers for DPSCs with inflammation compared to control. Silicon with/without inflammation showed similar collagen density and thickness as control.

Conclusion: Silicon, in the presence of inflammation, was found to induce odontoblastic differentiation at an early time point while regulating osteogenic differentiation – potentially stimulating pulp healing.