Novel in vitro comparative model of osteogenic and inflammatory cell response to dental implants.

OBJECTIVES: 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.

METHODS: 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).

RESULTS: 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.

SIGNIFICANCE: 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.