2020 Volume 29 Issue 1 Pages 37-44
Hyperlipidemia inhibits bone formation, which has an adverse impact on the success of dental implants. Fzd9 has been reported to be a positive regulator of osteogenesis. However, the role of Fzd9 in dental implants in hyperlipidemic conditions is still unknown. In current study, we investigated how Fzd9 impacts on implant osseointegration in hyperlipidemic conditions. Models of high-fat medium-stimulated rat bone marrow stromal stem cells (BMSCs) were established. Alkaline phosphatase (ALP), alizarin red S (ARS) and oil red O (ORO) staining were used to examine the osteogenic differentiation of BMSCs. Wistar rats were fed with high-fat diet to induced hyperlipidemia. Titanium implants were implanted into the proximal metaphysis of the bilateral femurs of rats after 8 weeks. Thereafter, 1 mm of bone around each implant was obtained. Implant osseointegration and micromorphology were analyzed with microcomputer tomography (micro-CT) and hematoxylin-eosin (HE) staining. The relative expression levels of Fzd9 and Runx2 were analyzed by quantitative real-time PCR in vitro and in vivo. Western blotting was used to analyzed the protein level of Fzd9. The expression levels of Fzd9 and Runx2 were decreased. Osteogenic differentiation of BMSCs were suppressed under high-fat medium. Less bone formation was observed in hyperlipidemic rats compared to the normal. Hyperlipidemic rats had lower osteoblasts and bone-implant combination (BIC), bone volume fraction (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N) but higher trabecular spacing (Tb.S), trabecular bone pattern factor (TBf) and osteoclasts. In conclusion, the lower expression of Fzd9 impairs osseointegration in hyperlipidemic conditions via Wnt signaling pathway-related Runx2. Fzd9 may serve as a promising strategy for hyperlipidemia osseointegration.