Conclusions
Our results showed the effects of atRA on suppressing inflammatory responses and promoting osteoblastic differentiation of BMSCs on titanium in an LPS-induced microenvironment. This indicates the potential therapeutic value of atRA for treating peri-implants inflammatory disease.
Methods
BMSCs were divided into four groups and treated with LPS (1 μg/mL), atRA (1 nmol/L), LPS + atRA, or left untreated. Cells were then cultured on titanium surfaces and cell function compared. BMSC proliferation and osteoblastic differentiation were assessed using the MTT assay, alkaline phosphatase (ALP) activity, alizarin red staining, and quantitative real-time polymerase chain reaction (RT-PCR). Expression levels of inflammatory factors were measured by quantitative RT-PCR and enzyme-linked immunosorbent assay.
Results
Increased mineralized nodule formation, ALP activity, osteocalcin, and osteopontin expression levels were detected in LPS + atRA-treated BMSCs after osteogenic induction, when compared with LPS-treated cells. In addition, the high levels of tumor necrosis factor-α, interleukin-1β, and receptor activator of nuclear factor-κ B ligand (RANKL) expression induced by LPS were inhibited after treatment with atRA. Conclusions: Our results showed the effects of atRA on suppressing inflammatory responses and promoting osteoblastic differentiation of BMSCs on titanium in an LPS-induced microenvironment. This indicates the potential therapeutic value of atRA for treating peri-implants inflammatory disease.