Steroid -induced osteonecrosis of the femoral head (SONFH )is a metabolic disease caused by the extensive use of glucocorticoid. The pathogenesis of steroid-induced osteonecrosis of the femoral head is still not completely clear, yet there are various hypotheses. Studies have shown that the inflammatory reaction of macrophages may be one of the important factors to impel the development of steroid-induced osteonecrosis of the femoral head.The TLR4/NF-κB inflammatory signaling pathway can be activated by excessive glucocorticoid in the short-term or long term, resulting in the activation of NF-κB, which changes the original structural state of NF-κB, and then transmits to the nuclear promoter gene expression to release a large number of inflammatory mediators,such as TNF-α, Il-1β, IL-6, etc. They inhibits osteoblast differentiation and bone formation, induces osteoblast apoptosis, at the same time，enhances osteoclast differentiation,increases bone resorption and destroys bone homeostasis, eventually leading to collapse and necrosis of femoral head. This article reviews the possible mechanism of TLR4/NF-ΚB signaling pathway in the progression of SONFH, provideing a new idea for the prevention and treatment of SONFH.