摘要Osteonecrosis of the femoral head (ONFH) is a leading cause of hip diseases in young adults and is frequently observed in patients treated with high dose of glucocorticoids.There have been various hypotheses about the pathogenesis of glucocorticoid-induced ONFH.Studies have shown that inflammation and inflammatory cytokines play a crucial role in many diseases and are also an important contributors in the glucocorticoid-induced ONFH.TLR4, a major member of Toll-like receptor family, is the most important pattern recognition receptor for endotoxin/lipopolysaccharide.It is a pivotal mediating factor in the development of glucocorticoid-induced ONFH.Studies showed that glucocorticoids could induce excessive activation of Myd88-dependent TLR4 signaling pathway with NF-κB transferred into nuclear and the release of inflammatory cytokines, such as TNF-α, IL-1βand IL-6.NF-κB could exert both promotion and inhibition effects on the osteogenic differentiation and calcium deposition of osteoblasts, promote bone resorption, destroy bone homeostasis and inhibit angiogenesis.A variety of inflammatory cytokines also have significant effects on the destruction, resorption and regeneration of the bone.Eventually it could lead to ONFH.The research on TLR4 signaling pathway could not only reveal the pathogenesis of glucocorticoid-induced ONFH, but also provide references for the prevention and treatment of ONFH.It is of great significance for the early treatment of glucocorticoid-induced ONFH and incidence reduction.