Denosumab (Dmab) was the first monoclonal antibody (mAb) approved for the treatment of osteoporosis. It blocks the receptor activator for nuclear factor κB ligand (RANKL) and acts as a potent antiresorptive agent. In contrast to classic antiresorptive agents, Dmab treatment leads to a progressive increase in bone mass, but the mechanisms remain controversial. Recently, RANKL signaling in osteoblastogenesis and bone formation and RANKL reverse signaling in coupling bone resorption and formation were demonstrated. Thus, here we discuss the roles of RANKL signaling and RANKL reverse signaling in the bone-forming effects of Dmab.

地诺单抗 (Dmab) 是第一个被批准用于治疗骨质疏松症的单克隆抗体 (mAb)。它阻断核因子 κB 配体 (RANKL) 的受体激活剂，并充当有效的抗再吸收剂。与经典的抗骨吸收药物相比，Dmab 治疗可导致骨量逐渐增加，但其机制仍存在争议。最近，证明了成骨细胞生成和骨形成中的 RANKL 信号传导以及骨吸收和形成耦合中的 RANKL 反向信号传导。因此，在这里我们讨论 RANKL 信号传导和 RANKL 反向信号传导在 Dmab 的骨形成作用中的作用。