Denosumab (Dmab) is a humanized monoclonal antibody that blocks RANKL (receptor activator for nuclear factor κB ligand), thereby exerting a potent bone antiresorptive action. Dmab treatment leads to a dramatic and sustained increase in bone mass through mechanisms that are currently under debate. It is also a matter of controversy whether this potent action of Dmab could lead to intrabone dystrophic mineralization. Recent research has uncovered a possible anabolic role of Dmab involving RANKL-dependent reverse signaling in osteoblasts, and that bone marrow adipocytes can modulate osteoclastogenesis through the production of RANKL. We comment here on potential pathways which might account for the anabolic action of Dmab. The impact of this proposed mechanism needs to be addressed in further research.

中文翻译：

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RANKL 封锁产生的意外骨骼形成

地诺单抗 (Dmab) 是一种人源化单克隆抗体，可阻断 RANKL（核因子 κB 配体的受体激活剂），从而发挥有效的骨抗吸收作用。Dmab 治疗通过目前正在辩论的机制导致骨量的显着和持续增加。Dmab 的这种强效作用是否会导致骨内营养不良性矿化，这也是一个有争议的问题。最近的研究揭示了 Dmab 可能的合成代谢作用，涉及成骨细胞中 RANKL 依赖性反向信号传导，并且骨髓脂肪细胞可以通过产生 RANKL 来调节破骨细胞生成。我们在此评论可能解释 Dmab 合成代谢作用的潜在途径。这种拟议机制的影响需要在进一步的研究中加以解决。