Current Osteoporosis Reports ( IF 4.2 ) Pub Date : 2022-10-06 , DOI: 10.1007/s11914-022-00756-5 Albert S Kim 1, 2, 3 , Christian M Girgis 3, 4, 5 , Michelle M McDonald 1, 2
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Purpose of Review
Inhibition of receptor activator of nuclear factor kappa-B ligand (RANKL) with denosumab is an effective treatment in a number of conditions including osteoporosis where suppression of bone resorption is desired. However, denosumab discontinuation is associated with rebound increase in bone resorption and subsequent loss in bone mass and a rapid return to baseline fracture risk. We review recent data on the rebound increase in bone resorption following denosumab discontinuation and the potential mechanisms behind this phenomenon.
Recent Findings
Osteoclasts have been considered to be highly specialised cells that undergo apoptosis after fulfilling their function of bone resorption. However, recent studies suggest that osteoclasts are longer lived cells which migrate through vasculature and are capable of undergoing fission into a novel cell type (the osteomorph) and re-fusion in a process termed osteoclast recycling.
Summary
The life cycle of the osteoclast is more complex than previously appreciated. Osteoclast recycling provides a novel mechanistic framework to examine changes in osteoclast biology in response to treatment of bone diseases and provides an exciting new avenue towards personalised medicine.
中文翻译：
破骨细胞回收和狄诺塞麦停药后的反弹现象
审查目的
用狄诺塞麦抑制核因子 kappa-B 配体受体激活剂 (RANKL) 是治疗多种疾病的有效方法，包括需要抑制骨吸收的骨质疏松症。然而，地诺塞麦停用与骨吸收反弹增加、随后骨量损失以及快速恢复至基线骨折风险相关。我们回顾了关于停用狄诺塞麦后骨吸收反弹增加的最新数据以及这种现象背后的潜在机制。
最近的发现
破骨细胞被认为是高度特化的细胞，在完成其骨吸收功能后发生凋亡。然而，最近的研究表明，破骨细胞是寿命较长的细胞，可以通过脉管系统迁移，并且能够分裂成新的细胞类型（骨形态），并在称为破骨细胞回收的过程中重新融合。
概括
破骨细胞的生命周期比以前想象的更复杂。破骨细胞回收提供了一个新颖的机制框架来检查破骨细胞生物学的变化对骨疾病治疗的反应，并为个性化医疗提供了一条令人兴奋的新途径。
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