Formation of mature bone-resorbing cells through osteoclastogenesis is required for the continuous remodeling and repair of bone tissue. In aging and disease this process may become aberrant, resulting in excessive bone degradation and fragility fractures. Interaction of receptor-activator of nuclear factor-κB (RANK) with its ligand RANKL activates the main signaling pathway for osteoclastogenesis. However, compelling evidence indicates that this pathway may not be sufficient for the production of mature osteoclast cells and that co-stimulatory signals may be required for both the expression of osteoclast-specific genes and the activation of osteoclasts. Osteoclast-associated receptor (OSCAR), a regulator of osteoclast differentiation, provides one such co-stimulatory pathway. This review summarizes our present knowledge of osteoclastogenesis signaling and the role of OSCAR in the normal production of bone-resorbing cells and in bone disease. Understanding the signaling mechanism through this receptor and how it contributes to the production of mature osteoclasts may offer a more specific and targeted approach for pharmacological intervention against pathological bone resorption.

通过破骨细胞形成形成成熟的骨吸收细胞对于骨组织的连续重塑和修复是必需的。在衰老和疾病中，该过程可能变得异常，导致过度的骨降解和脆性骨折。核因子-κB（RANK）受体激活剂与其配体RANKL的相互作用激活了破骨细胞形成的主要信号通路。然而，有力的证据表明该途径可能不足以产生成熟的破骨细胞，并且破骨细胞特异性基因的表达和破骨细胞的激活可能都需要共刺激信号。破骨细胞相关受体（OSCAR）是破骨细胞分化的调节剂，提供了一种这样的共刺激途径。这篇综述总结了我们目前关于破骨细胞生成信号的知识以及OSCAR在正常情况下的骨吸收细胞和骨疾病中的作用。了解通过该受体的信号传导机制及其如何促进成熟破骨细胞的产生，可能为针对病理性骨吸收的药理干预提供一种更具体和更有针对性的方法。