Teti Anna
Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila , L'Aquila, Italy.
Bonekey Rep. 2013 Dec 4;2:449. doi: 10.1038/bonekey.2013.183.
Should we believe that osteoclasts are only involved in bone resorption? What about their contribution to bone formation? In this article I will review evidence that bone formation can be regulated by osteoclasts. Why is this? Likely because in the physiologic condition of bone remodeling, bone resorption and formation are balanced, and there is no better way to control this equilibrium than through a concerted action between the two cell types. Although the influence of osteoblasts on osteoclastic bone resorption is well documented and consolidated over time, what osteoclasts do to regulate osteoblast activity is still matter of intense investigation. The original hypothesis that all is in the osteoblast-seeking factors stored in the bone matrix, released and activated during bone resorption, is now being challenged by several studies, suggesting that osteoclasts are also capable of producing 'clastokines' that regulate osteoblast performance. Indeed, several of them have been demonstrated to orchestrate osteoclast-osteoblast activities. However, we are probably still at the dawn of a new era, and future work will tell us whether any of these clastokines can be exploited to stimulate bone formation and rebalance bone remodeling in skeletal diseases.
我们是否应该认为破骨细胞仅参与骨吸收？它们对骨形成有何贡献？在本文中，我将综述破骨细胞可调节骨形成的证据。为什么会这样呢？可能是因为在骨重塑的生理状态下，骨吸收和形成是平衡的，而控制这种平衡的最佳方法莫过于这两种细胞类型之间的协同作用。虽然成骨细胞对破骨细胞性骨吸收的影响已有充分记录且随着时间推移得到了巩固，但破骨细胞如何调节成骨细胞活性仍是深入研究的课题。最初的假设认为，一切都取决于在骨吸收过程中释放并激活的、储存在骨基质中的成骨细胞趋化因子，现在这一假设正受到多项研究的挑战，这些研究表明破骨细胞也能够产生调节成骨细胞功能的“破骨细胞因子”。事实上，其中一些因子已被证明可协调破骨细胞与成骨细胞的活动。然而，我们可能仍处于一个新时代的开端，未来的研究将告诉我们，这些破骨细胞因子中的任何一种是否可用于刺激骨形成并重新平衡骨骼疾病中的骨重塑。
