Department of Operative Dentistry and Endodontics, School of Stomatology, Fourth Military Medical University, Xi'an, People's Republic of China.
J Bone Miner Res. 2011 May;26(5):1047-56. doi: 10.1002/jbmr.294.
The mechanisms by which inorganic phosphate (P(i)) homeostasis controls bone biology are poorly understood. Here we used Dmp1 null mice, a hypophosphatemic rickets/osteomalacia model, combined with a metatarsal organ culture and an application of neutralizing fibroblast growth factor 23 (FGF-23) antibodies to gain insight into the roles of P(i) in bone biology. We showed (1) that abnormal bone remodeling in Dmp1 null mice is due to reduced osteoclast number, which is secondary to a reduced ratio of RANKL/OPG expressed by osteoclast supporting cells and (2) that osteoblast extracellular matrix mineralization, growth plate maturation, secondary ossification center formation, and osteoblast differentiation are phosphate-dependent. Finally, a working hypothesis is proposed to explain how phosphate and DMP1 control osteocyte maturation.
无机磷酸盐（P(i)）稳态如何控制骨生物学的机制尚不清楚。在这里，我们使用 Dmp1 基因敲除小鼠（一种低磷性佝偻病/骨软化症模型），结合跖骨器官培养和中和成纤维细胞生长因子 23（FGF-23）抗体的应用，深入了解 P(i) 在骨生物学中的作用。我们发现：（1）Dmp1 基因敲除小鼠的异常骨重塑是由于破骨细胞数量减少所致，这是由于破骨细胞支持细胞表达的 RANKL/OPG 比值降低所致；（2）成骨细胞细胞外基质矿化、生长板成熟、次生骨化中心形成和成骨细胞分化均依赖于磷酸盐。最后，提出了一个工作假说来解释磷酸盐和 DMP1 如何控制骨细胞的成熟。
