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Unique roles of phosphorus in endochondral bone formation and osteocyte maturation
Author(s) -
Zhang Rong,
Lu Yongbo,
Ye Ling,
Yuan Baozhi,
Yu Shibin,
Qin Chunlin,
Xie Yixia,
Gao Tian,
Drezner Marc K,
Bonewald Lynda F,
Feng Jian Q
Publication year - 2011
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.294
Subject(s) - osteocyte , endochondral ossification , fibroblast growth factor 23 , osteoclast , osteoblast , endocrinology , bone remodeling , dmp1 , rankl , medicine , microbiology and biotechnology , hypophosphatemia , phex , chemistry , intramembranous ossification , biology , calcium , anatomy , immunology , rickets , parathyroid hormone , activator (genetics) , cartilage , vitamin d and neurology , biochemistry , receptor , viral matrix protein , virus , in vitro
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. © 2011 American Society for Bone and Mineral Research.