[Phosphate homeostasis and oral diseases].
FGF23 produced mainly by osteocytes plays a central role in phosphate homeostasis by increasing the renal phosphate excretion and suppressing the vitamin D activation. Mutations in FGF23 and its regulatory molecules such as PHEX, DMP1, and FAM20C have been shown to be responsible for hereditary hypophosphatemic diseases. Patients and animal models of these hypophosphatemic conditions often manifest dental defects, whose etiology may include hypophosphatemia and impaired vitamin D action. In addition, the mechanisms specific to each responsible gene such as accumulated ASARM peptides in PHEX deficiency and the reduced DSPP expression in DMP1 deficiency are also involved in the pathogenesis of these dental problems.
Department of Bone and Mineral Research,Osaka Medical Center and Research Institute for Maternal and Child Health, Japan.
Toshimi
T
Michigami
D000818:Animals; D001851:Bone Diseases, Metabolic / Q000378:metabolism*; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D010710:Phosphates / Q000172:deficiency / Q000378:metabolism*; D014070:Tooth / Q000378:metabolism*
C000717427:FGF23 protein, human; D010710:Phosphates; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23