Chapter 22: Fetal Calcium Metabolism Christopher S. Kovacs

Figure 1 Figure 1 Calcium sources in fetal life. Reproduced with permission from Pediatric Bone: Biology and Diseases, vol. 1, issue 1, Glorieux FH, Pettifor JM, Jüppner H, Fetal Mineral Homeostasis, pp. 271–302; Copyright Elsevier From the Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7 th Edition.

Figure 2 Figure 2 Fetal blood calcium regulation. PTH and PTHrP both contribute to blood calcium regulation, with blood calcium represented schematically as a thermometer (light gray, contribution of PTH; dark gray, contribution of PTHrP). In the absence of PTHrP, the blood calcium falls to the maternal level. In the absence of parathyroids (Hoxa3 null), the blood calcium falls well below the maternal calcium concentration, whereas in the absence of PTH (Pth null), the blood calcium equals the maternal level. In the absence of both PTHrP and PTH (Hoxa3/Pthrp double mutant), the blood calcium falls even further than in the absence of the parathyroids. Reproduced with permission from Pediatric Bone: Biology and Diseases, vol. 1, issue 1, Glorieux FH, Pettifor JM, Jüppner H, Fetal Mineral Homeostasis, pp. 271–302; Copyright Elsevier From the Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7 th Edition.

Figure 3 Figure 3 Schematic model of the relative contribution of PTH and PTHrP to endochondral bone formation and skeletal mineralization. PTHrP is produced within the cartilaginous growth plate and directs the development of this scaffold that will later be broken down and replaced by bone. PTH reaches the skeleton systemically from the parathyroids and directs the accretion of mineral by the developing bone matrix. Reproduced with permission from Pediatric Bone: Biology and Diseases, vol. 1, issue 1, Glorieux FH, Pettifor JM, Jüppner H, Fetal Mineral Homeostasis, pp. 271–302; Copyright Elsevier From the Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7 th Edition.