This review lecture will examine the available evidence about the roles of PTH and PTHrP in regulating mineral homeostasis during fetal development, and will demonstrate that these two hormones maintain interlocking, complementary, and at times overlapping roles. Each is unable to make up for loss of the other hormone. PTHrP is expressed within the growth plate, directs endochondral bone formation, and determines the fate of chondrocytes before bone formation can be initiated. It is expressed in placenta and is present at high levels in the fetal circulation. It stimulates placental calcium (and possibly magnesium) transfer, and raises blood minerals levels above ambient maternal values in order to effect mineralization of the skeleton. It does not upregulate in response to absence of PTH or hypocalcemia, and so its secretion may be regulated autonomously or in response to placental signals. Its actions on endochondral bone development require the PTH/PTHrP receptor (PTH1R); its actions on placental calcium transfer appear to require a midmolecular receptor; its actions to raise the blood calcium above the maternal level may require both receptors. PTH is expressed in fetal parathyroids and placenta. Despite circulating at low levels it has a more dominant effect than PTHrP in regulating the blood calcium and ensuring adequate mineralization of the skeleton by term. It probably does not affect the cartilaginous stages of endochondral bone development although it may influence bone formation in the steps that occur after the apoptosis of hypertrophic chondrocytes. Unlike PTHrP, it increases with fetal hypocalcemia, but its secretion is constrained by the calcium sensing receptor to maintain the adult calcium level, well below what the fetus normally achieves. PTH does have the ability to stimulate placental calcium transfer but whether this occurs normally or only in response to abnormal conditions (such as absence of PTHrP, or pharmacological treatment with PTH) remains unknown. Absence of PTH disrupts expression of calciotropic and other cation transporter genes within the placenta. All of the known actions of PTH require normal expression of the PTH1R. This article is part of a Special Issue entitled ECTS 2011. Disclosure of interest: None declared.