FACTORS THAT ALTER SKELETAL RESPONSES TO PTH

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 甲状旁腺激素(PTH)刺激骨质疏松妇女的骨形成和重建骨微结构，显著降低新骨折的发生率。但PTH并不能治愈许多患者的骨质疏松症，尽管它可以常规地治愈实验动物的骨质疏松症。甲状旁腺激素不能治愈所有人的一个原因是，甲状旁腺素刺激的骨形成增加随着甲状旁腺素治疗的继续而消散。这项研究测试了缓慢增加甲状旁腺素的剂量是否延长了它对骨形成的影响。此外，参与者中的研究调查了为什么甲状旁腺素对骨形成的影响在继续治疗的情况下下降。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Parathyroid hormone (PTH) stimulates bone formation and reconstitutes bone micro-architecture in women with osteoporosis and markedly reduces the incidence of new fractures. But PTH does not cure osteoporosis in many patients, even though it routinely cures osteoporosis in experimental animals. One reason PTH fails to cure all humans is that PTH-stimulated increases in bone formation dissipate as PTH therapy continues. This study tests whether slowly increasing the dose of PTH prolongs its effects on bone formation. In addition, studies among the participants investigate why PTH's effects on bone formation decline despite continued treatment.