CLINICAL TRIAL: FACTORS THAT ALTER SKELETAL RESPONSES TO PTH

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 甲状旁腺激素（PTH）刺激骨质疏松症妇女的骨形成和重建骨微结构，并显着降低新发骨折的发生率。 但是PTH不能治愈许多患者的骨质疏松症，即使它在实验动物中常规治愈骨质疏松症。 PTH不能治愈所有人的一个原因是PTH刺激的骨形成增加随着PTH治疗的继续而消失。 本研究测试缓慢增加PTH剂量是否会影响骨形成。 此外，参与者中的研究调查了为什么尽管持续治疗，PTH对骨形成的影响会下降。

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.