Kaji Hiroshi
Kobe University Graduate School of Medicine, Department of Internal Medicine, Division of Diabetes, Metabolism and Endocrinology.
Clin Calcium. 2007 Dec;17(12):1836-42.
The continuous treatment with parathyroid hormone (PTH) or endogenous PTH excess by primary hyperparathyroidism cause enhanced bone resorption and subsequent decreased bone volume. However, the intermittent treatment with PTH is expected as a drug for osteoporosis for its stimulation of bone formation and marked increase in bone volume. The mechanism of different PTH actions due to the administration method still remains unclear. Several reports suggested the hypothesis about the role of insulin-like growth factor-1, anti-apoptotic effects through Runx2 or Smad3 and the differences of its effects on bone resorption. The investigation about the mechanism of bone formation by PTH intermittent treatment would lead to the development of bone-forming reagent in the future.
甲状旁腺激素(PTH)持续治疗或原发性甲状旁腺功能亢进导致内源性PTH过量会引起骨吸收增强,随后骨量减少。然而,间歇性PTH治疗因其刺激骨形成和显著增加骨量而有望成为治疗骨质疏松症的药物。给药方式导致不同PTH作用的机制仍不清楚。一些报告提出了关于胰岛素样生长因子-1的作用、通过Runx2或Smad3的抗凋亡作用及其对骨吸收影响差异的假说。对PTH间歇性治疗促进骨形成机制的研究将有助于未来骨形成试剂的开发。