作者: Pedro Esbrit , María José Alcaraz
DOI: 10.1016/J.BCP.2013.03.002
关键词:
摘要: Osteoporosis is characterized by low bone mineral density and/or poor microarchitecture leading to an increased risk of fractures. The skeletal alterations in osteoporosis are a consequence relative deficit formation compared resorption. therapies have mostly relied on antiresorptive drugs. An alternative therapeutic approach for currently available, based the intermittent administration parathyroid hormone (PTH). Bone anabolism caused PTH therapy mainly accounted ability increase osteoblastogenesis and osteoblast survival. PTH-related protein (PTHrP)-an abundant local factor bone- interact with common type 1 receptor similar affinities osteoblasts. Studies rodent models limited data postmenopausal women suggest that N-terminal PTHrP peptides might be considered promising anabolic therapy. In addition, putative osteogenic actions ascribed not only its domain but also PTH-unrelated C-terminal region. this review, we discuss underlying cellular molecular mechanisms potential (PTHrP) mass improve regeneration.