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Effects Of a One‐Month Treatment With PTH(1–34) on Bone Formation on Cancellous, Endocortical, and Periosteal Surfaces of the Human Ilium
Author(s) -
Lindsay Robert,
Zhou Hua,
Cosman Felicia,
Nieves Jeri,
Dempster David W,
Hodsman Anthony B
Publication year - 2007
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1359/jbmr.070104
Subject(s) - cancellous bone , osteoblast , endocrinology , iliac crest , medicine , bone histomorphometry , bone remodeling , osteoporosis , bone formation , anabolism , chemistry , population , bone resorption , urology , anatomy , trabecular bone , biochemistry , environmental health , in vitro
Abstract Using bone histomorphometry, we found that a 1‐month treatment with PTH(1–34) [hPTH(1–34)] stimulated new bone formation on cancellous, endocortical, and periosteal bone surfaces. Enhanced bone formation was associated with an increase in osteoblast apoptosis. Introduction : The precise mechanisms by which hPTH(1–34) increases bone mass and improves bone structure are unclear. Using bone histomorphometry, we studied the early effects of treating postmenopausal women with osteoporosis with hPTH(1–34). Materials and Methods : Tetracycline‐labeled iliac crest bone biopsies were obtained from 27 postmenopausal women with osteoporosis who were treated for 1 month with hPTH(1–34), 50 μg daily subcutaneously. The results were compared with tetracycline‐labeled biopsies from a representative control group of 13 postmenopausal women with osteoporosis. Results : The bone formation rate on the cancellous and endocortical surfaces was higher in hPTH(1–34)–treated women than in control women by factors of 4.5 and 5.0, respectively. We also showed a 4‐fold increase in bone formation rate on the periosteal surface, suggesting that hPTH(1–34) has the potential to increase bone diameter in humans. On the cancellous and endocortical surfaces, the increased bone formation rate was primarily caused by stimulation of formation in ongoing remodeling units, with a modest amount of increased formation on previously quiescent surfaces. hPTH(1–34)–stimulated bone formation was associated with an increase in osteoblast apoptosis, which may reflect enhanced turnover of the osteoblast population and may contribute to the anabolic action of hPTH(1–34). Conclusions : These findings provide new insight into the cellular basis by which hPTH(1–34) improves cancellous and cortical bone architecture and geometry in patients with osteoporosis.