![]() We conclude that in cancellous bone, attenuation of osteoblast apoptosis by PTH increases osteoblast number because their rate of apoptosis is high, making this effect of the hormone profound. However, 14 days of pre-treatment with ganciclovir prevented PTH anabolism on periosteal bone. ![]() ![]() Consistent with high turnover of cancellous osteoblasts as compared to that of periosteal osteoblasts, ganciclovir-induced ablation of replicating osteoblast progenitors in mice expressing thymidine kinase under the control of the 3.6kb rat Col1A1 promoter resulted in disappearance of osteoblasts from cancellous bone over a 7–14 day period, whereas periosteal osteoblasts were unaffected. Thus, intermittent PTH does not increase cancellous or periosteal osteoblast number by stimulating the proliferation of osteoblast progenitors. Cancellous osteoblasts, on the other hand, were labeled under basal conditions, but PTH did not increase the percentage of BrdU-positive cells. Administration of BrdU for 4 days failed to label periosteal osteoblasts under either basal conditions or following administration of PTH. Moreover, PTH did not have a discernable effect on periosteal osteoblast apoptosis. However, the prevalence of apoptotic periosteal osteoblasts was only 0.2% in vehicle treated animals, which is ~20-fold lower than is the case for cancellous osteoblasts. ![]() We report that daily injections of 100 ng/g of PTH(1–34) to 4–6 month old mice increased the number of osteoblasts on the periosteum of lumbar vertebrae by 2–3 fold as early as after 2 days. Previous studies of ours in mice demonstrated that intermittent PTH increases cancellous osteoblast number at least in part by attenuating osteoblast apoptosis, but the mechanism responsible for the anabolic effect of the hormone on periosteal bone is unknown. Intermittent administration of parathyroid hormone (PTH) stimulates bone formation on the surface of cancellous and periosteal bone by increasing the number of osteoblasts.
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