This study demonstrates that intermittent administration of parathyroid hormone (PTH) increases bone formation by preventing osteoblast apoptosis, rather than by increasing the production of new osteoblasts. In mice with normal or reduced bone mass, daily PTH injections increased bone formation without affecting the generation of new osteoblasts. Instead, PTH extended the lifespan of mature osteoblasts by preventing their apoptosis, which is the typical fate of these cells under normal conditions. This antiapoptotic effect of PTH was confirmed in vitro using rodent and human osteoblasts and osteocytes. The findings support the principle that the work performed by a cell population can be increased by suppressing apoptosis. The study also suggests novel pharmacotherapeutic strategies for osteoporosis and other conditions where tissue mass reduction compromises functional integrity. The results indicate that PTH's anabolic effect on bone is primarily due to its ability to prevent osteoblast apoptosis, rather than by increasing osteoblast progenitor activity. The study also shows that PTH inhibits osteocyte apoptosis, further supporting its role in enhancing bone formation. The antiapoptotic effect of PTH is mediated through the PTH/PTHrP receptor and subsequent activation of adenylate cyclase, leading to cAMP-generated signals that interfere with some, but not all, death pathways. The findings have important implications for the treatment of osteoporosis and other bone-related diseases, as they highlight the potential of targeting apoptosis to enhance bone formation.This study demonstrates that intermittent administration of parathyroid hormone (PTH) increases bone formation by preventing osteoblast apoptosis, rather than by increasing the production of new osteoblasts. In mice with normal or reduced bone mass, daily PTH injections increased bone formation without affecting the generation of new osteoblasts. Instead, PTH extended the lifespan of mature osteoblasts by preventing their apoptosis, which is the typical fate of these cells under normal conditions. This antiapoptotic effect of PTH was confirmed in vitro using rodent and human osteoblasts and osteocytes. The findings support the principle that the work performed by a cell population can be increased by suppressing apoptosis. The study also suggests novel pharmacotherapeutic strategies for osteoporosis and other conditions where tissue mass reduction compromises functional integrity. The results indicate that PTH's anabolic effect on bone is primarily due to its ability to prevent osteoblast apoptosis, rather than by increasing osteoblast progenitor activity. The study also shows that PTH inhibits osteocyte apoptosis, further supporting its role in enhancing bone formation. The antiapoptotic effect of PTH is mediated through the PTH/PTHrP receptor and subsequent activation of adenylate cyclase, leading to cAMP-generated signals that interfere with some, but not all, death pathways. The findings have important implications for the treatment of osteoporosis and other bone-related diseases, as they highlight the potential of targeting apoptosis to enhance bone formation.