The study by Jilka et al. investigates the mechanism by which intermittent administration of parathyroid hormone (PTH) increases bone mass in mice. The authors found that PTH administration, whether in normal or osteopenic mice, increased bone formation without affecting the generation of new osteoblasts. Instead, PTH prolonged the lifespan of mature osteoblasts by preventing their apoptosis, which is a common fate for these cells under normal conditions. This antiapoptotic effect of PTH was confirmed in both rodent and human osteoblasts and osteocytes in vitro. The results suggest that the anabolic effect of PTH is mediated through its direct action on osteoblasts, via the PTH/PTHrP receptor, and through cAMP-generated signals that interfere with specific death pathways. The findings provide a novel mechanism for the therapeutic potential of PTH in conditions such as osteoporosis, where tissue mass reduction compromises functional integrity.The study by Jilka et al. investigates the mechanism by which intermittent administration of parathyroid hormone (PTH) increases bone mass in mice. The authors found that PTH administration, whether in normal or osteopenic mice, increased bone formation without affecting the generation of new osteoblasts. Instead, PTH prolonged the lifespan of mature osteoblasts by preventing their apoptosis, which is a common fate for these cells under normal conditions. This antiapoptotic effect of PTH was confirmed in both rodent and human osteoblasts and osteocytes in vitro. The results suggest that the anabolic effect of PTH is mediated through its direct action on osteoblasts, via the PTH/PTHrP receptor, and through cAMP-generated signals that interfere with specific death pathways. The findings provide a novel mechanism for the therapeutic potential of PTH in conditions such as osteoporosis, where tissue mass reduction compromises functional integrity.