PHYSICIANS have traditionally considered PTH to be an agent that is catabolic to the skeleton. However, as early as 60 yr ago, Albright and his colleagues (1) and later Selye (2) noted that the peptide extract could also be anabolic to the skeleton, producing increases in bone tissue in animals. The potential for an agent that can increase bone mass and hence reverse the skeletal defect in patients with osteoporosis is great, particularly if in doing so it also repairs microarchitectural damage. The agents currently available in the United States for treatment of osteoporosis, estrogens and salmon calcitonin, primarily stabilize bone mass and prevent further loss of bone, although a transient small increment in mass is often reported, particularly in patients with elevated levels of bone remodeling. This increase is not a true anabolic effect but is related to the temporal effects on turnover in which resorption declines initially followed by a reduction in formation that may take several months. Fluoride, in contrast, does increase bone mass by a true anabolic action, but there is controversy about the quality of the bone formed. Two recent controlled studies failed to find a reduction in fracture recurrence (3, 4), although the dose may have been excessive, and consequently, fluoride is currently not approved for treatment of osteoporosis in the United States. Thus, if PTH is capable of improving bone mass and quality, the peptide will have a potential therapeutic role in osteoporosis. This review summarizes the data available to date, starting at the cellular level.