Our object in this paper is to point out the existence of postmenopausal osteoporosis and to describe its clinical features. Some metabolic data showing the effects of therapy with estrogens and other agents are incorporated in other papers.1 It will probably be well to start by explaining and defining the term "osteoporosis." Adult bone is normally subject to two continuous processes—formation and resorption. The mass of bone may be deficient either because resorption is too great (hyperparathyroidism with osteitis fibrosa generalisata) or because formation is too little (osteoporosis or osteomalacia). Formation of bone may be too little, furthermore, either because the osteoblasts do not lay down sufficient osseous matrix or because the matrix, once laid down, is not calcified. The former condition is osteoporosis; the latter, osteomalacia or rickets (fig. 1). It is thought that stresses and strains are an important stimulus to osteoblastic activity and that the atrophy