As a model to investigate the pathogenesis of postmenopausal osteoporosis and the involvement of calcitonin in the bone alterations, we chose surgical menopause, studying the influence of castration on blood calcitonin. After surgery, the hormone and calcemia were raised significantly over preoperative values in castrated women, but not so in a control group of patients undergoing hysterectomy without oophorectomy. The elevated concentration of calcitonin was maintained during at least 4 months. It is speculated that this mechanism of control of calcitonin secretion by gonadal hormones might be activated in the pathogenesis of postmenopausal osteoporosis.