Oestrogen deficiency is by far the major factor contributing to the high rate of osteoporotic fractures in women. The anti-osteoporotic effect of estrogen may be explained by its property to regulate cytokine secretion and thus balance bone remodeling. In oestrogen deficiency, increased resorption and remodeling will occur leading to osteoporosis. It has been extensively shown that oestrogen replacement therapy (ERT) prevents postmenopausal bone loss and reduces fracture risk by half, provided that an appropriate dose is used. In order to optimize osteoporosis prevention, ERT should be started a early as possible in menopause and be maintained as long as possible. ERT may also be effective in elderly osteoporotic patients in preventing bone loss and, reducing fracture risk. The acceptance of ERT, however, at an older age has not been thoroughly evaluated. A reduction of cardiovascular disease and of climateric symptoms are among other benefits of ERT. So far, only few postmenopausal women are treated with ERT. ERT without progestins has been repeatedly found associated with an increased risk of developing endometrial cancer, but the cyclic addition of progestins protects from endometrial hyperplasia and carcinoma. Combined oestrogen-progestin therapy is as efficient as estrogen therapy alone, but not more so. Since progestins may oppose some of the beneficial effects of estrogens, the lowest dose with the least metabolic impact should be prescribed. Women who have had a hysterectomy, should probably be treated by estrogen replacement therapy only. Meta-analyses concerning breast cancer associated with ERT found a very moderately increased risk (RR = 1.06). Therefore ERT prescription should be discussed openly with women considering all risks and benefits. In women who have suffered from breast cancer, a bone sparing effect of tamoxifen has been shown.