The treatment of osteoporosis in subjects older than 65, defined by Albright and Reifenstein(2) as ''senile osteoporosis,'' requires a systematic approach that entails both short- and long-term considerations, an understanding of the needs and circumstances of the individual patient, and a familiarity with the pathophysiology of osteoporosis and of the treatment available. The evidence of clinical trials is of limited value both because most of them have been conducted on normal postmenopausal women and because they take little or no account of the apparent risk factors operating in different patients. The treatment options described in this article are therefore based more on first principles and clinical experience than on clinical trials. Osteoporosis represents a deficiency of whole bone, summed up in Albright and Reifenstein's elegant phrase that there is ''too little bone in the bone.''(2) With the advent of bone densitometry, we now equate this definition with low bone mineral density (BMD), bearing in mind that it refers to organ rather than tissue density and takes no account of osteomalacia. A low bone density may be genetic in origin or arise during growth, remain present but silent during maturity, and become clinically apparent only when routine densitometry or fracture brings it to light. Alternatively, and perhaps more often, bone density may be perfectly normal during young adult life but be subject to accelerated loss during aging and so present as vertebral or hip fracture later.(75) In both scenarios, it is the low bone density that increases the fracture risk.