The treatment of osteoporosis in subjects older than 65, defined by Al
bright and Reifenstein(2) as ''senile osteoporosis,'' requires a syste
matic approach that entails both short- and long-term considerations,
an understanding of the needs and circumstances of the individual pati
ent, and a familiarity with the pathophysiology of osteoporosis and of
the treatment available. The evidence of clinical trials is of limite
d value both because most of them have been conducted on normal postme
nopausal women and because they take little or no account of the appar
ent risk factors operating in different patients. The treatment option
s described in this article are therefore based more on first principl
es and clinical experience than on clinical trials. Osteoporosis repre
sents a deficiency of whole bone, summed up in Albright and Reifenstei
n's elegant phrase that there is ''too little bone in the bone.''(2) W
ith the advent of bone densitometry, we now equate this definition wit
h low bone mineral density (BMD), bearing in mind that it refers to or
gan rather than tissue density and takes no account of osteomalacia. A
low bone density may be genetic in origin or arise during growth, rem
ain present but silent during maturity, and become clinically apparent
only when routine densitometry or fracture brings it to light. Altern
atively, and perhaps more often, bone density may be perfectly normal
during young adult life but be subject to accelerated loss during agin
g and so present as vertebral or hip fracture later.(75) In both scena
rios, it is the low bone density that increases the fracture risk.