Corticosteroid-induced osteoporosis is a major cause of morbidity and is th
e leading secondary cause of osteoporosis today. Unfortunately, despite thi
s knowledge, patients receiving corticosteroid therapy are often not offere
d any preventative treatment. Recent research has focused attention on the
critical role the osteoblast has played in the pathophysiology of corticost
eroid-induced osteoporosis. In addition to an initial increase in bone reso
rption, there is evidence that corticosteroids induce osteoblast and osteoc
yte apoptosis and as a result are important contributors to bone loss. Inte
resting work has suggested that the bisphosphonates and calcitonin may help
to prevent osteoblast apoptosis from occurring. Large scale randomised con
trolled trials have also been completed with a variety of therapeutic agent
s. Of the many different therapies, it is now clear that the bisphosphonate
s have the greatest evidence to support their use. Increases in bone minera
l density when compared with a control group, not only at the spine but als
o at the hip, have been demonstrated. These studies have shown clinically s
ignificant reductions in vertebral fracture rates seen for the most part in
postmenopausal women. Other therapies may well be effective, as evidenced
by maintenance of bone mass in the spine; however, maintenance of bone mass
in the hip and reductions in fracture rate have yet to be demonstrated for
many of these therapies, Given our current knowledge and the evidence that
is outlined in this review, it is hoped that patients who require therapy
with corticosteroids for more than 3 months will be offered appropriate pre
ventative treatment.