abstract
- Corticosteroid-induced osteoporosis is a major cause of morbidity and is the leading secondary cause of osteoporosis today. Unfortunately, despite this knowledge, patients receiving corticosteroid therapy are often not offered any preventative treatment. Recent research has focused attention on the critical role the osteoblast has played in the pathophysiology of corticosteroid-induced osteoporosis. In addition to an initial increase in bone resorption, there is evidence that corticosteroids induce osteoblast and osteocyte apoptosis and as a result are important contributors to bone loss. Interesting work has suggested that the bisphosphonates and calcitonin may help to prevent osteoblast apoptosis from occurring. Large scale randomised controlled trials have also been completed with a variety of therapeutic agents. Of the many different therapies, it is now clear that the bisphosphonates have the greatest evidence to support their use. Increases in bone mineral density when compared with a control group, not only at the spine but also at the hip, have been demonstrated. These studies have shown clinically significant 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 preventative treatment.