Glucorticoid treatment is the most common cause of secondary osteoporosis in men and women.
One of the most important side effects of glucocorticoids is bone loss, which is biphasic, with a rapid reduction of bone mineral density (BMD) during the first year (6% to 12%), followed by a slower annual loss of about 3% for as long as glucocorticoids are administered. The relative risk of fracture increases more rapidly (up to 75% within the first 3 months), and fragility fractures often occur before a significant decline in BMD become evident, indicating that the use of corticosteroids does has an effect on fracture risk also independently of the effects on bone density.
In fact the detrimental actions of glucocorticoids on the skeleton are the direct consequences of their interaction with the bone cells, produce a decrease in osteoblastogenesis and an increase in osteoblasts apoptosis, leading to a continual decrease of cancellous osteoblasts, synthetic ability and bone formation. On the other hand, osteoclasts survival is improved by glucocorticoids, producing an increase of cancellous osteoclasts and bone resorption. A relevant effect on osteocytes has been also described, with increased osteocyte apoptosis and decreased canalicular circulation, leading to an alteration of bone quality.
General measures for fracture prevention in patients receiving glucocorticoids are excellent nutrition, appropriate calcium intake, physical exercise and avoid detrimental lifestyle factors (e.g., smoking cessation). Vitamin D supplementation should be always considered in order to attain and maintain an adequate vitamin D level (25-hydroxy-vitamin D >30 ng/ml), due to its implication for bone health and falls prevention. Finally, in patients at risk of falls, intervention to prevent falls by improving balance and strength should be implemented.
In RCTs of men and women receiving glucocorticoids, bisphosphonates and teriparatide showed significant beneficial effects in preserving and/or improving the bone mineral density. Some of these pharmacological agents also demonstrated to reduce the risk of vertebral fractures. Teriparatide represents the rational approach to glucocorticoid-induced osteoporosis, as it directly counteracts the detrimental effects of glucocorticoids on osteoblasts.
Although these data support the use of bisphosphonates and teriparatide in the management of glucocorticoid-induced osteoporosis their anti-fracture and long-term efficacy has not been fully clarified mainly due to the small samples studied and to the short-term follow-up of RCTs.
Disclosure of Interest None declared