Should bisphosphonates be used for long‐term treatment of glucocorticoid‐induced osteoporosis?

Skeletal mass is a reflection of the relative activities of bone synthesizing osteoblasts and resorbing osteoclasts. When the activity of the latter supersedes that of the former, bone loss occurs, which if profound, eventuates into osteoporosis (1). While their clinical manifestations may be similar, the causes of osteoporosis are many, the most common attending menopause. Estrogen-deficiency typically prompts a high turnover form of osteoporosis in which both formation and resorption are accelerated but the relative activity of the osteoclast is greater than that of the osteoblast (2–3). Thus, suppression of the osteoclast using hormone replacement was standard of care for decades. With the realization that estrogens increase risk of breast cancer and cardiovascular complications in older women, bisphosphonates have become the most common treatment for post-menopausal osteoporosis. Given the absolute increase in osteoclast activity in estrogen-deficient osteoporosis, the effectiveness of bisphosphonates is not surprising. Alendronate, for example, maintains bone mass and reduces fracture risk of post-menopausal, osteoporotic women for as long as a decade with minimal complications in the great majority of patients (4).