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Introduction: The use of low-dose glucocorticoids for the treatment of rheumatoid arthritis (RA) has been debated for many years. Glucocorticoids were first introduced as RA treatment in 1950 and Hench and Kendall received the Nobel Prize in Medicine for their efforts in discovering this novel treatment [1]. Over the subsequent years, adverse effects of glucocorticoids began to restrict their use to lower doses. Indeed, newer data on their apparent disease modifying properties have further rejuvenated their use and it is now estimated that at least 40% of RA patients in the United States receive glucocorticoids at some point during their disease course [2]. Despite their widespread use, the one glucocorticoid adverse event that has continued to generate the greatest discussion is osteoporosis. An observational study suggested that patients taking a mean of only 8.6 mg daily of prednisone had a 34% chance of experiencing a fracture after 5 years of follow-up [3]. Data of this type have reasonable generalizability, but suffer from selection biases inherent in therapeutic observational studies. The randomized, controlled trials (RCTs) recently have suggested mixed, but generally only modest effects of low-dose glucocorticoids on the bone [4–7]. Two recent studies have examined the use of low-dose prednisolone in combination with disease-modifying antirheumatic drugs (DMARDs) in early RA during a 2-year period. Both of these RCTs also have included data on the adverse effects of glucocorticoids—in particular, their effects on bone.