Intra-articular (IA) corticosteroids are recommended in several guidelines for the treatment of patients with knee osteoarthritis (OA).1 ,2 They are also widely used: a recent survey of rheumatologists in the United States suggesting that over 95% use them at least ‘sometimes’ and 53% ‘frequently’.3 Before considering mechanisms of action of IA corticsteroids we should first consider the evidence that they are effective in OA.

A recent systematic review ⁴ summarised evidence from five controlled studies of IA corticosteroid in patients with OA knee. Using a quality rating system (originally designed to assess methodology and reporting of NSAID studies), critical analysis showed that none of the studies achieved a score of more than 3 out of a possible 8 for design. It would not be unreasonable, therefore, to conclude that our knowledge of the efficacy of corticosteroid in OA is based on inadequate data. Table 1 summarises the five studies, and two more recent studies. Generally, they show a positive effect but one that is short lived and confounded by a powerful response to placebo (in all cases an equal volume of saline). In one study,5 for example, both placebo and corticosteroid groups showed significant decreases in pain at one week, lasting for the duration of the study (eight weeks). A more recent double blind, placebo controlled, crossover study ⁶found a significantly greater decrease in pain with corticosteroid than placebo at three weeks. The inability to detect an effect of corticosteroids beyond three weeks may reflect insensitivity of pain as an outcome measure, rather than a lack of corticosteroid effect.

There is, therefore, some discordance between the modest and short lived benefit over placebo …