Erosion healing in rheumatoid arthritis after anakinra treatment.

Disruption of the cortical plate and erosive destruction of the subchondral bone are characteristic features of active rheumatoid arthritis (RA), potentially leading to progressive damage. Until recently, damage progression as documented on radiographs has been regarded as an irreversible process. However, several case reports now indicate that this process may be stopped or even reversed, leading to healing or repair of bone lesions. Under physiological conditions there is a balance between bone resorption by osteoclasts and bone formation by osteoblasts. In a state of active inflammation, bone resorption usually exceeds new bone formation, resulting in bone destruction. However, as soon as the inflammatory process has been stopped in an individual joint, osteoblastic activity may exceed bone resorption, leading to new bone formation and repair. This process is regulated by osteoprotegerin. 2 Because bone formation takes time, reparative changes can be expected to be clearly visible on radiographs only 6–12 months after distinct clinical improvement occurred. These may present as reappearance of the cortical plate or filling in of erosions. As clinical remission rarely occurs within the timeframe of clinical trials, and as patients experiencing remission outside clinical trials often do not visit their rheumatologist, x ray pictures showing healing phenomena have only occasionally been reported. Recent clinical trials with tumour necrosis factor α inhibitors indicate that clinical improvement and halting of radiographic progression occur earlier than with conventional disease modifying antirheumatic drugs (DMARDs). They have also shown a reduction in the radiographic scores in a considerable number of patients, probably indicating repair if measurement error can be excluded. As interleukin 1 (IL1) plays an important part in bone destruction, its inhibition might also result in a preponderance of repair over further destruction in eroded joints. We wish to demonstrate here an example of healing during treatment with the IL1 receptor antagonist (IL1Ra) anakinra in a patient with active RA who did not respond sufficiently to conventional DMARD treatment.