[Pain in rheumatic diseases : What can biologics and JAK inhibitors offer?]

Persistent pain despite adequate inflammation control poses a big challenge in many rheumatic diseases for patients as well as physicians. The focus of drug development over the past years was on anti-inflammatory therapies. Enormous progress has been made and several treatment options have been added. It has been observed that pain triggered by inflammation can be effectively treated by inflammation control; however, the chronic pain component remains a problem, is little studied and specific treatment options are missing. Pain is influenced by inflammatory mediators, such as cytokines, which act on peripheral nociceptors and lead to peripheral sensitization. If inflammation continues, this can potentially lead to central sensitization and chronification of pain via immigration of immune cells and/or local activation of e.g. microglia. This leads to increasing autonomization and uncoupling of pain from the actual inflammatory process. The present review deals with the question if bDMARD or tsDMARD also show benefits concerning pain processes in addition to the profound inhibitory effects on inflammation. There are preclinical data that show an influence on sensitization following the use of cytokine inhibitors. On the other hand, so far clinical data show that bDMARDs as well as tsDMARDs consistently rapidly and reliably reduce nociceptive inflammatory pain across disease entities. An effect especially on the process of central sensitization and therefore on chronification of pain cannot be finally evaluated based on the currently available data.