Molecular mechanisms of the development of the phenomena of peripheral and central sensitization in rheumatoid arthritis

Modern tactics for the treatment of rheumatoid arthritis is aimed at achieving remission or low activity of the disease, the maximum elimination of the manifestations of the disease and the restoration of physical and social activity of patients. At the same time, despite the wide range of the most modern pathogenetic agents, a good therapeutic response can’t be obtained in all cases. A difficult problem is the so-called rheumatoid arthritis RA (difficult to treat), in which two or more sequentially prescribed genetically engineered biological drugs or JAK inhibitors are ineffective. One of the important factors negatively affecting the outcome of RA treatment are functional disorders of the nociceptive system, such as peripheral and central sensitization. These phenomena, associated with persistent activation of nociceptive neurons and the development of nociplastic changes, are caused by systemic autoimmune inflammation and the influence of various cytokines and chemokines on the neuronal membrane. This review considers the molecular biological aspects of the formation of peripheral and central sensitization in RA, with a separate analysis of the pathogenetic role of individual interleukins.