Pathogenesis of axial spondyloarthritis as the treatment basis — realities and prospects

Pathogenesis of axial spondyloarthritis as the treatment basis — realities and prospects

I.Z. Gaydukova^1,2, V.I. Mazurov^1,2 

¹I.I. Mechnikov North-Western State Medical University, St. Petersburg

²St. Petersburg Clinical Rheumatology Hospital No. 25, St. Petersburg 

Spondyloarthritis (SpA) is a group of chronic inflammatory diseases in the spine, joints, and entheses characterized by common clinical, radiological, and genetic patterns. This work was aimed at analyzing modern ideas about the etiology and pathogenesis of axial spondyloarthritis (axSpA) and pathogenetically justified ways to improve its treatment. The presented work is based on a literary search in the medical citation systems: eLibrary, PubMed Medline for the period from 01.01.1948 to 01.11.2023. The review included only full-text articles in Russian or English that corresponded to the search query and the study purpose. The following search words were used: "axial spondyloarthritis", "ankylosing spondylitis", "Bekhterev’s disease", "genetically engineered drug", "biological treatment", "biological agents", "axSpA pathogenesis", "axSpA treatment", "drug treatment", "non-drug therapy" and their English analogs. The authors presented an analysis of existing treatment methods of axSpA. It also showed the benefits and drawbacks of the applied therapeutic techniques and the authors’ opinions on ways to optimize them. Promising methods of axSpA pathogenetic treatment were also described, as well as depletion of autoreactive TRBV9+ T cells, their potential place in the disease treatment, the supposed benefits and drawbacks, and possible options for the disease treatment in the future. The final article section was the presentation of the authors’ opinion on the potential pathogenetically justified treatment of axSpA.

Keywords: spondyloarthritis, axial spondyloarthritis, ankylosing spondylitis, Bekhterev’s disease, depletion of TRBV9+ T cells, macrophages, tumor necrosis factor-α, interleukin-17, interleukin-12, interleukin-23, interleukin-36.

For citation: Gaydukova I.Z., Mazurov V.I. Pathogenesis of axial spondyloarthritis as the treatment basis — realities and prospects. RMJ. 2023;7:6–14.