Spondyloarthritis: aspects of pathogenesis and diagnostics

Abstract

Spondyloarthritis (SpA) has extremely high social importance due to patient’s risk of early disability and a persistent decline in the quality of life. The last decade has brought important knowledge on its genetic mechanisms and pathophysiological aspects, as well as diagnosis and treatment. Axial spondyloarthritis (axSpA) is characterized by a pathological tissue response to immune and mechanical triggers, predominant lesion of the axial skeleton (spine, sacroiliac joints). It is divided into ankylosing spondylitis (AS) and non-radiological axSpA. Mechanical stress is proven to affect specific localization of inflammation and tissue damage in SpA. Areas of inflammation and erosion are limited to those having increased susceptibility and unique microanatomy. It is shown that a number of genes located outside the main histocompatibility complex significantly affect susceptibility to AS. A study of genes and polymorphisms not related to HLA-B27 revealed different pathogenesis mechanisms in various ethnic groups and formed a new understanding of AS pathogenesis and treatment. A family history of AS or anterior uveitis is useful to detect axSpA, as it is associated with the carrier of genetic marker HLA-B27. Researchers are strongly focused on studying AS patients» autoantibodies, where antibodies to CD74 are of the greatest diagnostic value. An imbalanced microbiome can trigger SpA development. Approximately 50 % of all SpA patients have microscopic signs of intestinal inflammation. The development and use of highly sensitive imaging methods in the future will lead to improved approaches for axSpA classification and more precise disease prognosis and therapeutic decisions. 18-fluorodeoxyglucose positron emission tomography is a sensitive method to determine syndesmophytes and sacroiliac joints in axSpA patients.