Literature review of modern hypotheses of seronegative spondyloarthropathies

Abstract

Seronegative spodyloarthropathies (SpA) are a set of disorders marked by chronic inflammation of axial joints. These are portrayed by similar clinical syndromes, genetic susceptibility, and constitutional symptoms, with prominent tissue inflammation and joint destruction. Specific clinical types comprise of Ankylosing Spondylitis (AS), Reactive arthritis (RA) with Spondylitis, Psoriatic Arthritis (PA), Enteropathic Arthritis (EA) and Undifferentiated SpA. This review summarizes the proposed classification of major pathogenic mechanisms of seronegative SpA. It also considers the hypotheses of its etiology and pathogenesis in recent times. The current understanding of SpA pathogenesis is obscure. Subsequently, knowledge of early tissue, cellular, and molecular changes is incomplete. However, many researchers recognize the influence of the environment, immunologic processes, and genetics as factors of disease source and development. Majority of the focus is on HLA- B27 in predisposed individuals, immunologic processes like molecular mimicry and arthritogenic peptide hypothesis. Recent studies also highlight the pivotal roles of cytokines, tumor necrosis factor alpha (TNF-a), and angiogenesis in immune deregulation which results in disease morbidity. The most promising new direction has been the involvement of cytokines. By elucidating the central role of cytokines in etiology and pathogenesis of SpA, diagnostic and therapeutic significance is apparent.