REACTIVE ARTHRITIS: CONTEMPORARY INSIGHTS INTO PATHOGENESIS, DIAGNOSTIC CHALLENGES, AND EVOLVING THERAPEUTIC STRATEGIES

Reactive arthritis (ReA) is an inflammatory condition that occurs in the spondyloarthritis spectrum, triggered by infections in the gastrointestinal, genitourinary, or, less commonly, respiratory systems. Enteric pathogens including Campylobacter jejuni, Salmonella spp., Shigella spp., and Yersinia spp., along with urogenital Chlamydia trachomatis, continue to be the most frequently identified triggers. Recent developments in molecular diagnostics show that microbial DNA, RNA, and antigen remnants can remain in synovial tissues, especially in Chlamydia-related ReA, challenging the conventional belief that post-infectious arthritis is sterile. Host genetic susceptibility, particularly HLA-B27, significantly influences the pathogenesis of ReA by affecting antigen presentation, cytokine dynamics, and the survival of intracellular pathogens. Immunological imbalances characterized by changes in TNF-α, IFN γ, IL-10, and TGF-β activity distinguish acute from chronic disease patterns and influence diverse clinical outcomes. Diagnostic evaluation still depends on clinical criteria along with PCR-based identification of microbial elements, although no singular conclusive test is available. Present management is still symptom-focused, utilizing NSAIDs as primary treatment, additional intra-articular corticosteroids for peripheral joint issues, and DMARDs for persistent or resistant situations. Although antibiotics have minimal effectiveness for post-enteric ReA, extended combination treatments may hold therapeutic potential in diseases related to Chlamydia. Even with advancements in grasping microbial persistence and immune responses, indicators of chronicity and effective long-term treatment approaches are still unclear. Ongoing studies are essential to enhance diagnostic instruments, discover biomarkers of disease advancement, and formulate targeted treatments that can change the persistent trajectory of ReA.