The interconnection between obstructive sleep apnoea and spondyloarthritis: pathophysiology, clinical evidence, and future perspectives.

Obstructive sleep apnoea (OSA) and spondyloarthritis (SpA) are chronic inflammatory disorders associated with substantial cardiometabolic morbidity and impaired quality of life. Increasing evidence suggests that these conditions frequently coexist and may share overlapping pathogenic mechanisms involving intermittent hypoxia, oxidative stress, endothelial dysfunction, autonomic dysregulation, and activation of TNF-α and the IL-17/IL-23 axis. This narrative review summarises current evidence on the epidemiological, mechanistic, and clinical relationship between OSA and SpA, with emphasis on axial spondyloarthritis and psoriatic arthritis. Available studies indicate an increased prevalence of OSA in ankylosing spondylitis and psoriatic arthritis, although evidence remains heterogeneous and limited by small cohorts, cross-sectional designs, and inconsistent use of polysomnography. Structural spinal restriction, obesity, metabolic syndrome, chronic inflammation, and altered sleep architecture may all contribute to OSA susceptibility in SpA populations. Conversely, OSA-related intermittent hypoxia may amplify inflammatory pathways relevant to SpA pathobiology, potentially worsening fatigue, pain, disease activity, and cardiovascular risk. Preliminary evidence also suggests that continuous positive airway pressure and biologic therapies may favourably influence inflammatory and sleep-related outcomes, although disease-specific interventional evidence remains limited. Current evidence suggests a clinically relevant association between OSA and SpA, but the directionality and clinical significance of this interaction remain incompletely understood. Prospective longitudinal and mechanistic studies integrating objective sleep assessment, inflammatory biomarkers, and rheumatologic outcomes are needed to clarify causality and guide multidisciplinary management strategies.