Ankylosing Spondylitis: Axial Spondyloarthritis
Ankylosing spondylitis (AS) is a chronic inflammatory arthritis primarily affecting the spine and sacroiliac joints, causing progressive stiffness and potential fusion of spinal vertebrae. Like other spondyloarthropathies, AS has strong genetic associations (HLA-B27) but environmental triggers modulate disease expression and severity.
PFAS and Entheseal Inflammation
Entheses—where tendons and ligaments insert onto bone—are the primary sites of inflammation in AS. PFAS compounds promote IL-17 production by Th17 cells and innate lymphoid cells, inflammatory mediators that drive entheseal inflammation. Elevated IL-17 levels in both PFAS-exposed populations and AS patients suggest shared inflammatory pathways.
Gut Microbiome and AS Connection
AS has strong associations with gut dysbiosis—particularly alterations in Prevotella and Klebsiella species—through gut-joint immune axis interactions. PFAS-induced gut microbiome disruption may amplify the gut dysbiosis contributing to AS pathogenesis, creating a mechanistic pathway from environmental PFAS exposure to exacerbation of genetically primed spondyloarthritis.
Rheumatological Practice
Rheumatologists managing AS patients in PFAS-contaminated communities should assess environmental exposure history as part of disease burden evaluation. Microbiome-supportive dietary interventions and PFAS exposure reduction may complement standard biologic and NSAID therapies for AS, particularly in patients with active gut inflammatory disease.