The spondyloarthropathies (SpA) are a group of interrelated inflammatory conditions unified by enthesitis as the primary pathology, axial skeletal involvement, asymmetrical peripheral arthritis, and a strong HLA-B27 association. The family includes axial spondyloarthritis (axSpA - ankylosing spondylitis [AS] and non-radiographic axSpA), psoriatic arthritis (PsA), reactive arthritis (ReA), and enteropathic arthritis. axSpA affects around 0.5-1% of UK adults, and historical diagnostic delay of 8-10 years from symptom onset is unacceptable. NICE NG65 promotes earlier recognition and referral. The cardinal message: inflammatory back pain in a young person (under 45) should prompt consideration of axSpA. Do not exclude SpA solely because HLA-B27 is negative, inflammatory markers are normal, or X-rays appear normal - all can be normal in active early disease.
The enthesis - the tendon, ligament, or capsule insertion into bone - is the primary target. The 'enthesis organ' concept (Benjamin and McGonagle) extends this functional unit to adjacent fibrocartilage, bone, and periosteum, explaining bony changes around insertions and the functional enthesitis of dactylitis (inflammation of the digital flexor tendon sheath and surrounding structures).
This is the fundamental distinction from rheumatoid arthritis: SpA is enthesitis-driven, while RA is synovitis-driven. SpA also produces pathological new bone formation - syndesmophytes in the spine, enthesophytes peripherally - alongside erosion, in contrast to the purely destructive process of RA. IL-23 and IL-17 are the dominant cytokines, alongside TNF-alpha. Bridging syndesmophytes can fuse vertebrae into the 'bamboo spine' of advanced AS.\n\nHLA-B27 is a class I MHC allele present in around 8% of White UK populations (varies by ethnicity), in over 90% of AS, around 70% of axSpA overall, ~60% of ReA, ~50% of enteropathic SpA, and ~20% of PsA. It supports the diagnosis in the right clinical context but is not diagnostic; most carriers never develop SpA, and negativity does not exclude disease.
A gut-joint axis is implicated: subclinical gut inflammation is found in up to 60% of SpA patients, and IBD is both a cause and an association. The sacroiliac joints are synovial anteriorly and syndesmotic posteriorly and are the earliest and most consistent site of axial involvement.
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