Spondyloarthritis (SpA), also known as spondyloarthropathy, is a collection of syndromes connected by genetic predisposition and clinical symptoms.

[2] Symptoms of spondyloarthritis include back pain, arthritis, and enthesitis, inflammation at bone-adhering ligaments, tendons, or joint capsules.

[8] In all subtypes of spondyloarthritis, inflammatory back pain and/or asymmetrical arthritis, mainly affecting the lower limbs, are the most common symptoms.

[10] Inflammatory back pain associated with ankylosing spondylitis usually starts slowly, has a dull feel to it, and spreads into the gluteal areas.

They suggest that HLA-B27's genesis may be autoinflammatory rather than autoimmune, as it plays a part in initiating innate immune responses instead of its traditional function of presenting antigens.

[2] According to the first hypothesis, HLA-B27 heavy chains devoid of β2 microglobulin can form disulphide-linked homodimers that are produced at the cell surface and can be recognized directly by KIR3DL2 killer immunoglobulin-like receptors, regardless of the associated peptide.

[19][20] According to the second hypothesis, the B pocket's Cys 67 residue causes HLA-B27 heavy-chain misfolding in the endoplasmic reticulum before assembling into complexes with peptide and β2 microglobulin.

[21][22] As a result, the unfolded protein response (UPR) modifies the immune cells' cytokine output and reactivity to various innate immunological stimuli.

According to the current criteria for ankylosing spondylitis, a person must exhibit clinical symptoms of inflammatory back pain and limited spinal mobility together with radiological sacroiliitis.

[5] Criteria for the early diagnosis of axial spondyloarthritis have been developed in light of the emergence of effective treatments.

[26] MRI imaging of the spine and entheses has made it possible to distinguish between inflammatory spinal lesions associated with ankylosing spondylitis and those unrelated to it earlier than is feasible with traditional radiography.

Aggressive psoriatic arthritis erosions can result in the articular surface of the proximal bone of the joint being destroyed and taking on the look of a "pencil in cup.

Normochromic normocytic anemia, increased C reactive protein, and erythrocyte sedimentation rate are frequently present nonspecific indicators.

[6][7] A person must meet two requirements to be considered for a diagnosis of axial spondyloarthritis: they must be under 45 years old and have experienced back pain of any kind for at least three months.

[34] Non-steroidal anti-inflammatory drugs (NSAIDs) should be administered first to those with active, primarily axial signs of spondyloarthritis.

If NSAID medication is contraindicated, does not work, or causes side effects, people are then treated with tumor necrosis factor (TNF) blockers.

Because there is insufficient evidence of treatment efficacy, those with axial spondyloarthritis who do not exhibit peripheral disease signs do not receive traditional disease-modifying antirheumatic drugs (DMARDs).

But if peripheral arthritis is present, those with spondyloarthritis should get treatment with conventional DMARDs before TNF-blocker medication and after the failure of NSAID therapy.

[35] Recreational exercise, whether performed in a group setting or alone, helps people with ankylosing spondylitis feel less stiff and in pain.

Back exercise also helps these people function better, but the effects vary depending on how long the disease has been present.

The best NSAID for treating those with ankylosing spondylitis appears to be tolmetin or indomethacin, although there is insufficient evidence to support this theory in rheumatologic practice.

These studies demonstrated that TNF-blocker therapy improves clinical symptoms, CRP levels, and MRI-detectable inflammation in the spine or sacroiliac joints.

[5] According to recent statistics, people with ankylosing spondylitis, particularly those who are older and have had the condition longer, may be more likely than population controls to be work handicapped or not engage in the labor market.

[31] People with ankylosing spondylitis experience up to 50% more sick leave episodes, an overall 8% loss of productivity, and a thrice higher rate of disability than the general population.

[48] Furthermore, increasing evidence indicates that cardiovascular illness puts those with ankylosing spondylitis at risk for early death.

[58][59][60] Reactive arthritis prevalence is unknown and likely varies with time based on endemic rates of the enteric (Shigella, Salmonella, Campylobacter) and sexually acquired (chlamydia) infections that cause it.