⚕️ Educational information only — not medical advice. Read the full disclaimer

Ankylosing Spondylitis and Axial Spondyloarthritis: Causes, Signs and What Helps

Ankylosing spondylitis (AS) is a long-term inflammatory disease of the spine and the sacroiliac joints, where the spine meets the pelvis. Rheumatologists now treat it as one end of a wider condition called axial spondyloarthritis (axSpA), which also includes people whose X-rays still look normal. It usually starts before 40, often as back pain that is worse after rest and better with movement, and it is frequently mistaken for ordinary back trouble for years. This page explains what drives it (the HLA-B27 gene, the IL-23/IL-17 immune axis and a close link with the gut), how inflammatory back pain differs from mechanical back pain, why diagnosis takes so long, and why exercise sits alongside medicines at the centre of treatment. Every major claim is graded for evidence strength.

Important: This page is general educational information, not medical advice. Axial spondyloarthritis must be diagnosed and managed by a qualified clinician, usually a rheumatologist. Always consult a healthcare professional before changing your diet, supplements, exercise or medication, and never stop or change a prescribed medication without speaking to your doctor or pharmacist.

Key takeaways

  • "Ankylosing spondylitis" is now called radiographic axSpA. People with the same symptoms but normal X-rays have non-radiographic axSpA; early on, the two look clinically alike.12 Strong
  • HLA-B27 is the strongest genetic risk factor: about 60–90% of people with axSpA carry it, depending on the population. But only 1.3% of HLA-B27 carriers in the general population developed AS in a classic Dutch study.34 Strong
  • Blocking TNF or IL-17A works in axSpA; blocking IL-23 did not work in a trial in AS, even though it works in psoriasis and psoriatic arthritis.56 Strong
  • About 46% of people with spondyloarthritis in one cohort had microscopic gut inflammation on ileocolonoscopy without gut symptoms, and about 7% of people with AS have inflammatory bowel disease.78 Strong (link) Emerging (cause)
  • Diagnosis takes a pooled average of 6.7 years from first symptoms, and this delay has not improved over time.9 Strong
  • Smoking is linked to earlier onset, more disease activity and faster spinal damage.1011 Strong (association)
  • Exercise and physiotherapy are core treatment, not extras. In a randomised trial, 3 months of high-intensity exercise lowered disease activity.1213 Strong

Ankylosing spondylitis vs non-radiographic axSpA Strong

Axial spondyloarthritis is a chronic inflammatory disease that mainly affects the axial skeleton (the spine and sacroiliac joints). Its most common symptoms are chronic back pain and spinal stiffness, but it often affects other areas too: peripheral joints, the entheses (where tendons and ligaments attach to bone), the eyes, the skin and the gut.14 It belongs to the spondyloarthritis family, along with psoriatic arthritis, reactive arthritis and arthritis linked to inflammatory bowel disease.

The Assessment of SpondyloArthritis international Society (ASAS) uses the umbrella term axSpA for two groups.214

The two forms of axial spondyloarthritis
FeatureRadiographic axSpA (ankylosing spondylitis)Non-radiographic axSpA (nr-axSpA)
Defining featureDefinite sacroiliitis visible on a plain X-ray (modified New York criteria)No definite X-ray damage; inflammation may show on MRI, or HLA-B27 plus typical features
Sex ratioAbout 2 men : 1 womanAbout 1 : 1
Typical onsetUsually in the third decade of life (the 20s)
Symptoms and disease activityEarly on, very similar: same rates of HLA-B27, inflammatory back pain, arthritis, enthesitis and uveitis
Treatment approachLargely the same in current guidelines

The German Spondyloarthritis Inception Cohort compared 226 people with early nr-axSpA with 236 people with AS. The two groups did not differ in how often they were HLA-B27 positive, had inflammatory back pain, arthritis, enthesitis or uveitis, and they had similar disease activity. This suggests the two are stages or variants of the same disease. Male sex and a raised CRP were linked to X-ray damage.1 When ASAS developed its classification criteria, 60.2% of 649 people with unexplained chronic back pain that began before age 45 were diagnosed with axSpA, and 70% of those did not meet the X-ray criteria for AS.15

Not everyone with nr-axSpA progresses. In the same German cohort, 11.6% of people with nr-axSpA moved to definite AS on X-ray over two years; a raised CRP was a strong predictor.16 US guidelines make similar treatment recommendations for AS and nr-axSpA.17

6.7 yrspooled mean delay from first symptoms to diagnosis (64 studies)9
25.8%of people with AS have had uveitis (eye inflammation)8
46.2%of a SpA cohort had microscopic gut inflammation on ileocolonoscopy7
1.3%of HLA-B27-positive adults (45+) in a general population had AS4

How common is it? Strong

How common AS is depends on where you live, largely because the frequency of HLA-B27 varies between populations. A systematic review of 36 studies estimated mean AS prevalence at 23.8 per 10,000 people in Europe, 31.9 in North America, 16.7 in Asia, 10.2 in Latin America and 7.4 in Africa. That works out to an estimated 1.30–1.56 million cases in Europe and 4.63–4.98 million in Asia.18

In the United States, national survey data put AS prevalence at 0.52–0.55% and the wider axSpA group at 1.0–1.4% of adults. The same work found that chronic back pain affects 19.4% of US adults, and nearly a third of them have inflammatory features, which shows how much ordinary back pain doctors must sort through.19 A Berlin study of HLA-B27-tested blood donors estimated AS prevalence at 0.86% and spondyloarthritis overall at 1.9%, making it one of the more common rheumatic diseases in white populations.20

HLA-B27 and genetics Strong (association) Emerging (how it causes disease)

AS is one of the most strongly inherited common diseases: heritability has been estimated at more than 90%, and the strongest single genetic association is with HLA-B27.2 HLA-B27 is a version of an immune gene that helps show protein fragments (peptides) to T cells. A 2024 review by leading axSpA researchers summarises the key numbers:3

  • About 8% of people in central Europe carry HLA-B27, and the vast majority stay healthy. (In the US, 6.1% of adults carry it, 7.5% of non-Hispanic white adults.19)
  • Roughly 60–90% of people with axSpA worldwide are HLA-B27 positive, with the share varying by region. In a 24-country study of 2,269 tested people with axSpA, 1,753 (about 77%) were positive.21
  • HLA-B27 explains only about 30% of the genetic risk; more than 116 other risk variants have been identified.322

Most HLA-B27 carriers never get AS. In a Dutch population study of people aged 45 and over, only 1.3% of HLA-B27-positive individuals had AS. Among HLA-B27-positive first-degree relatives of people with AS, the figure was 21%, about 16 times higher. Family history matters on top of the gene.4 In the Berlin blood-donor study, 13.6% of HLA-B27-positive donors had some form of spondyloarthritis, compared with 0.7% of HLA-B27-negative donors.20

Mechanism: why HLA-B27? (still unsolved)

Fifty years after the link was found, nobody knows for certain how HLA-B27 causes disease.22 The leading idea is the "arthritogenic peptide" hypothesis: HLA-B27 may present certain microbial or self peptides that set off T cells against the body's own tissues.3 One clue is that the common HLA-B*27:05 subtype is linked to AS, while HLA-B*27:09, which differs by a single amino acid, is not.22 Some researchers place more emphasis on the innate immune system (γδ T cells, innate lymphoid cells, neutrophils and mast cells at the entheses and in the gut), and the current view is that AS has both autoinflammatory and autoimmune features.23

HLA-B27 status also shapes how the disease looks. In the 24-country study, HLA-B27-positive people were diagnosed younger (mean 31.6 vs 37.7 years) and were more often male. HLA-B27-negative people had a longer diagnostic delay and more psoriasis, inflammatory bowel disease, enthesitis and peripheral arthritis, but less uveitis.21

Testing tip: A positive HLA-B27 test does not mean you have axSpA, and a negative test does not rule it out. The test is useful when a doctor already suspects axSpA from your symptoms; testing people without symptoms is not useful for diagnosis. See autoimmune markers on the biomarkers page.

The IL-23/IL-17 axis Strong (TNF and IL-17) Emerging (where IL-23 fits)

Evidence from drug trials shows that two signalling proteins, TNF-α and interleukin-17, play an important part in axSpA.2 Animal research points to where the inflammation starts. In a 2012 Nature Medicine study, raising IL-23 levels in mice caused enthesitis and new bone formation at the entheses, the hallmarks of spondyloarthritis. The IL-23 acted on a previously unknown group of T cells that live in the enthesis and release IL-17 and IL-22.24

Mechanism: a surprising split between IL-23 and IL-17

IL-23 sits upstream of IL-17, so you might expect blocking either one to work. In AS, it does not:

  • Blocking IL-17A works. In the phase 3 MEASURE 1 trial of secukinumab, 61% of people on the 150 mg dose reached an ASAS20 response at week 16 compared with 29% on placebo, and the benefit was sustained through 52 weeks.5
  • Blocking IL-23 did not. In a phase 2 trial of risankizumab in 159 people with active AS, ASAS40 responses at week 12 were no better than placebo (15.0% at the top dose vs 17.5%). The authors concluded that IL-23 may not be an important driver of established AS.6

One interpretation is that, once the disease is established, IL-17 in the spine can be produced without needing IL-23. This is still being studied. In practice, it means drugs that work well for skin psoriasis and psoriatic arthritis (IL-23 blockers) are not used for axial disease.

The gut connection in axSpA is real and well documented:

  • Hidden gut inflammation. In a Belgian cohort, 65 people with axial and peripheral spondyloarthritis had ileocolonoscopy with biopsies. 46.2% had microscopic gut inflammation, and rates were similar in nr-axSpA and AS. In axial disease, gut inflammation was more likely in men, younger people and those with higher disease activity and more restricted spinal movement.7
  • IBD in AS. A meta-analysis found a pooled IBD (Crohn's disease or ulcerative colitis) prevalence of 6.8% in people with AS.8
  • AS in IBD. Going the other way, a meta-analysis of 71 studies found sacroiliitis in 10% and AS in 3% of people with IBD.25
  • Shared biology. SpA and IBD share many genetic risk factors, show similar changes in gut bacteria, and both respond to TNF blockers.26

What is not settled is the direction. The popular idea that inflammation starts in the gut and travels to the joints is attractive, but a 2020 Nature Reviews Rheumatology review points to contradictions. IL-17A blockers work in the joints but not the gut, and the IBD drug vedolizumab, which stops immune cells reaching the gut, can be followed by new or worsening SpA.26 In the secukinumab trials, new Crohn's disease occurred at 0.7 cases per 100 patient-years.5 That is why a rheumatologist will ask about bowel symptoms before choosing a drug.

The claim that a "leaky gut" causes AS, or that a gut-healing protocol can reverse it, has not been shown in trials Contested. Our leaky gut and arthritis page reviews the spondyloarthritis-IBD evidence in more depth, including what it does and does not support.

Inflammatory vs mechanical back pain Strong

Most back pain is mechanical: it comes from muscles, discs or joints and is worse with activity. The back pain of axSpA behaves in the opposite way. ASAS experts examined real patients and identified the five features that best predicted inflammatory back pain (IBP). In order of strength, they were: improvement with exercise (odds ratio 23.1), pain at night (20.4), insidious onset (12.7), age at onset under 40 (9.9) and no improvement with rest (7.7).27

Inflammatory back pain (ASAS expert criteria) compared with typical mechanical back pain
FeatureInflammatory back pain (axSpA)Typical mechanical back pain
Age at onsetUnder 40 (ASAS criterion)Any age; more common with increasing age
How it startsInsidious: creeps in over weeks to months (ASAS criterion)Often sudden, after lifting, twisting or strain
Effect of exerciseImproves with movement (ASAS criterion)Often worse with activity or certain movements
Effect of restNo improvement with rest (ASAS criterion)Usually eases with rest
Night painPain at night, often in the second half, improving on getting up (ASAS criterion)Night pain uncommon unless changing position
Morning stiffnessOften prolonged (30 minutes or more)Usually brief
DurationChronic (3 months or more)Often settles within weeks
Other cluesAlternating buttock pain, heel pain, uveitis, psoriasis, IBD, family history, good response to NSAIDsUsually none

Under the ASAS definition, inflammatory back pain is present when at least 4 of the 5 criteria are met. In the validation cohort this had a sensitivity of 79.6% and a specificity of 72.4%.27 That is useful, but it is not a diagnosis. Many people with chronic back pain have some inflammatory features without having axSpA.19 The rows without "ASAS criterion" are widely used clinical clues rather than part of the formal definition. For a wider comparison of stiffness patterns across arthritis types, see morning stiffness and how pain behaves.

How doctors diagnose and classify axSpA Strong

No single test confirms axSpA. A rheumatologist recognises a pattern from the history, examination, blood tests and imaging.14 The ASAS classification criteria (2009) apply to people with back pain for at least 3 months that began before age 45. They are met by either:15

  • the imaging arm: sacroiliitis on X-ray or MRI plus at least one SpA feature; or
  • the clinical arm: HLA-B27 plus at least two other SpA features.

SpA features include inflammatory back pain, arthritis, heel enthesitis, uveitis, dactylitis, psoriasis, Crohn's disease or colitis, a good response to NSAIDs, a family history of SpA, and a raised CRP. Overall, the criteria had a sensitivity of 82.9% and specificity of 84.4%, and the imaging arm alone had a specificity of 97.3%.15 These are classification criteria, built so that research studies enrol similar patients. They are valid for that purpose but are not meant to be used as a diagnostic checklist.14

Blood tests play a supporting role. CRP is raised in only some people with active axSpA, and a normal result does not rule it out. When CRP is raised, it predicts progression on X-ray.16 See inflammatory markers and CRP vs ESR. Unlike rheumatoid arthritis, axSpA is seronegative: rheumatoid factor and anti-CCP are usually negative.

The diagnostic delay Strong

A 2021 meta-analysis of 64 studies found a pooled mean delay of 6.7 years (95% CI 6.2–7.2) between first symptoms and an axSpA diagnosis, much longer than the 2.6 years for psoriatic arthritis. The delay has not improved over time. Longer delays were linked to lower education, younger age at symptom onset, and the absence of extra-articular features such as uveitis or psoriasis, which often prompt referral.9 The authors note that longer delays are associated with worse function and quality of life.

Why so long? Back pain is extremely common, the patient is often young and otherwise well, blood tests may be normal, and X-ray changes can take years to appear. That is why nr-axSpA was defined in the first place: so that people can be recognised and treated before damage shows on X-ray.12

Practical tip: if you are under 45 and have had back pain for more than 3 months, note whether it is worse after rest, better with movement, and wakes you in the second half of the night. Also note any heel pain, eye inflammation, psoriasis, bowel symptoms or family history. Bring this to your doctor and ask whether a rheumatology referral is appropriate. Our flare tracker can help you record it.

Imaging: X-ray and MRI Strong

X-ray. Plain X-rays show the results of inflammation: erosion, sclerosis and eventually fusion of the sacroiliac joints, and later bony bridges (syndesmophytes) between vertebrae. Definite sacroiliitis on X-ray is what separates radiographic axSpA (AS) from nr-axSpA. These changes can take years to appear, and only a minority of people progress over two years.162

MRI. MRI can show active inflammation (bone marrow oedema) before X-ray damage appears, and is the most important imaging method for early axSpA.2 But MRI findings need careful interpretation. In a Dutch study, 23.4% of healthy volunteers with no history of back pain had an MRI that met the ASAS definition of sacroiliitis, as did 12.5% of frequent runners and 4 of 7 women with postpartum back pain. Deep, extensive bone marrow oedema, however, was found almost only in people with axSpA.28

Why this matters: a "positive" sacroiliac MRI on its own does not mean axSpA, especially after childbirth or in athletes. The result needs to be read by an experienced radiologist or rheumatologist alongside your symptoms and other findings.

US guidelines advise against routine repeat spine X-rays just to monitor progress, and suggest MRI may help when disease activity is unclear.17

Beyond the spine: eyes, skin and gut Strong

A meta-analysis of 156 studies estimated how often people with AS have the three classic "extra-articular" conditions (now often called extramusculoskeletal manifestations):8

Extra-articular manifestations in ankylosing spondylitis (pooled prevalence)
ConditionPooled prevalence in ASWhat to look out forEffect on treatment
Acute anterior uveitis25.8%; more common with longer disease durationA painful red eye, light sensitivity, blurred vision, usually in one eye at a timeTNF monoclonal antibodies preferred for recurrent uveitis12
Psoriasis9.3%Scaly skin plaques, scalp or nail changesIL-17 inhibitors considered for significant psoriasis12
Inflammatory bowel disease6.8%Persistent diarrhoea, blood in stool, abdominal pain, weight lossTNF monoclonal antibodies preferred12

Prevalence varied widely between studies and regions.8 Enthesitis (especially heel pain), peripheral arthritis and dactylitis are also common.14 The presence of these features often shortens the time to diagnosis.9

Smoking and progression Strong (association)

Smoking is one of the few modifiable factors with consistent evidence in axSpA:

  • In 210 people with early axSpA followed for two years in the German inception cohort, cigarette smoking independently predicted spinal X-ray progression (OR 2.75). So did syndesmophytes already present at baseline (OR 6.29) and raised ESR or CRP.10
  • In 647 people with early inflammatory back pain in the French DESIR cohort, smokers had earlier symptom onset, higher disease activity, worse function, more MRI inflammation and structural damage in the sacroiliac joints and spine, and poorer quality of life.11

These are observational studies, so they cannot prove smoking causes faster damage. But the findings are consistent, and guidelines encourage people with axSpA to stop smoking. Smoking also adds to cardiovascular and lung risk.

Bottom line: if you smoke, stopping is one of the most useful things you can do for your spine as well as your general health. Ask your doctor or pharmacist about stop-smoking support, including medicines that can help. See lifestyle and toxins for more.

Exercise and physiotherapy: core treatment Strong

In axSpA, movement is treatment. The ASAS-EULAR 2022 recommendations put non-pharmacological management first in the treatment pathway, alongside NSAIDs: patient education, regular exercise and physiotherapy.12 A 2021 review describes NSAIDs as first-line drug treatment "besides physiotherapy".14

  • High-intensity exercise reduced disease activity. In a multicentre randomised trial of 100 people with axSpA, 3 months of high-intensity cardio and strength training reduced disease activity compared with usual care (ASDAS −0.6; BASDAI −1.2 on a 0–10 scale). It also improved inflammation markers, physical function and cardiovascular health. 97 of 100 participants completed the trial. The authors concluded this "debunks concerns" that hard exercise worsens axSpA.13
  • Supervised beats unsupervised, and both beat nothing. A Cochrane review of 11 trials (763 participants) found that home or supervised exercise programmes were better than no intervention, that supervised group physiotherapy was better than home exercise, and that a spa-exercise programme followed by group physiotherapy was better than group physiotherapy alone. Much of the evidence was of low to moderate quality.29
Putting it into practice: a physiotherapist experienced in axSpA can build a programme that combines spinal mobility and posture work, stretching, strengthening and aerobic fitness, adapted to your current disease activity. Daily movement matters because stiffness builds with rest. Our physical therapy and pain rule sections give general guidance. If your spine is already fused or you have osteoporosis, ask your team which activities are safe, because a stiff spine fractures more easily.

Treatment overview Strong

This section describes how international guidelines organise treatment, so that you can have an informed conversation with your rheumatologist. It is not a recommendation for any individual.

Key principles from ASAS-EULAR 2022 and ACR/SAA/SPARTAN 2019 (summary)
TopicSummary
Non-drug careEducation, regular exercise and physiotherapy, and stopping smoking, are part of management from the start12
NSAIDsFirst-choice drug treatment1214
Glucocorticoids and conventional DMARDsLong-term glucocorticoids discouraged. Conventional DMARDs (such as sulfasalazine or methotrexate) discouraged for purely axial disease. ACR 2019: sulfasalazine only for persistent peripheral arthritis when TNF inhibitors are not an option1217
When to escalateBiologics or JAK inhibitors if disease stays active (ASDAS ≥2.1) after at least two NSAIDs, and there is raised CRP, MRI sacroiliac inflammation or X-ray sacroiliitis12
First advanced therapyASAS-EULAR: current practice is a TNF inhibitor or IL-17 inhibitor. ACR 2019: TNF inhibitors recommended over IL-17 inhibitors as the first biologic1217
Uveitis or IBDTNF monoclonal antibodies preferred12
Significant psoriasisIL-17 inhibitors considered12
IL-23 inhibitorsNot used for axial disease; a trial in AS showed no benefit over placebo6
If treatment failsRe-check the diagnosis and look for other causes of pain; if axSpA is confirmed and active, switch to another advanced therapy12
Sustained remissionASAS-EULAR: tapering (rather than stopping) a biologic can be considered. ACR 2019: tapering not routinely recommended. This is a decision for you and your rheumatologist1217
Surgery and fracturesHip replacement for severe hip damage; be alert to spinal fracture after even minor trauma12
Do not stop or change axSpA medicines on your own. NSAIDs carry stomach, kidney and cardiovascular risks that need to be weighed with your doctor. Biologics and JAK inhibitors need screening and care around infections, vaccines, pregnancy and surgery. Stopping them can lead to flares. Discuss side effects, cost or a wish to try a different approach with your rheumatologist, doctor or pharmacist. More general information is on the medications page.
Dietary & supplement note: No specific diet or supplement has been shown in good-quality trials to change the course of axSpA. A balanced, Mediterranean-style eating pattern supports general and cardiovascular health. Statements about foods and dietary supplements on this site have not been evaluated by the U.S. Food and Drug Administration (FDA) and are not intended to diagnose, treat, cure, or prevent any disease.

Red flags: when to see a doctor Strong

Seek urgent, same-day medical care if you have:
  • a painful red eye, light sensitivity or blurred vision. This may be uveitis, which needs prompt eye assessment to protect your sight;
  • new back pain with leg weakness, numbness in the saddle area, or loss of bladder or bowel control;
  • sudden new or different spinal pain after a fall or even a minor injury, especially if you have long-standing AS or a fused spine (possible fracture);
  • fever, chills or signs of infection while taking a biologic or JAK inhibitor;
  • chest pain or breathlessness;
  • back pain with fever, unexplained weight loss, or a history of cancer.

Book a prompt (non-emergency) appointment, and ask whether a rheumatology referral is appropriate, if you have:

  • back or buttock pain for more than 3 months that began before age 45, especially if it is worse after rest, better with exercise, or wakes you at night;
  • chronic back pain plus uveitis, psoriasis, inflammatory bowel disease, heel pain, a swollen finger or toe, or a family history of spondyloarthritis;
  • back pain that gets much better within a day or two of taking an NSAID and returns when you stop;
  • persistent diarrhoea, blood in the stool or abdominal pain alongside back symptoms.

Frequently asked questions

What causes ankylosing spondylitis?

The exact cause is unknown. Ankylosing spondylitis is strongly inherited, with heritability estimated at more than 90%, and the HLA-B27 gene variant is the biggest single genetic risk factor. The immune signals TNF and IL-17 drive the inflammation, which often starts where tendons and ligaments attach to bone. The gut is closely linked: nearly half of people with spondyloarthritis in one study had hidden gut inflammation. Environmental triggers are less well understood, but smoking is linked to earlier onset and faster spinal damage. This is educational information, not medical advice.

If I am HLA-B27 positive, will I get ankylosing spondylitis?

Most likely not. Around 6 to 8% of people of European ancestry carry HLA-B27, and the vast majority stay healthy. In a Dutch population study, only 1.3% of HLA-B27-positive adults aged 45 or over had ankylosing spondylitis, compared with 21% of HLA-B27-positive relatives of people with the disease. HLA-B27 testing is useful only when a doctor already suspects axial spondyloarthritis from symptoms.

What is the difference between ankylosing spondylitis and non-radiographic axial spondyloarthritis?

Both are forms of axial spondyloarthritis. Ankylosing spondylitis, also called radiographic axial spondyloarthritis, means definite damage to the sacroiliac joints is visible on plain X-ray. In non-radiographic axial spondyloarthritis the X-ray is not yet clearly abnormal, though MRI may show inflammation. Early on, symptoms and disease activity are very similar, and current guidelines treat the two in much the same way. About 12% of people with the non-radiographic form progressed to visible X-ray changes over two years in one large cohort.

How is inflammatory back pain different from ordinary back pain?

Inflammatory back pain usually starts before age 40, comes on gradually, improves with exercise, does not improve with rest, and causes pain at night that eases on getting up. Experts from the Assessment of SpondyloArthritis international Society define it as having at least four of these five features. Ordinary mechanical back pain often starts suddenly after strain, is worse with activity and eases with rest. Inflammatory back pain is a reason to see a doctor, but it does not by itself mean you have axial spondyloarthritis.

Does exercise help ankylosing spondylitis?

Yes. Exercise and physiotherapy are core treatment in the ASAS-EULAR 2022 recommendations, alongside NSAIDs. In a randomised trial of 100 people with axial spondyloarthritis, three months of high-intensity cardio and strength training reduced disease activity, inflammation and cardiovascular risk markers compared with usual care. A Cochrane review found supervised group physiotherapy works better than home exercise alone. Ask your rheumatologist or a physiotherapist to tailor a programme, especially if your spine is fused or you have osteoporosis.

References

  1. Rudwaleit M, Haibel H, Baraliakos X, et al. The early disease stage in axial spondylarthritis: results from the German Spondyloarthritis Inception Cohort. Arthritis Rheum. 2009;60(3):717–727. PubMed 19248087
  2. Sieper J, Poddubnyy D. Axial spondyloarthritis. Lancet. 2017;390(10089):73–84. PubMed 28110981
  3. Braun J, Rudwaleit M, Sieper J. The role of HLA-B27 in the pathogenesis and diagnosis of axial spondyloarthritis: 50 years after discovery of the strong genetic association [article in German]. Z Rheumatol. 2024;83(2):125–133. PubMed 38112753
  4. van der Linden SM, Valkenburg HA, de Jongh BM, Cats A. The risk of developing ankylosing spondylitis in HLA-B27 positive individuals: a comparison of relatives of spondylitis patients with the general population. Arthritis Rheum. 1984;27(3):241–249. PubMed 6608352
  5. Baeten D, Sieper J, Braun J, et al. Secukinumab, an interleukin-17A inhibitor, in ankylosing spondylitis. N Engl J Med. 2015;373(26):2534–2548. PubMed 26699169
  6. Baeten D, Østergaard M, Wei JC, et al. Risankizumab, an IL-23 inhibitor, for ankylosing spondylitis: results of a randomised, double-blind, placebo-controlled, proof-of-concept, dose-finding phase 2 study. Ann Rheum Dis. 2018;77(9):1295–1302. PubMed 29945918
  7. Van Praet L, Van den Bosch FE, Jacques P, et al. Microscopic gut inflammation in axial spondyloarthritis: a multiparametric predictive model. Ann Rheum Dis. 2013;72(3):414–417. PubMed 23139267
  8. Stolwijk C, van Tubergen A, Castillo-Ortiz JD, Boonen A. Prevalence of extra-articular manifestations in patients with ankylosing spondylitis: a systematic review and meta-analysis. Ann Rheum Dis. 2015;74(1):65–73. PubMed 23999006
  9. Zhao SS, Pittam B, Harrison NL, et al. Diagnostic delay in axial spondyloarthritis: a systematic review and meta-analysis. Rheumatology (Oxford). 2021;60(4):1620–1628. PubMed 33428758
  10. Poddubnyy D, Haibel H, Listing J, et al. Baseline radiographic damage, elevated acute-phase reactant levels, and cigarette smoking status predict spinal radiographic progression in early axial spondylarthritis. Arthritis Rheum. 2012;64(5):1388–1398. PubMed 22127957
  11. Chung HY, Machado P, van der Heijde D, D'Agostino MA, Dougados M. Smokers in early axial spondyloarthritis have earlier disease onset, more disease activity, inflammation and damage, and poorer function and health-related quality of life: results from the DESIR cohort. Ann Rheum Dis. 2012;71(6):809–816. PubMed 21989541
  12. Ramiro S, Nikiphorou E, Sepriano A, et al. ASAS-EULAR recommendations for the management of axial spondyloarthritis: 2022 update. Ann Rheum Dis. 2023;82(1):19–34. PubMed 36270658
  13. Sveaas SH, Bilberg A, Berg IJ, et al. High intensity exercise for 3 months reduces disease activity in axial spondyloarthritis (axSpA): a multicentre randomised trial of 100 patients. Br J Sports Med. 2020;54(5):292–297. PubMed 30745314
  14. Navarro-Compán V, Sepriano A, El-Zorkany B, van der Heijde D. Axial spondyloarthritis. Ann Rheum Dis. 2021;80(12):1511–1521. PubMed 34615639
  15. Rudwaleit M, van der Heijde D, Landewé R, et al. The development of Assessment of SpondyloArthritis international Society classification criteria for axial spondyloarthritis (part II): validation and final selection. Ann Rheum Dis. 2009;68(6):777–783. PubMed 19297344
  16. Poddubnyy D, Rudwaleit M, Haibel H, et al. Rates and predictors of radiographic sacroiliitis progression over 2 years in patients with axial spondyloarthritis. Ann Rheum Dis. 2011;70(8):1369–1374. PubMed 21622969
  17. Ward MM, Deodhar A, Gensler LS, et al. 2019 update of the American College of Rheumatology/Spondylitis Association of America/Spondyloarthritis Research and Treatment Network recommendations for the treatment of ankylosing spondylitis and nonradiographic axial spondyloarthritis. Arthritis Rheumatol. 2019;71(10):1599–1613. PubMed 31436036
  18. Dean LE, Jones GT, MacDonald AG, et al. Global prevalence of ankylosing spondylitis. Rheumatology (Oxford). 2014;53(4):650–657. PubMed 24324212
  19. Reveille JD, Weisman MH. The epidemiology of back pain, axial spondyloarthritis and HLA-B27 in the United States. Am J Med Sci. 2013;345(6):431–436. PubMed 23841117
  20. Braun J, Bollow M, Remlinger G, et al. Prevalence of spondylarthropathies in HLA-B27 positive and negative blood donors. Arthritis Rheum. 1998;41(1):58–67. PubMed 9433870
  21. Chaudhary H, López-Medina C, Khan MA, Dougados M, Magrey M. Clinical profile and treatment utilisation based on HLA-B*27 status in axial spondyloarthritis: results from ASAS-PerSpA study. RMD Open. 2023;9(3):e003179. PubMed 37491128
  22. Khan MA. HLA-B*27 and ankylosing spondylitis: 50 years of insights and discoveries. Curr Rheumatol Rep. 2023;25(12):327–340. PubMed 37950822
  23. Mauro D, Thomas R, Guggino G, et al. Ankylosing spondylitis: an autoimmune or autoinflammatory disease? Nat Rev Rheumatol. 2021;17(7):387–404. PubMed 34113018
  24. Sherlock JP, Joyce-Shaikh B, Turner SP, et al. IL-23 induces spondyloarthropathy by acting on ROR-γt+ CD3+CD4−CD8− entheseal resident T cells. Nat Med. 2012;18(7):1069–1076. PubMed 22772566
  25. Karreman MC, Luime JJ, Hazes JMW, Weel AEAM. The prevalence and incidence of axial and peripheral spondyloarthritis in inflammatory bowel disease: a systematic review and meta-analysis. J Crohns Colitis. 2017;11(5):631–642. PubMed 28453761
  26. Gracey E, Vereecke L, McGovern D, et al. Revisiting the gut-joint axis: links between gut inflammation and spondyloarthritis. Nat Rev Rheumatol. 2020;16(8):415–433. PubMed 32661321
  27. Sieper J, van der Heijde D, Landewé R, et al. New criteria for inflammatory back pain in patients with chronic back pain: a real patient exercise by experts from the Assessment of SpondyloArthritis international Society (ASAS). Ann Rheum Dis. 2009;68(6):784–788. PubMed 19147614
  28. de Winter J, de Hooge M, van de Sande M, et al. Magnetic resonance imaging of the sacroiliac joints indicating sacroiliitis according to the Assessment of SpondyloArthritis international Society definition in healthy individuals, runners, and women with postpartum back pain. Arthritis Rheumatol. 2018;70(7):1042–1048. PubMed 29513924
  29. Dagfinrud H, Kvien TK, Hagen KB. Physiotherapy interventions for ankylosing spondylitis. Cochrane Database Syst Rev. 2008;(1):CD002822. PubMed 18254008