Ankylosing spondylitis affects roughly 0.5 percent of American adults — about one person in 200. Estimates from US population data put it at 0.52 to 0.55 percent, within a wider published range of 0.2 to 0.5 percent depending on how cases are counted. The broader disease family it belongs to, axial spondyloarthritis, affects 1.0 to 1.4 percent of adults — closer to one person in 80.
According to PubMed, those figures come from analyses of the National Health and Nutrition Examination Survey, the same nationally representative survey used to track blood pressure and diabetes in the United States (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):431-6. DOI; and Reveille JD. Epidemiology of spondyloarthritis in North America. Am J Med Sci. 2011;341(4):284-6. DOI).
Not in the way most people mean by “rare.” A condition affecting one adult in 200 is not a medical curiosity — for comparison, the same national survey data put chronic back pain in US adults at 19.4 percent, and roughly a third of that is inflammatory in character. The disease is sitting inside a very large and very ordinary-looking population.
What is genuinely uncommon is being diagnosed with it promptly. That is a different problem, and it is the one that actually harms patients.
According to PubMed, a systematic review and meta-analysis of 64 studies found the pooled mean delay between symptom onset and diagnosis in axial spondyloarthritis to be 6.7 years (95% CI 6.2 to 7.2). The same analysis found a pooled delay of 2.6 years in psoriatic arthritis — the same specialty, the same clinics, less than half the wait — and found that the delay had not improved over time when the studies were stratified by year of publication (Zhao SS, et al. Rheumatology (Oxford). 2021;60(4):1620-1628. DOI).
The delay is not distributed evenly. According to PubMed, a 2024 systematic review and meta-analysis found diagnostic delay averaged 1.48 years longer in women than in men (95% CI 0.83 to 2.14), and reported that the classification criteria used to identify the disease were originally studied largely in male populations (Bandinelli F, et al. J Pers Med. 2024;14(1):91. DOI).
So the accurate answer to “is it rare” is: the disease is not rare, the diagnosis is late, and the delay is longer if you are a woman. A patient in their forties who was told at 25 that they had ordinary mechanical back pain is not an unusual case. They are the typical case.
Because the presenting complaint — back pain in a young adult — is one of the most common complaints in medicine, and almost none of it is inflammatory.
According to PubMed, chronic back pain in the US adult population runs around 19.4 percent, with nearly a third of that meeting criteria for inflammatory back pain (Reveille and Weisman 2013, DOI). An earlier NHANES analysis put inflammatory back pain at 0.8 percent of adults aged 25 to 49 overall, and at 6.7 percent among those who had experienced a back pain episode lasting two weeks or more (Dillon CF, Hirsch R. Am J Med Sci. 2011;341(4):281-3. DOI).
The signal is there. It is buried in a very large amount of noise, and it is only findable if someone asks the specific questions that separate inflammatory from mechanical back pain.
This is the part worth reading closely, because the pattern is nearly the reverse of ordinary mechanical back pain.
Beyond the spine, features that raise the probability substantially: a red painful eye that has recurred (acute anterior uveitis), psoriasis, inflammatory bowel disease, heel pain at the Achilles insertion or under the heel, a swollen finger or toe, and a family history of any of these. Fatigue that is out of proportion to the pain is common and is a genuine feature of the disease rather than a personality trait.
HLA-B27 is a genetic marker strongly associated with ankylosing spondylitis, and it is the source of a great deal of confusion in both directions.
According to PubMed, the age-adjusted prevalence of HLA-B27 in the United States is 6.1 percent (95% CI 4.6 to 8.2) — roughly one American in 16. By group, it was 7.5 percent in non-Hispanic whites, 4.6 percent in Mexican Americans, and 3.5 percent across all other US racial and ethnic groups combined (Reveille JD, Hirsch R, Dillon CF, Carroll MD, Weisman MH. Arthritis Rheum. 2012;64(5):1407-11. DOI).
Set that against a disease prevalence of about 0.5 percent and the arithmetic is unforgiving in both directions. The overwhelming majority of people who carry HLA-B27 will never develop ankylosing spondylitis. A positive test in someone without the clinical picture means very little. And a negative test does not exclude the disease, because a meaningful minority of patients with axial spondyloarthritis are B27-negative — this is one of the reasons the diagnosis is missed more often in women.
The test is one input into a diagnosis that is made by a rheumatologist, combining history, examination, inflammatory markers, and imaging of the sacroiliac joints. It is not a screening test for back pain, and it should not be ordered as one.
Diagnosis and disease-modifying treatment belong with rheumatology. We want to be plain about that rather than blur it. Ankylosing spondylitis is an immune-mediated disease, and the medications that alter its course — anti-inflammatories used at anti-inflammatory doses, and biologic agents targeting TNF or IL-17 — are prescribed and monitored by rheumatologists. If your history matches the pattern above and you have never been evaluated by one, that referral is the single most useful thing that can happen for you, and we will help make it happen.
Where an interventional pain practice does have a role:
Surgery is not part of the treatment plan for ankylosing spondylitis itself. The disease is driven by immune-mediated inflammation and new bone formation. No operation modifies that process, and there is no procedure that treats the underlying condition.
There are two situations in a patient with AS where surgery is squarely the right conversation, and neither is a treatment for the disease:
Dr. Gurpreet Singh Padda, MD, MBA, MHP is a licensed physician and surgeon with surgical privileges, and this practice performs minimally invasive spinal procedures. For ankylosing spondylitis specifically, the sequence that helps patients is early rheumatology involvement, sustained exercise, and interventional treatment of the mechanical pain generators that accumulate alongside the disease — not an operation aimed at the disease.
Back pain that started before 45, is worse after rest, better with movement, and wakes you in the second half of the night is a specific pattern with a specific meaning, and it deserves to be named rather than managed indefinitely. We see patients from across St. Louis, Clayton, St. Charles and the Illinois Metro East. Call (314) 481-5000 or request an evaluation.
About 0.5 percent of US adults, or one person in roughly 200, based on national survey data — published estimates run from 0.2 to 0.55 percent depending on case definition. The wider disease family, axial spondyloarthritis, affects 1.0 to 1.4 percent, closer to one person in 80. Those are population figures for adults, not lifetime risk figures. Read more: The scale of autoimmune disease.
Not by the usual meaning of rare. Around one adult in 200 has it, and it sits inside a population where chronic back pain runs at 19.4 percent — which is exactly why it hides. What is genuinely unusual is a prompt diagnosis: the pooled average delay from symptom onset to diagnosis is 6.7 years, and it is longer in women. Read more: When autoimmunity is the source of pain.
Because the presenting symptom is back pain in a young adult, which is extremely common and almost never inflammatory. Distinguishing the two takes specific questions — age at onset, whether rest makes it worse, morning stiffness beyond 30 minutes, whether it wakes you in the second half of the night — that are not routinely asked. The pooled delay is 6.7 years, and it has not improved over time. Read more: When the scan does not match the pain.
Probably not. About 6.1 percent of Americans carry HLA-B27, while ankylosing spondylitis affects about 0.5 percent — so the overwhelming majority of carriers never develop it. The marker raises probability in someone whose history already fits; it does not make a diagnosis on its own, and a negative result does not rule the disease out. Read more: Autoimmune risk and what modifies it.
Diagnosis and disease-modifying treatment belong with rheumatology, and we will say so plainly rather than blur the line. What an interventional pain practice contributes is recognizing the pattern in someone who has not been evaluated, and treating the mechanical pain generators that accumulate alongside the disease in patients whose inflammation is already controlled but who still hurt. Read more: Pain is a signal, not the disease.
Because disease activity and pain are correlated but not identical. A meta-analysis of 14 studies found anti-TNF therapy improved disease activity and function markedly while showing no significant effect on radiographic progression — the inflammation and the structural consequences are separable. Persistent focal pain in a treated patient is often a distinct, testable mechanical generator rather than a sign the medication has failed. Read more: Why pain treatments stop working.
No — and in this disease that instinct is particularly costly. Inflammatory back pain characteristically improves with movement and worsens with rest, and sustained exercise is a core part of long-term management rather than an optional extra. What changes is how you exercise, not whether. Read more: Walking as treatment for low back pain.
Treat it as an emergency and go to an emergency department. A long-standing fused spine breaks like a long bone, these fractures are frequently unstable, they are easy to miss on plain X-rays, and they can involve the spinal cord. New, sharply changed or unusually severe pain after even a minor fall is not something to schedule. Read more: Sudden back pain and vertebral fracture.
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