Anti-Inflammatories vs Biologics for Ankylosing Spondylitis: How the Choice Is Made

He was thirty-four, standing at the kitchen counter at six in the morning because sitting hurt more than standing, reading the leaflet that came with his new prescription. Three lines in, he stopped: the rheumatologist had said “we’ll start with an anti-inflammatory and see,” and then, almost in passing, “if that isn’t enough there are stronger options.” What he wanted to know, and hadn’t quite asked, was why the stronger option wasn’t first.

That question sits at the heart of nearly every conversation about biologics vs NSAIDs for ankylosing spondylitis. On one side, a familiar class of tablets many people have taken for a sprained ankle. On the other, engineered proteins delivered by injection that target a single molecule in the immune system. They sound like different leagues. In practice they are two steps on the same staircase, and the order is not about cost-cutting or caution for its own sake.

This explainer walks through how each works, who is usually offered which, what the first months typically look like, and where the honest gaps in the evidence still are.

Biologics vs NSAIDs for ankylosing spondylitis: what the choice is really about

Ankylosing spondylitis (AS) is a long-term inflammatory arthritis that mainly affects the spine and the sacroiliac joints, the two joints where the base of the spine meets the pelvis. It belongs to a wider family that rheumatologists call axial spondyloarthritis. When damage is visible on a plain X-ray the label is AS or “radiographic” disease; when inflammation shows only on MRI, it is called non-radiographic axial spondyloarthritis. The treatment logic is broadly the same for both, which is why you will see the terms used side by side.

The debate over anti-inflammatories versus biologics is not a contest between a weak drug and a strong one. It is a question of matching the intensity of treatment to the intensity of disease, then adjusting as the picture changes. Every mainstream guideline, including the NHS pathway that follows NICE recommendations, describes a stepped approach: exercise and physiotherapy for everyone, NSAIDs as the first medicine, and biologics when inflammation stays active despite those measures.

Three things drive the decision at each step. First, how active the disease is, measured by symptoms, blood markers of inflammation such as CRP, and imaging. Second, how much the current treatment is achieving, judged at planned review points rather than on a bad morning. Third, the rest of the person: stomach and kidney health, heart risk, infection history, plans for pregnancy, and what they can realistically fit into their life.

The reader in the kitchen was not being fobbed off with the lesser option. He was being placed on the step the evidence says most people should start on, with a clear plan for what happens if that step is not enough.

How NSAIDs for ankylosing spondylitis actually work

NSAIDs, non-steroidal anti-inflammatory drugs, block enzymes called cyclo-oxygenases (COX-1 and COX-2) that the body uses to make prostaglandins. Prostaglandins are short-lived chemical messengers that amplify pain, swelling and the stiffness you feel after lying still. Reduce them and the inflamed joint quietens down. The effect is broad rather than targeted: the same mechanism that eases a stiff sacroiliac joint also dampens the protective lining of the stomach and alters blood flow through the kidneys, which is where most NSAID side effects come from.

In ankylosing spondylitis specifically, NSAIDs do something that many other painkillers do not. The inflammatory back pain of AS characteristically improves with movement and worsens with rest, and it tends to respond to anti-inflammatory medicine in a way that mechanical back pain often does not. Rheumatologists sometimes use that response as one supporting clue in diagnosis, alongside imaging and the HLA-B27 blood test, a genetic marker carried by most people with AS but also by many people who never develop it (NIH NIAMS).

Several NSAIDs are used, and the choice between them is individual. There is no single “best anti-inflammatory for ankylosing spondylitis” established by evidence; comparative reviews find the class works broadly similarly, with differences in duration of action and side-effect profile rather than in raw effectiveness. That is why the NHS pathway describes trying one NSAID and, if it does not help or is not tolerated, switching to another before concluding the class has failed.

What NSAIDs do not do is reprogram the immune response driving the disease. They turn down the volume on inflammation’s consequences. Whether that also slows the bony changes of AS is a separate question, addressed later.

How do biologics work for ankylosing spondylitis?

A biologic is a medicine made from living cells rather than synthesised in a chemical plant, usually an antibody or receptor protein engineered to bind one specific target. Because these are large proteins, they cannot be swallowed; the stomach would digest them. They are given by injection under the skin or by infusion into a vein.

Two biologic classes are established for ankylosing spondylitis. TNF inhibitors block tumour necrosis factor alpha, a signalling protein that sits near the top of the inflammatory cascade in AS and drives recruitment of immune cells into the joints and the spine’s ligament attachments. IL-17 inhibitors block interleukin-17, a different messenger produced by a subset of immune cells that appears to be particularly active at the sites where tendons and ligaments meet bone, the classic location of AS inflammation (Mayo Clinic).

The practical difference from an NSAID is precision. Instead of lowering prostaglandins everywhere, a biologic removes one lever the immune system is pulling. The upside is that inflammation can settle more completely, including inflammation that never fully responded to NSAIDs. The downside is that TNF and IL-17 also have day jobs in fighting infection, so blocking them raises infection risk, and screening for latent tuberculosis is standard before starting a TNF inhibitor (Mayo Clinic).

A third, newer group deserves a mention even though it is not a biologic in the strict sense. JAK inhibitors are small-molecule tablets that interrupt the signalling machinery inside immune cells. They are listed by Mayo Clinic among options for people who have not responded to earlier treatment, and they carry their own safety considerations that a prescriber will discuss. Which class suits which person is the subject of a later section; the point here is that all of them act on the disease process itself, not just its symptoms.

Why anti-inflammatories are usually tried first

It would be easy to assume the step-up order is about money. Biologics are far more complex to manufacture and the systems that pay for them do weigh that, but the clinical case for starting with NSAIDs stands on its own.

Many people with ankylosing spondylitis get meaningful relief from an NSAID alone, combined with a structured exercise program. For them, escalating to an injectable immune-modulating medicine would add risk without adding benefit. The only way to find out who those people are is to try the simpler treatment properly. “Properly” matters: the NHS describes trying an NSAID at an effective anti-inflammatory level, switching to a second if the first does not help, and judging the result over weeks rather than days.

The safety calculation also runs in NSAIDs’ favour at the start. Their risks, stomach irritation and bleeding, kidney strain, raised blood pressure and a modest increase in cardiovascular events with long-term use, are well characterised and can be monitored, and they are reversible if the medicine is stopped (MedlinePlus). Biologic risks centre on infection, including reactivation of dormant TB, and on rarer immune effects, and they require screening blood tests and ongoing vigilance.

There is a diagnostic benefit too. A clear response to an NSAID reinforces that the back pain is inflammatory. A poor response, in someone whose imaging and blood tests show active inflammation, is exactly the information a rheumatologist needs to justify moving up a step.

None of this means anyone should stay on a treatment that is not working. The step-up model has built-in exits. What it avoids is exposing people who would have done well on a tablet to a more powerful medicine they never needed.

When to start biologics for ankylosing spondylitis: who qualifies and who is asked to wait

The clearest candidates for a biologic are people whose disease remains active despite an adequate NSAID trial. In the NHS, which applies NICE guidance, that usually means having tried at least two different NSAIDs without adequate control, alongside evidence of ongoing inflammation. Rheumatologists typically document activity with a validated questionnaire called the BASDAI (Bath Ankylosing Spondylitis Disease Activity Index), which scores fatigue, spinal pain, joint pain, tenderness and morning stiffness, together with a spinal pain rating, blood tests and imaging.

Beyond that core group, a few situations tend to push the decision towards earlier biologic use, always at the treating team’s discretion. Someone who cannot take NSAIDs at all, because of kidney disease, a history of stomach bleeding, inflammatory bowel disease or heart failure, has effectively already failed the first step and may be considered sooner. Recurrent anterior uveitis, inflammation of the front of the eye that affects a substantial minority of people with AS, is another factor, because some biologic classes also reduce eye flares (Cleveland Clinic).

People often asked to wait include those whose symptoms are troubling but whose objective markers are quiet, those who have not yet had a fair NSAID trial, and those with an active or untreated infection, which must be dealt with first. Pregnancy planning does not rule out biologics but changes which agents are considered and when, and needs an unhurried conversation.

Waiting is not the same as being ignored. During a period of watchful management the team should still be reviewing exercise, sleep, pain and function, and should have set a date to look again. If that review date is missing, it is reasonable to ask for one.

TNF inhibitors vs IL-17 inhibitors: how a rheumatologist picks a biologic class

People frequently ask which is the best biologic for ankylosing spondylitis. The honest answer is that head-to-head evidence does not crown a winner for the spine itself; both TNF and IL-17 inhibitors are recommended by mainstream guidance, and the choice is made on the features around the spine.

The features that matter most are the ones that travel with AS. Inflammatory bowel disease, Crohn’s or ulcerative colitis, coexists in a meaningful share of people with axial spondyloarthritis. TNF inhibitors are established treatments for those bowel conditions, whereas IL-17 inhibitors have been associated with worsening of bowel inflammation and are generally avoided when it is present (Mayo Clinic). Psoriasis pulls the other way; IL-17 blockade is highly active against skin disease, so a person with prominent plaques may be steered towards it. Recurrent uveitis has generally favoured certain TNF inhibitors.

History also counts. If a first biologic has stopped working, a rheumatologist may switch within the same class or across classes depending on why it failed, whether the body has formed antibodies against it, and what the disease is doing elsewhere. Some TNF inhibitors are given by fortnightly injection, others by periodic infusion; that practical difference is part of the discussion.

JAK inhibitors, the tablet-form option, are typically positioned for people who have not responded to a biologic, and they carry specific cautions around cardiovascular and clotting risk in older adults and those with existing heart disease that a prescriber will weigh.

So the question “which is best?” becomes “best for someone with this combination of spine, gut, skin and eye involvement, this history and these preferences.” That is a decision for the prescribing rheumatologist, and it is a decision that can be revisited.

Anti-inflammatories and biologics side by side

A table cannot capture an individual conversation, but it can make the structure of the decision visible. The rows below summarise how the two approaches differ on the questions people actually raise in clinic. Every entry describes typical patterns in mainstream guidance, not a guarantee for any one person.

Question	NSAIDs	Biologics (TNF or IL-17 inhibitors)
How is it taken?	Tablet or capsule, sometimes gel	Injection under the skin or intravenous infusion
What does it target?	Prostaglandin production throughout the body	One specific immune signalling protein
Usual place in the pathway	First medicine, with exercise	After an adequate trial of two NSAIDs, or when NSAIDs cannot be used
Main safety concerns	Stomach bleeding, kidney strain, blood pressure, cardiovascular risk with long use	Infection, latent TB reactivation, injection-site reactions, class-specific effects on bowel or skin
Screening before starting	Kidney function, blood pressure, bleeding history	TB test, hepatitis screening, infection history, vaccination review
When response is judged	Over weeks, then switch if inadequate	Formal review around 12 weeks (NHS)
Effect on X-ray progression	Uncertain; evidence mixed	Uncertain; some long-term data suggest slowing, not proven to halt
Extra-spinal benefit	Peripheral joint pain	May also treat uveitis, psoriasis or bowel disease depending on class

Two rows deserve emphasis. The screening row explains why a biologic cannot be started the same day it is discussed; the tests protect against the specific harms of switching off part of the immune system. The progression row explains why neither treatment is sold as a way to stop the disease in its tracks, a point expanded below.

What the first weeks and months usually look like

Starting an NSAID is undramatic. Most people notice a change in morning stiffness and night pain relatively quickly, and the rheumatologist or GP will want to know, after a few weeks, whether the change is enough. If it is not, the next move is usually a different NSAID rather than an immediate jump to a biologic, because individuals genuinely vary in which one suits them (NHS). During this phase the team will also check blood pressure and kidney function and ask about indigestion or black stools.

Starting a biologic has more moving parts. Before the first injection there is a screening period: a blood or skin test for latent tuberculosis, checks for hepatitis B and C, a review of vaccination status because live vaccines are generally avoided once treatment begins, and a baseline of blood counts and liver tests. Someone with a positive TB test may need a course of preventive treatment before the biologic can start.

Then comes teaching. Most subcutaneous biologics are self-injected at home after a nurse demonstrates the technique, and the first dose is often given in clinic. Infused biologics mean a scheduled visit to a day unit. Injection-site redness is common and usually settles.

The response to a biologic is judged formally rather than by feel. The NHS pathway describes reassessment at around 12 weeks, using the BASDAI score and a spinal pain rating, and continuing only if a defined improvement is documented. Some people feel a shift within the first few weeks; others need most of that window. If the first biologic does not meet the bar, the conversation turns to a switch, not to giving up.

Do biologics stop progression of ankylosing spondylitis?

This is the question with the least satisfying answer, and it deserves a straight one. “Progression” in AS means structural change on X-ray: new bone forming at the edges of vertebrae, eventually bridging them, and the sacroiliac joints fusing. It is distinct from inflammation, which is what causes pain, and the two do not always move together.

Biologics are very good at controlling inflammation; that is why they are recommended. Whether they also slow new bone formation is less settled. Early trials of TNF inhibitors, which ran over roughly two years, did not show a clear difference in X-ray progression compared with what would have been expected without treatment, which surprised many researchers. Longer observational follow-up has since suggested that people on sustained TNF blockade over several years may accumulate less new bone, particularly when treatment begins earlier, but observational data cannot fully separate the effect of the drug from differences in who gets prescribed it. Evidence on IL-17 inhibitors and structural change is still maturing.

NSAIDs have their own version of this uncertainty. One line of research suggested that taking an NSAID continuously rather than only when needed might slow radiographic change; a subsequent trial designed to test that idea did not confirm it. Mainstream sources now describe the effect of NSAIDs on progression as unproven (Johns Hopkins).

What is reasonably well established is indirect: persistent inflammation is associated with later bony change, and both drug classes reduce inflammation. So the honest framing is that good disease control is the best current strategy for protecting the spine, not that any medicine has been shown to stop fusion. Anyone promising otherwise is ahead of the evidence.

Where steroids, exercise and the rest of the plan fit in

Because the headline choice is between anti-inflammatories and biologics, the other components of AS care can get lost. They should not, and some of them change how the drug decision plays out.

Exercise is the one treatment recommended for everyone at every stage. A physiotherapist-designed program of stretching, posture work and aerobic activity is described by the NHS as a core part of management, not an optional extra, because mobility in the spine and chest wall is what long-term function depends on. A person whose NSAID is taking the edge off pain enough to exercise properly may do better than one on a more powerful drug who has stopped moving.

Corticosteroids play a smaller role than many people expect. Long-term oral steroids are not recommended for the spinal disease of AS because the side effects outweigh the benefit; a steroid injection into a single inflamed peripheral joint or the sacroiliac joint can be useful for a localised flare (Mayo Clinic). Steroid eye drops are the standard first response to a uveitis flare, which is why prompt eye assessment matters.

Conventional disease-modifying tablets used in rheumatoid arthritis, such as sulfasalazine or methotrexate, have not shown benefit for the spine in AS. Sulfasalazine is sometimes used when peripheral joints are the main problem (NHS). If a prescriber suggests one, the reason will be joints outside the spine, not the back itself.

Smoking is linked to more active disease and faster structural change in axial spondyloarthritis, and stopping is one of the few levers entirely in a person’s own hands (Cleveland Clinic). Sleep, weight, and cardiovascular risk management round out a plan that the drug choice sits within, rather than replaces.

What people often get wrong about biologics vs NSAIDs for ankylosing spondylitis

“Being started on an anti-inflammatory means my disease isn’t taken seriously.” The reverse is closer to the truth. An NSAID trial is the first move in every guideline-based pathway, and it generates the evidence a rheumatologist needs to escalate. Skipping it would be the unusual choice.

“There is a best biologic, and I should insist on it.” No trial has established one agent as superior for spinal disease across the board. The right class depends on gut, skin and eye involvement, prior treatments and practical factors. A person for whom an IL-17 inhibitor is ideal may be a poor candidate for the same drug if they develop bowel inflammation.

“Biologics stop the spine from fusing.” They control inflammation; their effect on bone formation is suggested by long-term observational data but not proven. Treat that claim as hopeful, not settled.

“NSAIDs are just painkillers I can take as I please.” Used regularly at anti-inflammatory levels, they carry real stomach, kidney and cardiovascular risks that need monitoring (MedlinePlus). They also interact with common medicines, including some blood pressure tablets and blood thinners.

“The 6 As are a checklist I should test myself against.” The “6 As” is a memory aid used in medical training for features that can accompany AS: anterior uveitis, aortic valve involvement, apical lung fibrosis, amyloidosis, Achilles tendon inflammation, and autoimmune bowel disease. Most people with AS will experience few or none of them. Its purpose is to remind clinicians to ask, not to prompt self-diagnosis.

“If a biologic works, I can stop everything else.” Exercise remains central regardless, and some people continue an NSAID alongside a biologic for residual symptoms under their team’s guidance.

Weighing the safety trade-offs honestly

Neither option is risk-free, and the risks differ in kind, which is why the comparison is not a simple ranking.

NSAID harms are mostly dose- and duration-related and fall on organs that bear the brunt of reduced prostaglandins. Stomach and upper-gut irritation is the most familiar, ranging from indigestion to ulcers and bleeding; prescribers often add a stomach-protecting medicine for people at higher risk. The kidneys can be affected, particularly in older adults, in dehydration, or alongside certain blood pressure medicines. Blood pressure may rise. Long-term regular use is associated with a modest increase in heart attack and stroke risk, a concern that weighs more heavily in someone who already has cardiovascular disease (MedlinePlus). People with a history of ulcers, kidney disease, heart failure or aspirin-sensitive asthma may be steered away from the class altogether.

Biologic harms follow from blocking a piece of immune defence. Infections are more common and can be more serious; respiratory and skin infections are the most frequent. Latent tuberculosis can reactivate under TNF blockade, which is why screening is universal before starting (Mayo Clinic). IL-17 inhibitors are associated with fungal infections such as thrush and, as noted, with worsening or new inflammatory bowel disease. Injection-site reactions are common and usually minor. Rarer concerns, including effects on the nervous system or blood counts, are monitored through periodic blood tests and reporting of new symptoms.

The trade-off, then, is between a class whose risks are well understood, monitorable and reversible on stopping, and a class that is more targeted and often more effective for persistent inflammation but demands infection vigilance for as long as it is used. Where a given person sits on that balance is precisely what the prescribing conversation is for.

Questions to ask your care team

A good consultation about anti-inflammatories and biologics is a two-way exchange. These questions tend to surface the information that matters most, and none of them is out of place.

• How active do you consider my disease right now, and what measures are you basing that on: symptoms, blood tests, MRI or X-ray?
• Have I had what you would count as an adequate trial of anti-inflammatories, and if not, what would make it adequate?
• Are there reasons in my medical history, kidneys, stomach, heart, bowel or eyes, that push you towards or away from a particular class?
• If we start a biologic, which class are you leaning towards and why, given my skin, gut and eye history?
• What screening tests will I need first, and how long does that stage usually take?
• How and when will we judge whether the treatment is working, and what happens if it is not?
• What symptoms should make me contact you between appointments, and how do I reach the team quickly?
• Which vaccinations should I have before starting, and which should I avoid afterwards?
• Does this treatment affect plans for pregnancy or fatherhood, and how far ahead should we discuss that?
• Should I continue my anti-inflammatory alongside a biologic, or stop it, and who decides?
• Who is coordinating my exercise and physiotherapy, and how does that fit with the medicine plan?

It helps to write the answers down or to bring someone who can. If a question cannot be answered on the day, asking when it will be is entirely reasonable. The decision about which step you are on, and when to move, rests with the treating rheumatologist, but it should be a decision you understand and have shaped.

When to call your doctor

Most people on either treatment go long stretches without needing unscheduled contact. Some situations should not wait for the next routine appointment.

Seek urgent medical care, the same day or through emergency services, for: vomiting blood or passing black, tar-like stools, which can signal gut bleeding on an NSAID; sudden severe chest pain or breathlessness; a high fever with shaking chills, especially on a biologic; a red, painful eye with blurred vision or light sensitivity, which may be uveitis and needs same-day eye assessment; new weakness, numbness or loss of bladder or bowel control; or a sudden, severe change in back or neck pain after a fall or minor injury, because a stiffened spine fractures more easily (Cleveland Clinic).

Contact your rheumatology team promptly, within a day or two, for: a cough, sore throat or infection that is not settling, or any infection needing antibiotics while on a biologic; a persistent cough, night sweats or unexplained weight loss, which prompt a TB check; new or worsening diarrhoea, abdominal pain or blood in the stool, particularly on an IL-17 inhibitor; a spreading rash or significant reaction at an injection site; swelling of the ankles, a marked rise in blood pressure, or reduced urine output on an NSAID; a planned surgery, dental procedure or live vaccine; or a possible pregnancy.

Finally, call if the treatment simply is not working. A flare that lasts, sleep broken by pain most nights, or a return of morning stiffness after a period of control are all reasons to bring forward a review rather than wait it out. The pathway has next steps built into it, but only if the team knows you have reached the edge of the current one.

Frequently asked questions

What is the best biologic for treating ankylosing spondylitis?

No single biologic has been shown to be best for everyone with ankylosing spondylitis. TNF inhibitors and IL-17 inhibitors are both recommended by mainstream guidance for spinal disease. Rheumatologists choose between them based on what else is present: TNF inhibitors are favoured when inflammatory bowel disease or recurrent uveitis coexists, while IL-17 inhibitors are attractive when psoriasis is prominent. Prior treatment history and practical factors also matter.

What is the best anti-inflammatory for ankylosing spondylitis?

Comparative reviews have not identified one NSAID as clearly superior for ankylosing spondylitis; the class performs broadly similarly, with differences in how long each lasts and in side-effect profile. Individuals do respond differently, which is why guidance describes trying a second NSAID if the first does not help. The choice depends on stomach, kidney and heart history and is made with the prescribing clinician.

What are the 6 As of ankylosing spondylitis?

The 6 As is a teaching mnemonic for features that can accompany ankylosing spondylitis: anterior uveitis (eye inflammation), aortic valve involvement, apical lung fibrosis, amyloidosis, Achilles tendon inflammation and autoimmune bowel disease. It exists to remind clinicians to ask about these areas. Most people with AS will experience few or none of them, so it should not be used as a self-diagnosis checklist.

Do biologics stop progression of ankylosing spondylitis?

Biologics reliably reduce inflammation, but they have not been proven to stop the new bone formation that fuses the spine. Early trials of TNF inhibitors showed no clear difference in X-ray progression over two years. Longer observational studies suggest people on sustained treatment may accumulate less new bone, but such studies cannot fully separate drug effect from patient differences. Good inflammation control remains the best current strategy.

When should you start biologics for ankylosing spondylitis?

Biologics are usually considered when ankylosing spondylitis remains active despite an adequate trial of at least two different NSAIDs, or when NSAIDs cannot be used because of kidney, stomach, bowel or heart problems. Rheumatologists document activity with symptom scores such as the BASDAI, blood markers and imaging before escalating. Active infection must be treated first, and the timing decision rests with the treating team.

How do biologics work for ankylosing spondylitis?

Biologics are engineered proteins that bind and block a single inflammatory messenger. TNF inhibitors neutralise tumour necrosis factor, which sits high in the inflammatory cascade; IL-17 inhibitors block interleukin-17, which is active where tendons and ligaments attach to bone. Because they are large proteins, they must be injected or infused rather than swallowed. Blocking these signals also lowers infection defences, which is why screening and monitoring are needed.

Can you take NSAIDs and biologics together for ankylosing spondylitis?

Some people continue an NSAID alongside a biologic, particularly for residual pain or peripheral joint symptoms, and others are able to reduce or stop it once inflammation is controlled. Whether to combine them depends on how well the biologic is working, on stomach, kidney and cardiovascular risk, and on other medicines being taken. That decision should be made with the rheumatology team rather than independently.

How long do biologics take to work for ankylosing spondylitis?

Response to a biologic is judged formally rather than by feel. The NHS pathway describes reassessing at around 12 weeks using the BASDAI score and a spinal pain rating, and continuing treatment only if a defined improvement is documented. Some people notice a change within the first few weeks; others need most of that window. If the first agent falls short, switching to another is the usual next step.

What tests are needed before starting a biologic for AS?

Before a biologic starts, screening typically includes a blood or skin test for latent tuberculosis, checks for hepatitis B and C, baseline blood counts and liver tests, and a review of vaccination history because live vaccines are generally avoided once treatment begins. A positive TB test may require preventive treatment first. These steps exist because TNF and IL-17 blockade lowers the body’s defences against certain infections.

Are TNF inhibitors or IL-17 inhibitors safer for ankylosing spondylitis?

Neither class is universally safer; they carry different risks. TNF inhibitors are associated with reactivation of latent tuberculosis and a broader infection risk, and they are the established choice when inflammatory bowel disease coexists. IL-17 inhibitors carry a risk of fungal infections such as thrush and have been linked to new or worsening bowel inflammation. The safer option is the one that fits an individual’s medical history.

References

• NHS: Ankylosing spondylitis: Treatment
• NIH NIAMS: Ankylosing Spondylitis
• MedlinePlus: Ankylosing Spondylitis

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.