MRI for Ankylosing Spondylitis

What Is Ankylosing Spondylitis?

Ankylosing spondylitis (AS) is a chronic inflammatory condition that primarily affects the spine and sacroiliac joints. It belongs to a family of conditions called spondyloarthropathies (SpA), which share common features including spinal inflammation, enthesitis (inflammation where tendons and ligaments attach to bone), and association with the HLA-B27 gene.

The term "ankylosing spondylitis" describes the end stage of the disease — "ankylosing" meaning stiffening or fusion, and "spondylitis" meaning spinal inflammation. Modern terminology increasingly uses "axial spondyloarthritis" (axSpA) as the broader term, with AS representing the subset that has structural damage visible on X-ray (radiographic axSpA). Non-radiographic axSpA (nr-axSpA) is the earlier stage where inflammation is present but X-ray changes haven't yet developed.

AS affects approximately 1 in 200 people in the UK — around 200,000 adults. It typically begins between ages 17 and 45, with a mean age of onset around 24. Historically considered a male-dominant disease, it's now recognised that the male-to-female ratio is closer to 2:1 (rather than the previously quoted 9:1), with women being more commonly misdiagnosed or diagnosed later.

The average delay from symptom onset to diagnosis in the UK remains stubbornly long — 8.5 years according to the National Ankylosing Spondylitis Society (NASS). This delay matters because effective biological therapies exist and work best when started early, before irreversible structural damage occurs.

Why MRI Is Used for Ankylosing Spondylitis

MRI has transformed the diagnosis and management of AS by detecting inflammation years before X-ray changes develop:

• Early diagnosis: The ASAS classification criteria for axial SpA include two pathways — one based on X-ray sacroiliitis plus clinical features, and one based on MRI sacroiliitis plus clinical features. MRI enables diagnosis at the nr-axSpA stage, potentially 5-10 years before X-ray changes would appear.
• SI joint assessment: MRI detects bone marrow oedema (active inflammation) and structural changes (erosions, fat metaplasia, sclerosis) in the SI joints with far greater sensitivity than X-ray.
• Spinal inflammation: MRI shows active inflammation at the corners of vertebral bodies (spondylitis), at the facet joints (facet arthritis), along the posterior elements, and at the costovertebral joints — all sites of disease activity that are invisible on X-ray until structural damage occurs.
• Treatment response monitoring: Objective measurement of inflammatory burden on MRI (using scoring systems like SPARCC or the Berlin modification of the ASspiMRI-a score) allows quantitative assessment of treatment response to biological therapies.
• Distinguishing from mechanical back pain: The MRI pattern of inflammatory sacroiliitis and spondylitis is distinct from degenerative changes, helping clinicians differentiate AS from much more common mechanical back pain.
• Assessing complication risk: MRI can identify vertebral fractures (which occur with increased frequency in AS due to spinal rigidity and osteoporosis) and spinal cord compression.

MRI Sequences Used

• STIR coronal oblique through SI joints: The single most important sequence. Active sacroiliitis appears as bright bone marrow oedema adjacent to the SI joint surfaces. The ASAS/OMERACT definition requires at least two slices with definite BMO or at least two areas of BMO on a single slice.
• T1-weighted coronal oblique through SI joints: Shows structural changes — erosions (cortical breaks), fat metaplasia (bright T1 signal replacing previously inflamed bone), sclerosis (dark on T1 and T2), and ankylosis (bony bridging).
• STIR sagittal of the entire spine: Detects vertebral corner inflammatory lesions (VCILs or "Romanus lesions") — bright areas at the anterior or posterior corners of vertebral bodies. Also shows inflammation at the facet joints, spinous processes, and interspinous ligaments.
• T1-weighted sagittal of the entire spine: Shows structural spinal changes — corner fatty lesions (bright on T1, indicating previous inflammation), syndesmophytes (bony bridges between vertebrae, though CT shows these better), and vertebral body shape changes.
• T2-weighted sequences: Complementary to STIR for detecting oedema and assessing disc integrity.
• Post-gadolinium T1 fat-saturated (optional): Can detect synovitis and entheseal enhancement, but STIR/T2 fat-sat protocols are now considered sufficient for most clinical purposes, and gadolinium-free protocols are preferred to minimise contrast exposure in a disease requiring repeated imaging.

What Radiologists Look For

• Sacroiliac joint — active inflammation:
  • Bone marrow oedema on STIR — the defining feature of active sacroiliitis on MRI
  • Capsulitis — high signal around the joint capsule
  • Enthesitis — inflammation at ligament attachments around the joint
  • Joint fluid — not always present, and less specific than BMO
• Sacroiliac joint — structural changes:
  • Erosions — irregular joint surface with cortical breaks
  • Fat metaplasia — bright T1 signal in subchondral bone, indicating healed inflammation
  • Sclerosis — dense, dark signal on both sequences
  • Ankylosis — complete bony fusion of the joint
• Spine — active lesions:
  • Anterior and posterior corner inflammatory lesions (spondylitis/Romanus lesions)
  • Lateral corner lesions (visible on coronal or axial images)
  • Facet joint inflammation
  • Costovertebral joint inflammation
  • Spinous process oedema
  • Andersson lesion — inflammatory discovertebral lesion resembling a fracture non-union
• Spine — structural changes:
  • Corner fatty lesions (bright on T1)
  • Vertebral body squaring (loss of normal concavity)
  • Syndesmophytes (better seen on CT/X-ray)
  • Vertebral fractures (particularly through ankylosed segments — "chalk stick" fractures)
• SPARCC scoring: The Spondyloarthritis Research Consortium of Canada score quantifies SI joint inflammation across 6 consecutive coronal oblique slices, scoring each quadrant for BMO, deep BMO, and intense signal. Maximum score 72. Used primarily in clinical trials and research but increasingly in clinical practice for monitoring treatment response.

How to Prepare for the Scan

• No special preparation — continue all medications including NSAIDs and biological therapies
• Wear comfortable, non-metallic clothing
• If your spine is very stiff and you have difficulty lying flat, inform the department when booking — they can use pillows and supports to make you comfortable
• If you have a fused kyphotic spine and can't lie flat, the department may be able to accommodate you with additional pillows or a different starting position
• The scan may cover SI joints alone (20-25 minutes) or SI joints plus whole spine (40-60 minutes) — confirm with your referring clinician what's been requested

What Happens During the Scan

You'll lie on your back. For SI joint imaging, a surface coil is placed over the pelvis. For combined SI joint and spine imaging, the spine coil (built into the table) is used alongside pelvic coils.

An SI joint-only scan takes 20-25 minutes. Combined SI joints plus whole spine takes 40-60 minutes. No breath-holds are required — the spine and pelvis are relatively still structures unaffected by breathing.

If lying flat is uncomfortable due to spinal stiffness, let the radiographer know — they'll adjust your position with supports. Some patients with advanced kyphosis find lying flat impossible; the radiographer has strategies to accommodate this.

Contrast is not routinely used for AS assessment. The STIR and T1 protocol provides all the necessary diagnostic information.

What MRI Can't Show

• Syndesmophytes reliably: The bony bridges between vertebrae that characterise AS are calcified/ossified structures — CT and X-ray show these better than MRI. For structural damage assessment and monitoring, modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS) uses lateral X-rays of the cervical and lumbar spine.
• Non-specific oedema: BMO at the SI joints occurs in many conditions — degenerative disease, mechanical loading (runners, gymnasts, pregnant women), infection, and other inflammatory arthropathies. BMO alone is not specific for axSpA. The clinical context, distribution pattern, and associated features are critical for interpretation.
• Disease activity with one number: While MRI quantifies visible inflammation, it doesn't capture all dimensions of disease activity. Patient-reported outcomes (BASDAI), blood markers (CRP), and clinical examination complement imaging in assessing overall disease status.
• Peripheral joint and entheseal disease: AS often involves peripheral entheses (Achilles, plantar fascia, costochondral junctions) and sometimes peripheral joints. These aren't covered by a standard SI joint/spine MRI protocol and need separate clinical assessment or targeted imaging.

Treatment Pathways After Diagnosis

• NSAIDs: First-line treatment. Used continuously (not just as needed) for active inflammatory symptoms. At least two different NSAIDs should be tried for a minimum of 4 weeks total before considering them ineffective.
• Exercise and physiotherapy: A structured exercise programme is fundamental — NICE recommends this for all patients with AS. Regular exercise (hydrotherapy, stretching, strengthening, and cardiovascular fitness) improves spinal mobility, reduces pain, and complements drug therapy. The NASS website provides specific exercise programmes.
• Biologic therapy — anti-TNF agents: Adalimumab, certolizumab, etanercept, golimumab, and infliximab. Indicated when ≥2 NSAIDs have failed and disease remains active (BASDAI ≥4 and spinal pain VAS ≥4). These drugs reduce inflammation, pain, and stiffness, and may slow radiographic progression. NICE Technology Appraisals govern access criteria in the UK.
• Biologic therapy — IL-17 inhibitors: Secukinumab and ixekizumab. Effective alternatives to anti-TNF, particularly useful when anti-TNF has failed or is contraindicated.
• JAK inhibitors: Tofacitinib and upadacitinib — oral targeted synthetic DMARDs. Licensed for AS, providing another option when biological therapies are unsuitable.
• Conventional DMARDs: Sulfasalazine and methotrexate have limited evidence for axial disease but may help with peripheral joint involvement.
• Surgery: Total hip replacement for end-stage hip involvement. Spinal osteotomy for severe fixed kyphotic deformity (highly specialised surgery). Urgent stabilisation for spinal fractures in ankylosed spines.
• Multidisciplinary care: Rheumatologist-led care coordinating with physiotherapy, occupational therapy, ophthalmology (for acute anterior uveitis, which affects 25-40% of AS patients), gastroenterology (for IBD, associated in 5-10%), and dermatology (for psoriasis).

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