Ankylosis spondylosis

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Ankylosing Spondylitis (AS)

Note on terminology: The term "Ankylosing Spondylosis" is a common misnomer. The correct condition is Ankylosing Spondylitis (AS) - spondylosis refers to degenerative disc disease, while spondylitis refers to inflammation. AS is now classified as radiographic axial spondyloarthritis (r-AxSpA) under modern terminology.

Definition

Ankylosing spondylitis is a multisystem inflammatory spondyloarthropathy primarily affecting the axial skeleton. It belongs to the family of spondyloarthritides, which also includes psoriatic arthritis, reactive arthritis, and enteropathic arthritis. The Assessment of SpondyloArthritis international Society (ASAS) classifies it as radiographic axial spondyloarthritis - structural damage visible on plain radiographs of the sacroiliac (SI) joint distinguishes it from non-radiographic axial spondyloarthritis.

Goldman-Cecil Medicine, 26e, Ch. 244

Epidemiology

Prevalence parallels that of HLA-B27 in any given population
Predominantly affects HLA-B27-positive adolescents and young adults
Male-to-female ratio roughly 2-3:1 (though females are increasingly recognized)
About 90% of AS patients are HLA-B27 positive
HLA-B27 prevalence is ~7% in Northern Europeans/North American Whites; virtually absent in Australian aboriginals; ~1% in Japan; up to 50% in some Western Canadian indigenous tribes
May be as common as rheumatoid arthritis

Pathobiology

Genetic Susceptibility

The strongest genetic association is with HLA-B27 on the short arm of chromosome 6. Over 30 subtypes of B27 exist; B2705 is the primordial subtype. Notably, subtypes B2706 and B2709 do NOT appear to confer susceptibility to AS. Non-HLA genes (ERAP1, IL-23R, IL-17 pathway genes) also contribute.

Mechanism of Inflammation and New Bone Formation

The primary pathological target is the enthesis - the site where tendons, ligaments, and joint capsules attach to bone. Inflammation at entheses (enthesitis) leads to:

Erosive bone destruction
Reactive new bone formation (syndesmophytes)
Progressive ossification and fusion

The IL-17/IL-23 axis and TNF-alpha are key cytokine drivers. Paradoxically, TNF inhibitors suppress inflammation but may not halt new bone formation (syndesmophyte progression), suggesting these two processes are partly uncoupled.

Clinical Features

Hallmark: Inflammatory Back Pain

Distinguishing features from mechanical back pain:

Feature	Inflammatory (AS)	Mechanical
Onset	Insidious, <40 yrs	Acute or insidious, any age
Morning stiffness	>1 hour	Brief (<30 min)
Response to exercise	Improves	Worsens
Response to rest	Worsens	Improves
Night pain	Yes, wakes patient	Uncommon

Axial Involvement

Sacroiliitis - hallmark; bilateral and symmetrical in AS (unlike psoriatic/reactive arthritis which is asymmetrical)
Lumbar, thoracic, and cervical spine involvement
Costovertebral joint involvement reducing chest expansion
Cervical spine fusion in advanced disease

Peripheral Joint Involvement

Seen in up to 30% of patients
Hip joint is the second most commonly affected joint after the SI joint
Lower limb oligoarthritis pattern (similar to other spondyloarthritides)
Enthesitis - Achilles tendinitis, plantar fasciitis are common

Extra-articular Manifestations

System	Manifestation
Eyes	Acute anterior uveitis - most common extra-articular feature
Heart	Aortitis, aortic regurgitation, conduction defects
Lungs	Upper lobe bilateral reticulonodular infiltrates with cyst formation (apical fibrobullous disease) - no effective therapy known
Kidneys	IgA nephropathy, secondary amyloidosis
Bowel	Subclinical gut inflammation in ~60%; frank IBD in some

Radiological Features

Sacroiliac Joints

MRI detects the earliest change - subchondral bone marrow oedema (active sacroiliitis), before plain radiograph changes.

Plain X-ray/CT progression:

Erosions + subchondral sclerosis
Joint space irregularity
Bony ankylosis (complete fusion)

MRI of sacroiliac joints in AS - T1 weighted (A) showing erosions and T2 fat-suppressed (B) showing extensive subchondral oedema

T1 (A): erosions in the SIJ with joint space loss (damage). T2 fat-suppressed (B): extensive subchondral oedema reflecting active disease activity - Grainger & Allison's Diagnostic Radiology

Spine - Sequential Changes

Romanus lesions - sclerotic "shiny corners" at vertebral body corners (enthesitis at Sharpey fiber insertion). On MRI, this appears as bone oedema at vertebral body corners before sclerosis is visible on plain X-ray.
Squared vertebral bodies - erosion + anterior longitudinal ligament ossification
Syndesmophytes - thin, vertically oriented bone outgrowths (contrast with the bulky, nonmarginal, asymmetrical syndesmophytes of reactive arthritis)
Bamboo spine - complete fusion of vertebral bodies AND sacroiliac joints in advanced/untreated disease

Bamboo spine with bridging syndesmophytes (A) and complete bony fusion of sacroiliac joints (B)

Classic "bamboo spine" - bridging vertical syndesmophytes around intervertebral discs with no facet joint spaces visible, indicating posterior fusion (L3-S1). AP pelvis showing complete bony fusion of both sacroiliac joints - Grainger & Allison's

Lumbar spondylitis: symmetrical marginal bridging syndesmophytes in AS (left) vs bulky asymmetrical syndesmophytes of reactive arthritis (right)

Left: AS showing symmetrical marginal bridging syndesmophytes with spinal ligament calcification. Right: reactive arthritis showing bulky, nonmarginal, asymmetrical syndesmophytes - Goldman-Cecil Medicine

Spinal Fracture Risk

Despite apparent sclerosis, patients are osteopenic. A fused, rigid spine is extremely vulnerable to transverse fractures - these are highly unstable and frequently catastrophic, even from minimal trauma.

Hip Joint

Diffuse joint space loss with preserved bone density. A cuff of entheseal new bone around the femoral head creates a somewhat flattened appearance that can mimic a cam deformity (femoroacetabular impingement).

Andersson Lesion

In a largely fused spine, movement at unfused levels can cause an inflammatory discovertebral lesion (Andersson lesion) - the irregularity and sclerosis can be mistaken for infection.

Diagnosis

ASAS Classification Criteria for Axial Spondyloarthritis

Age of onset <45 years + chronic back pain ≥3 months, PLUS:

Imaging arm: Sacroiliitis on MRI or X-ray + ≥1 SpA feature
Clinical arm: HLA-B27 positive + ≥2 SpA features

SpA features include: Inflammatory back pain, arthritis, enthesitis (heel), uveitis, dactylitis, psoriasis, Crohn's/UC, good response to NSAIDs, family history of SpA, HLA-B27, elevated CRP.

Laboratory

HLA-B27: positive in ~90%
CRP/ESR: elevated (correlates with disease activity but can be normal)
Rheumatoid factor and ANA: negative (seronegative arthritis)

Imaging Summary

Plain X-ray: First-line; shows late changes (sclerosis, erosions, syndesmophytes, bamboo spine)
MRI: Best for early disease - detects active bone marrow oedema (sacroiliitis) before X-ray changes
CT: Best for assessing bony detail, erosions, and ankylosis but involves radiation
Scintigraphy: Historical role; now superseded by MRI (lower sensitivity/specificity)

Treatment

Non-pharmacological

Physiotherapy and exercise - maintain spinal mobility and posture
Swimming, hydrotherapy
Smoking cessation (smoking accelerates structural damage)

Pharmacological

Step 1 - NSAIDs

First-line therapy (Grade A evidence - Cochrane review)
Continuous NSAIDs may slow radiographic progression (unlike in RA)
Options: indomethacin, naproxen, diclofenac, celecoxib

Step 2 - Biologics (for inadequate NSAID response)

Class	Agents	Notes
TNF inhibitors	Etanercept, adalimumab, infliximab, certolizumab, golimumab	First biologic class proven effective; rapidly reduce inflammation
IL-17A inhibitors	Secukinumab, ixekizumab	Effective in TNF-naive and TNF-inadequate responders; preferred if IBD absent (may worsen IBD)
IL-12/23 inhibitor	Ustekinumab	Less robust evidence for AS vs PsA
JAK inhibitors	Tofacitinib, upadacitinib	Oral options; evidence accumulating

Step 3 - Local therapy

Intra-articular corticosteroid injections (peripheral joints, SI joints under imaging guidance)
Systemic corticosteroids are generally NOT effective for axial disease

Note on conventional DMARDs

Sulfasalazine and methotrexate have limited efficacy for axial disease but may help peripheral arthritis.

Surgical

Total hip replacement - for severe hip disease
Spinal surgery (osteotomy) for severe fixed kyphosis
No role for surgery in axial disease prophylactically

Prognosis and Complications

The clinical course is highly variable. Key points:

The strongest predictor of new syndesmophyte formation is the presence of syndesmophytes at baseline
Osteoporosis is a significant complication (both local chronic inflammation and abnormal biomechanical loading)
Late complications: cauda equina syndrome, osteoporotic compression fractures, spondylodiscitis, restrictive lung disease
Intervertebral fracture can occur after minimal trauma in late disease
Patients with refractory new spinal pain need urgent imaging to exclude fracture

Sources:

Goldman-Cecil Medicine, International Edition (26e), Chapter 244 - Spondyloarthritis
Grainger & Allison's Diagnostic Radiology, Chapter 44 - Ankylosing Spondylitis
Murray & Nadel's Textbook of Respiratory Medicine - Pulmonary manifestations of AS

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