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Spondyloarthropathies – What Are They?

Lower back pain can also occur as a form of inflammation, and its onset can be very uncomfortable. Learn how to recognize it and how it is treated.

Spondyloarthropathies or spondyloarthritis are a group of inflammatory rheumatic diseases that share certain characteristics and a hereditary predisposition. The main feature of this group of diseases is lower back pain, which differs from “ordinary” back pain and is called inflammatory-type back pain.

The spondyloarthropathy group includes the following rheumatic diseases:

  • Ankylosing spondylitis (AS)

  • Psoriatic arthritis (PsA)

  • Reactive arthritis (ReA)

  • Arthritis associated with inflammatory bowel disease (IBD)

  • Undifferentiated spondyloarthritis

  • Juvenile chronic arthritis

  • Juvenile ankylosing spondylitis

Spondyloarthropathies often show familial clustering, meaning these diseases occur more frequently in individuals with certain genetic traits (primarily HLA-B27 positive). Patients usually have a negative rheumatoid factor (RF)—an antibody typical in other inflammatory rheumatic diseases, especially rheumatoid arthritis—and lack subcutaneous nodules and other RA features.

Spondyloarthropathies often affect the spine and sacroiliac joints (between the sacrum and pelvic bones), and sometimes peripheral joints, usually asymmetrically and more often in the legs than the arms.

A newer term, axial spondyloarthropathy, describes cases in which spinal and sacroiliac involvement predominates.

Spondyloarthropathies may also present extra-articular manifestations, such as:

  • Eye inflammation (uveitis or iridocyclitis)

  • Skin and mucous changes

  • Intestinal changes

Because of the wide range of symptoms, their frequency, and sometimes subtle or gradual onset, diagnosis is often delayed, sometimes by up to 10 years. Early diagnosis is crucial, as earlier treatment slows disease progression and preserves mobility, especially with modern treatment options. New diagnostic strategies and referral algorithms improve early and accurate diagnosis.


How Is Spondyloarthropathy Diagnosed?

There is no specific diagnostic test for spondyloarthropathies. Expert evaluation by a rheumatologist is essential.

Classification criteria exist for research purposes but are sometimes used for diagnosis. These criteria generally combine:

  • Clinical symptoms

  • Radiographic changes (primarily sacroiliitis)

Modern diagnostic algorithms incorporate patient complaints, clinical findings, HLA-B27 status, and imaging, with MRI preferred for early detection.


Inflammatory-Type Lower Back Pain

Inflammatory-type back pain occurs in about 70% of spondyloarthropathy patients.

Characteristics that distinguish it from mechanical back pain (e.g., disc herniation compressing spinal nerves):

  • Deep, dull, poorly localized pain in the lower back and gluteal region, sometimes radiating to the thighs

  • Pain can shift sides, worse at night, especially in the second half of the night or early morning

  • Typically begins before age 40

  • Prolonged morning stiffness, lasting several hours

  • Pain improves with activity and worsens with rest

  • Responds well to NSAIDs

The two most common spondyloarthropathies are ankylosing spondylitis and psoriatic arthritis.


Ankylosing Spondylitis (AS)

Ankylosing spondylitis is an inflammatory rheumatic disease in the seronegative spondyloarthropathy group, characterized by progressive inflammation of the sacroiliac joints and spine.

  • Prevalence: ~1% of the general population, though many remain undiagnosed

  • Onset: usually ages 15–40

  • More common in men than women (2–3:1)

Cause and Disease Development

The exact cause is unknown, but disease development involves both genetic and environmental factors.

  • Environmental triggers: bacterial infections (e.g., Shigella, Yersinia, Klebsiella)

  • Genetics: HLA-B27 positive individuals have a 30% risk if a first-degree relative has AS, compared to 1–4% in HLA-B27 positive controls

  • Other genes and cytokines also play roles, especially in sacroiliac and enthesis (tendon/ligament insertion) inflammation

Inflammation at entheses leads over time to ossification and bone growths bridging vertebrae, resulting in characteristic spinal rigidity.

Symptoms and Signs

Typical AS patient: young male with persistent, dull lower back pain and stiffness.

  • Early: alternating hip and thigh pain; may mimic sciatica

  • Night pain improves with movement

  • Non-specific early symptoms: fatigue, low-grade fever, chills, or weight loss

  • Pain often localized to gluteal region or sacroiliac joints

  • Progression: thoracic and cervical spine involvement after 5–8 years

  • Women: often milder symptoms, cervical spine involvement more common

  • Chest pain may occur due to costovertebral or costosternal joint inflammation

  • Enthesitis: swelling at heel, hip, or ischial tuberosities

  • Peripheral joint involvement in ~30% (shoulder, hip)

Rarely, atlantoaxial joint involvement can cause neurological symptoms.


Clinical Examination

  • Reduced spinal mobility in all directions

  • Early limitation: lumbar region; later: thoracic and cervical

  • Decreased chest mobility; diaphragmatic breathing

  • Possible shoulder and hip involvement with pain and stiffness

  • Persistent flexed posture (“skier’s stance”)


Tests

  • Laboratory: nonspecific; HLA-B27 positive in ~90%

  • Imaging: X-rays sufficient in most cases; CT more sensitive; MRI preferred for early detection

  • DEXA: recommended for osteoporosis assessment


Treatment

Since the cause is unknown, treatment focuses on:

  • Reducing pain and stiffness

  • Suppressing inflammation

  • Maintaining functional mobility

Treatment categories:

  1. General measures and education

  2. Functional therapy

  3. Pharmacologic therapy

  4. Surgical treatment

Medications:

  • NSAIDs (first-line)

  • Disease-modifying drugs: sulfasalazine

  • Analgesics: paracetamol, tramadol

  • Local glucocorticoid injections for enthesitis or affected joints

  • Biologics (anti-TNF-α) reduce pain, stiffness, and structural progression

Physical therapy:

  • Maintain mobility, strength, prevent deformities, improve independence

  • Regular medical gymnastics is crucial

  • Main exercise groups: spine, hips/shoulders, breathing

  • Abdominal lying for 20–30 minutes, twice daily, helps prevent fixed flexion


Psoriatic Arthritis (PsA)

Psoriatic arthritis is a chronic inflammatory rheumatic disease associated with psoriasis.

Main features:

  • Asymmetric joint inflammation

  • Enthesitis (tendon/ligament insertion inflammation)

  • Dactylitis (swelling of entire fingers/toes)

  • Spine and sacroiliac involvement

Prevalence: 5–7% of psoriasis patients; up to 40% in severe psoriasis

Sequence:

  • Skin changes precede arthritis in 75%

  • Simultaneous onset: 10–15%

  • Arthritis precedes skin lesions: 13–17%

Gender: equal in men and women
Typical onset: 30–40 years, but can occur at any age


Cause and Development

Cause unknown; influenced by:

  • Genetic factors (HLA-Bw38, HLA-DR4, HLA-DR7, HLA-B27)

  • Environmental triggers: infections (e.g., Staphylococcus aureus), trauma

  • Family history increases risk; more frequent in monozygotic twins


Symptoms and Signs

  • Pain, swelling, stiffness of joints and entheses

  • Clinical forms:

    • Asymmetric arthritis (≤4 joints)

    • Symmetric arthritis (≥5 joints)

    • Distal joint involvement (“classic” form)

    • Arthritis with destructive changes

    • Axial involvement ± peripheral arthritis

  • Enthesitis common: heel, pelvis

  • Dactylitis in 16–48%

  • Spinal/sacroiliac inflammation: pain and stiffness improving with movement

  • Skin and nail psoriasis may aid diagnosis, including hidden areas (scalp, behind ears, under breasts)


Tests

  • Laboratory: negative RF; anti-CCP may help differentiate from RA

  • Acute-phase markers may or may not be elevated

  • Imaging: X-rays usually sufficient; CT/MRI for early or unclear cases

  • Spinal X-rays: ossification of ligaments and entheses; often asymmetric compared to AS


Treatment

Goals:

  • Reduce pain, stiffness, and inflammation

  • Maintain functional mobility

Conservative treatment:

  • Education, functional therapy, medications, surgery

Medications:

  • NSAIDs

  • Local corticosteroids (entheses/joints)

  • Disease-modifying drugs: leflunomide, sulfasalazine, methotrexate

  • Biologics (anti-TNF-α) effective for joint and skin symptoms

Physical therapy:

  • Electrotherapy, thermotherapy, individualized medical gymnastics