Ankylosing Spondylitis vs. Reactive Arthritis: Understanding Differences, Symptoms, and Treatments

What is the Difference Between Ankylosing Spondylitis and Reactive Arthritis?

While both Ankylosing Spondylitis (AS) and Reactive Arthritis (ReA) are types of spondyloarthritis that can affect the spine and other joints, the fundamental difference lies in their etiology: AS is a chronic, progressive autoimmune disease with a strong genetic predisposition, whereas ReA is an acute, sterile arthritis triggered by a preceding infection elsewhere in the body.

Understanding Spondyloarthritis

Ankylosing Spondylitis and Reactive Arthritis fall under the umbrella of spondyloarthritis (SpA), a group of inflammatory rheumatic diseases that primarily affect the spine and sacroiliac (SI) joints, but can also involve peripheral joints, entheses (where tendons or ligaments attach to bone), and various non-skeletal organs. Despite sharing common features like inflammatory back pain, enthesitis, and a strong association with the HLA-B27 gene, their distinct origins and clinical courses necessitate a clear understanding of their differences.

Ankylosing Spondylitis (AS)

Ankylosing Spondylitis is a chronic, systemic inflammatory disease primarily affecting the axial skeleton (spine and SI joints). It is the prototypic form of axial spondyloarthritis.

• Definition and Nature: AS is characterized by chronic inflammation of the sacroiliac joints (sacroiliitis) and the spine, leading to pain, stiffness, and potentially progressive structural damage. Over time, inflammation can lead to new bone formation, causing the vertebrae to fuse (ankylosis), which can severely reduce spinal mobility and result in a hunched posture.
• Causes: The exact cause of AS is unknown, but it is considered an autoimmune disease with a strong genetic component. The HLA-B27 gene is present in a large majority (80-95%) of individuals with AS, though not everyone with HLA-B27 develops the condition. Environmental factors are also thought to play a role in triggering the disease in genetically susceptible individuals.
• Key Symptoms:
  • Chronic Inflammatory Back Pain: Typically insidious in onset, worse with rest or inactivity (especially in the morning), improves with exercise, and can wake individuals from sleep.
  • Stiffness: Predominantly morning stiffness lasting more than 30 minutes.
  • Sacroiliitis: Pain in the buttocks or hips, often alternating sides.
  • Enthesitis: Inflammation at tendon/ligament insertion points, commonly affecting the Achilles tendon, plantar fascia (causing heel pain), or ribs.
  • Peripheral Arthritis: Less common than axial involvement, but can affect large joints like hips and shoulders.
  • Extra-Articular Manifestations:
    • Acute Anterior Uveitis: Eye inflammation, causing pain, redness, and light sensitivity.
    • Inflammatory Bowel Disease (IBD): Such as Crohn's disease or ulcerative colitis.
    • Psoriasis: A skin condition.
    • Fatigue.
• Progression: AS is a chronic, lifelong condition with a variable course. While some individuals experience mild symptoms, others face severe progression leading to significant spinal fusion and disability.

Reactive Arthritis (ReA)

Reactive Arthritis, formerly known as Reiter's Syndrome, is an acute form of arthritis that develops in response to an infection in another part of the body, typically the gastrointestinal (GI) or genitourinary (GU) tract. It is characterized by sterile joint inflammation, meaning the bacteria causing the initial infection are not present in the joint fluid.

• Definition and Nature: ReA is a post-infectious, inflammatory arthritis that typically manifests within weeks to a few months after the initial infection. It is considered "reactive" because the immune system's response to the infection mistakenly attacks the joints and other tissues.
• Causes: ReA is triggered by specific bacterial infections. Common culprits include:
  • Gastrointestinal infections: Salmonella, Shigella, Campylobacter, Yersinia.
  • Genitourinary infections: Chlamydia trachomatis (most common), Ureaplasma urealyticum.
  • Less commonly, other infections like Clostridium difficile or Borrelia burgdorferi (Lyme disease) have been implicated.
• Key Symptoms:
  • Asymmetric Peripheral Arthritis: Most commonly affects large joints in the lower limbs (knees, ankles, feet) in an asymmetric pattern.
  • Dactylitis ("Sausage Digits"): Swelling of an entire finger or toe.
  • Enthesitis: Similar to AS, often affecting the Achilles tendon or plantar fascia.
  • Classic Triad (not always present):
    • Arthritis: Joint inflammation.
    • Urethritis: Inflammation of the urethra (painful urination, discharge).
    • Conjunctivitis: Eye inflammation (redness, irritation).
  • Mucocutaneous Lesions:
    • Keratoderma blennorrhagicum: Psoriasis-like skin lesions, especially on the soles of the feet and palms of the hands.
    • Circinate balanitis: Painless shallow ulcers on the glans penis.
    • Oral ulcers.
  • Fatigue and low-grade fever.
• Course: ReA is often self-limiting, with symptoms typically resolving within 3-12 months. However, in a significant percentage of individuals (20-50%), the condition can recur or become chronic, resembling AS in some aspects, especially if linked to HLA-B27.

Key Differentiating Factors

Understanding the primary distinctions between AS and ReA is crucial for accurate diagnosis and management.

• Etiology (Cause):
  • AS: Primarily an autoimmune disease with a strong genetic predisposition (HLA-B27), chronic and idiopathic (no identifiable external trigger).
  • ReA: Triggered by a specific bacterial infection elsewhere in the body, leading to an acute inflammatory response.
• Onset:
  • AS: Insidious onset, symptoms develop gradually over months to years.
  • ReA: Acute onset, typically within 1-4 weeks following a documented infection.
• Primary Joint Involvement:
  • AS: Predominantly axial skeleton (sacroiliac joints, spine), often symmetric. Peripheral arthritis, if present, is less common and usually affects larger joints.
  • ReA: Primarily peripheral joints, especially lower limbs (knees, ankles, feet), and often asymmetric. Axial involvement (sacroiliitis) can occur but is less common and usually milder than in AS.
• Course and Prognosis:
  • AS: Chronic, progressive disease that can lead to permanent structural changes and disability.
  • ReA: Often acute and self-limiting, with symptoms resolving within months. However, chronic or recurrent forms can occur, especially in HLA-B27 positive individuals.
• Genetic Predisposition (HLA-B27):
  • AS: Present in 80-95% of individuals, strongly associated with disease development and severity.
  • ReA: Present in 30-50% of individuals, associated with a higher likelihood of axial involvement, chronicity, and recurrence. While present, the infectious trigger remains the primary initiator.
• Extra-Articular Manifestations:
  • AS: Uveitis, IBD, psoriasis are common.
  • ReA: The classic triad of arthritis, urethritis, and conjunctivitis is characteristic. Mucocutaneous lesions (keratoderma blennorrhagicum, circinate balanitis) are also distinctive. There is some overlap in eye and skin involvement.

Diagnosis

Diagnosing both conditions involves a combination of clinical evaluation, imaging, and laboratory tests.

• Clinical Evaluation: A thorough medical history (including infectious exposures for ReA) and physical examination assessing joint swelling, tenderness, range of motion, and signs of enthesitis.
• Imaging:
  • X-rays: May show sacroiliitis (inflammation of SI joints) and spinal changes (e.g., squaring of vertebrae, syndesmophytes, "bamboo spine" in advanced AS).
  • MRI: More sensitive for detecting early inflammatory changes in the SI joints and spine before they are visible on X-rays.
• Laboratory Tests:
  • Inflammatory Markers: Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) indicate inflammation but are non-specific.
  • HLA-B27 Testing: Helps assess genetic predisposition, but is not diagnostic on its own.
  • Infection Screening (for ReA): Stool cultures for enteric pathogens or urine/genital swabs for Chlamydia trachomatis or other organisms may be performed to identify the triggering infection.

Management and Treatment

While the underlying causes differ, the management of the inflammatory arthritis in both conditions shares some commonalities, particularly in symptom relief and disease modification.

• Nonsteroidal Anti-inflammatory Drugs (NSAIDs): First-line treatment for pain and stiffness in both conditions.
• Physical Therapy and Exercise: Crucial for maintaining mobility, flexibility, and posture in AS, and for restoring joint function in ReA.
• Disease-Modifying Anti-Rheumatic Drugs (DMARDs):
  • Conventional DMARDs (e.g., sulfasalazine, methotrexate): More effective for peripheral arthritis in both conditions, less so for axial symptoms in AS.
  • Biologics (e.g., TNF inhibitors like adalimumab, etanercept): Highly effective for severe axial and peripheral symptoms in AS, and for chronic, severe ReA that doesn't respond to other treatments.
• Specific Considerations:
  • For ReA: Antibiotics may be used to treat the initial infection, but they do not typically alter the course of the established arthritis. Corticosteroid injections into affected joints can provide localized relief.
  • For AS: Emphasizes long-term management, including regular exercise to prevent spinal fusion, and lifestyle modifications.

Conclusion

Ankylosing Spondylitis and Reactive Arthritis, while both belonging to the spondyloarthritis family, are distinct entities with different origins and disease courses. AS is a chronic, genetically influenced autoimmune disease primarily affecting the spine, leading to potential fusion. ReA is an acute, post-infectious condition, typically affecting peripheral joints, with a generally self-limiting course, though it can become chronic. Accurate diagnosis, based on a comprehensive understanding of their unique features, is paramount for effective management and improving patient outcomes.