What is the physiology and physiopathology of arthritis and arthrosis?

Physiology and Physiopathology of Arthritis and Arthrosis

Arthritis and arthrosis (osteoarthritis) are distinct joint disorders with different underlying mechanisms, though they share common pathways of cartilage damage and joint dysfunction.

Physiological Structure of Joints

• Normal joint structure consists of:
  • Articular cartilage: Smooth, avascular tissue covering bone ends
  • Synovial membrane: Produces synovial fluid for lubrication
  • Subchondral bone: Provides structural support
  • Periarticular structures: Ligaments, tendons, and muscles

Pathophysiology of Osteoarthritis (Arthrosis)

Definition and Characteristics

• Osteoarthritis is a degenerative joint disease characterized by cartilage breakdown, subchondral bone changes, and limited inflammation 1
• Primarily affects weight-bearing joints (knees, hips) and hands
• Typically involves joint space narrowing, osteophyte formation, and subchondral sclerosis

Key Pathophysiological Mechanisms

1. Initial Subchondral Bone Changes

   • Recent evidence shows subchondral bone lesions often precede cartilage degeneration 1
   • Leads to altered biomechanical properties and stress distribution

2. Cartilage Degeneration Process

   • Begins with increased cell proliferation and matrix protein synthesis
   • Progresses to imbalance between matrix synthesis and degradation
   • Chondrocytes attempt to recapitulate early cartilage development but cannot replicate original architecture 2

3. Low-Grade Inflammation

   • Chronic, low-grade synovial inflammation is now recognized as central to OA pathophysiology
   • Involves production of inflammatory mediators, cytokines, and proteinases 1

4. Biomechanical Factors

   • Abnormal joint loading and mechanical stress contribute to pathogenesis
   • Resembles aspects of embryonic bone formation through endochondral ossification 3

Pathophysiology of Inflammatory Arthritis

Definition and Types

• Inflammatory arthritis includes conditions like rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis
• Characterized by pronounced inflammation of the synovial membrane

Key Pathophysiological Mechanisms

1. Immune-Mediated Inflammation

   • Both innate and adaptive immune responses drive inflammation and tissue destruction 1
   • In RA, early cartilage damage triggers cellular reactions in the synovium 3

2. Synovial Hyperplasia

   • Formation of pannus (inflamed synovial tissue) that invades cartilage
   • Produces inflammatory cytokines (TNF-α, IL-1, IL-6) that promote cartilage destruction

3. Site-Specific Autoimmunity

   • RA represents a site-specific manifestation of systemic autoimmunity
   • Early cartilage damage in the context of immune activation leads to specific joint responses 3

4. Joint Destruction Pattern

   • More rapid and aggressive cartilage and bone erosion compared to OA
   • Characteristic marginal erosions and periarticular osteopenia

Comparative Pathophysiology

Similarities

• Both conditions ultimately lead to cartilage damage and joint dysfunction
• Both involve inflammatory mediators and matrix-degrading enzymes
• Pain is the predominant symptom in both conditions 4

Key Differences

• Primary Trigger:

  • OA: Biomechanical stress, aging, and metabolic factors
  • Inflammatory arthritis: Immune dysregulation and autoimmunity

• Inflammation Pattern:

  • OA: Low-grade, chronic inflammation
  • Inflammatory arthritis: More pronounced, systemic inflammation

• Disease Progression:

  • OA: Typically slower progression
  • Inflammatory arthritis: Often more rapid joint destruction without treatment

Specific Joint Involvement

Hip Arthropathy

• In ankylosing spondylitis, hip involvement occurs in up to 80% of patients 5
• Haemochromatosis arthropathy typically affects metacarpophalangeal joints and ankles with exuberant osteophytes and rapid cartilage loss 6
• Radiographs show degenerative changes with joint space narrowing, osteophytes, and subchondral cysts, with chondrocalcinosis present in 50% of cases 6

Relationship Between Inflammation, Damage and Disability

• Inflammation causes pain and stiffness, leading to reversible disability
• Inflammation also induces structural damage which is usually irreversible
• Damage-induced disability is permanent, meaning that with increasing damage, physical functioning cannot fully recover even when inflammation is controlled 6

Clinical Implications

• Understanding these distinct pathophysiological mechanisms is crucial for appropriate treatment approaches
• OA management focuses on pain control and maintaining function
• Inflammatory arthritis requires controlling immune-mediated inflammation with disease-modifying drugs to prevent joint destruction
• Pain management should be guided by a patient-centered framework that considers biological, psychological and social factors 6

By recognizing the different pathophysiological processes in arthritis and arthrosis, clinicians can better target treatments to address the specific underlying mechanisms of joint damage and dysfunction.