Osteoarthritis

Chronic disease involving the imbalance between wear and repair of articular (hyaline) cartilage leading to progressive cartilage loss and accompanying periarticular change

Aetiology

Primary OA

  • Primary OA is defined as a 'common complex disorder' with multiple risk factors
    • Genetic factors - 40-60%
    • Constitutional factors - aging, female sex, obesity
    • Biomechanical factors - joint injury, occupational/recreational usage, reduced muscle strength, joint laxity, joint malalignment (e.g. genu varum can lead medial knee OA, genu valgum can lead to lateral knee OA)
  • Affects weightbearing or active joints
  • Presents > 50 years

Secondary OA

  • Secondary OA occurs when OA affects an unexpected site due to overuse, previous injury or previous arthritis
  • Examples of conditions which can lead to secondary OA include rheumatoid arthritis and gout

Pathophysiology

  • Metabolically active dynamic process that involves all joint tissues - cartilage, bone, synovium/capsule, ligaments and muscle
  • Involves an imbalance between the wear and repair of cartilage between joints
  • Key pathological changes include localised loss of hyaline cartilage and remodeling of adjacent bone with new bone formation (osteophyte) at joint margins
  • Leads to increased pressure on the bony surfaces and inflammation leads to pain, swelling (inflammatory effusion), thickening of the capsule and stiffness
  • Any synovial joint can be affected but knees, hands and hips are the most commonly affected joints

Development of OA

  1. Chondrocyte injury - genetic and biochemical factors
  1. Chondrocytes proliferate - release inflammatory mediators, proteases, collagen and proteoglycans
  1. Remodelling and degradation of cartilage
  1. Stimulates inflammatory changes in synovium and subchondral bone
  1. Repetative injury and chronic inflammation
  1. Long term consequences:
    1. Cartilage completely worn away - bone on bone
    2. Subchondral cysts (synovial fluid accumulation)
    3. Surface becomes 'polished' - eburnation (subchondral sclerosis)
    4. Formation of osteophytes (disorganised bone remodelling) - can irritate nerves
      1. notion image

Types of OA

  • Localised OA: can affect hips, knees, finger interphalangeal joints, facet joints of lower cervical and lower lumbar spines
  • Generalised OA: defined as OA at either the spinal or hand joints and in at least 2 other joint regions (e.g. DIP joints, thumb bases, first MTP joints, knees, hips)
    • Clinical marker of generalised OA is the presence of multiple Herbeden's nodes

Clinical presentation

Symptoms

  • Pain - worse with joint use
  • Pain at night
  • Morning stiffness lasting less than 30 mins
  • Inactivity gelling
  • Instability
  • Poor grip in thumb OA

Signs

  • Joint line tenderness
  • Crepitus
  • Deformity
  • Stiff on testing ROM
  • Bony swelling - osteophytes
    • Caused by bony spurs due to chronic trauma
    • Heberden's node (DIP joints) - only seen in OA (not in RA)
    • Bouchard's node (PIP joints) - less common, also seen in RA
  • 1st CMC OA - squaring of the thumb
    • notion image

How different joints may be affected

Knee OA
  • Osteophytes
  • Effusions
  • Crepitus and restriction of movement
  • Genu varus and valgus deformities
  • Baker's cysts
Hip OA
  • Pain may be felt in groin, radiating to knee or anterior thigh
  • Pain felt in hip may be radiating from the lower back
  • Hip movements restricted
Spine OA
  • Cervical - pain and restriction of movement, occipital headaches may occur
    • Osteophytes may impinge on nerve roots
  • Lumbar - osteophytes can cause spinal stenosis if they encroach on the spinal canal

Investigations

  • Clinical based on S+S
  • Imaging - plain x-rays, MRI scans, USS
    • Don't tend to perform imaging unless there is doubt over diagnosis

X-ray - LOSS

  • Loss of joint space
  • Marginal osteophytes
  • Sclerosis (subchondral)
  • Subchondral cysts
  • Pitfalls - insensitive particularly with early disease, correlate poorly with disease activity, common incidental asymptomatic finding in older people

Management

Medical management

Non-pharmacological
  • Education - ensure patient continues to exercise
  • Lifestyle management e.g. weight loss, exercise, walking aids
  • Physiotherapy
  • Activity modification e.g. occupational therapy, hobbies
Pharmacological
  • Analgesia - paracetamol, NSAIDs (avoid opiates) as needed
  • Local intra-articular steroid injections for flare-up
    • Can give up to 3 per year
    • If given too many can damage joint further and accelerate OA

Surgical management

  • Joint replacements e.g. knee, hip
  • Arthroscopic surgery to remove loose bodies etc.