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

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

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.