Key Facts

OA is primarily a disease of articular cartilage failure, but it involves the entire joint including subchondral bone, synovium, ligaments, and periarticular muscles. It is a clinical diagnosis and does not require imaging for typical presentations.

Epidemiology

• Most common joint disease worldwide
• UK prevalence: ~8.75 million people with symptomatic OA
• Risk increases markedly with age (>50% of over 65s have radiographic evidence)
• F:M 2:1 (hand and knee OA); equal for hip OA
• Knee OA most common symptomatic site

Aetiology

• Primary (idiopathic): age-related, genetic predisposition
• Secondary: post-traumatic, obesity, joint instability, previous inflammatory arthritis, developmental abnormalities (DDH), metabolic (haemochromatosis, Wilson, acromegaly, CPPD)
• Risk factors: age >45, female sex, obesity (strongest modifiable risk factor), previous joint injury, occupational (kneeling, heavy lifting), family history, joint malalignment

Pathophysiology

• Not simply "wear and tear" – active biological process
• Cartilage: chondrocyte dysfunction → matrix degradation (MMPs, aggrecanases) → fibrillation, fissuring, loss
• Subchondral bone: sclerosis (increased density), cyst formation
• Osteophytes: new bone formation at joint margins (attempted repair)
• Synovium: secondary low-grade synovitis (unlike RA, this is secondary to cartilage debris)
• Ligament and muscle: laxity and wasting contribute to joint instability

Typical Features

• Joint pain: worse with activity, relieved by rest (mechanical pattern)
• Morning stiffness: <30 minutes (unlike RA which is >30-60 minutes)
• Reduced range of motion: progressive
• Joint crepitus: grating sensation on movement
• Bony enlargement: Heberden nodes (DIP), Bouchard nodes (PIP)
• Joint instability: giving way, particularly knees

Distribution

• Knees: most common symptomatic joint
• Hips: groin pain, reduced internal rotation
• Hands: DIP, PIP, 1st CMC (thumb base – "squaring")
• Spine: cervical and lumbar spondylosis
• 1st MTP: can mimic gout

Red Flags (Suggest Alternative Diagnosis)

• Significant morning stiffness >60 minutes → inflammatory arthritis
• Multiple joint swelling with systemic features → RA, SLE
• Rapid onset monoarthritis → septic arthritis, gout
• Joint pain with erythema, warmth, fever → infection

Clinical Diagnosis (NICE NG226)

• No investigations required for typical presentation (age ≥45, activity-related pain, ≤30 min morning stiffness)
• Investigations only to exclude other diagnoses

If Atypical Features

• X-ray: LOSS features (Loss of joint space, Osteophytes, Subchondral sclerosis/cysts)
• FBC, ESR/CRP: normal in OA (elevated = consider inflammatory arthritis)
• RF, anti-CCP: negative in OA
• Serum urate: if gout suspected
• Ferritin/transferrin saturation: if haemochromatosis suspected (OA in unusual joints)
• Joint aspiration: if acute monoarthritis (exclude sepsis/crystal arthropathy)

Imaging

• X-ray: not needed for diagnosis but useful if atypical or pre-surgical planning
• MRI: not routine; occasionally for soft tissue assessment pre-surgery
• Poor correlation between X-ray severity and symptoms

Non-pharmacological (First-Line – Most Important)

• Exercise: strengthening, aerobic, flexibility; most effective intervention (NICE NG226)
• Weight loss: 5-10% body weight reduces pain by 25-50% in knee OA
• Patient education: self-management support, Versus Arthritis resources
• Physiotherapy: tailored exercise programme
• Walking aids: stick (opposite hand to affected hip/knee)
• Footwear advice: shock-absorbing insoles
• Occupational therapy: aids, adaptations, joint protection

Pharmacological (NICE NG226)

• Topical NSAIDs (diclofenac gel): first-line pharmacological for knee/hand OA
• Oral NSAIDs (naproxen 250-500mg BD + PPI; ibuprofen 400mg TDS + PPI): short-term, lowest effective dose
  • Consider CV risk (avoid in heart failure, IHD)
  • COX-2 selective (etoricoxib 30-60mg) if traditional NSAIDs not tolerated
• Topical capsaicin cream: 0.025-0.075% QDS; adjunct for knee/hand
• Paracetamol: NICE NG226 no longer recommends as sole analgesic for OA (limited efficacy)
• Intra-articular corticosteroid injection: for acute flares (short-term benefit)
• Duloxetine 30-60mg: emerging evidence for chronic OA pain (off-label)

NOT recommended (NICE):

• Hyaluronic acid injections
• Glucosamine/chondroitin supplements
• Acupuncture
• Opioids (avoid long-term; limited benefit, significant harm)

Surgical

• Total joint replacement (hip/knee): when non-surgical measures exhausted and significant impact on quality of life
• Refer regardless of age, BMI, or smoking status (NICE)
• >90% prosthesis survival at 10 years for knee and hip
• Alternatives: osteotomy (younger patients with malalignment), arthroscopy (very limited role)

Referral Criteria

• Failure of conservative management with significant functional limitation → orthopaedics
• Diagnostic uncertainty → rheumatology
• Night pain, rest pain, significant impact on daily activities → consider surgical referral

• Progressive condition with no disease-modifying drugs available
• Many patients manage well with lifestyle modifications and analgesia
• Knee OA: 30-50% progress to severe disease requiring arthroplasty over 10-15 years
• Hip replacement: 95% survival at 10 years; 85% at 25 years (National Joint Registry data)
• Knee replacement: 95% survival at 10 years
• Cardiovascular risk: OA-related inactivity and NSAID use increase CV risk
• Obesity: single most important modifiable risk factor for both prevention and management

OA vs RA Comparison

Heberden and Bouchard Nodes