Key Facts

Osteoarthritis is a clinical syndrome characterised by joint pain, stiffness, and functional limitation due to progressive loss of articular cartilage. It is the most common form of arthritis and a major cause of disability. Primary care management focuses on self-management, exercise, and analgesia.

Epidemiology

• Affects approximately 8.75 million people in the UK
• Knee OA: most common; hip OA: second most common
• Prevalence increases with age: >30% of adults aged >60 have radiographic knee OA
• More common in women (especially hand and knee OA) after age 50

Aetiology

• Primary (idiopathic): multifactorial — age, genetic predisposition, obesity, mechanical overload
• Secondary: previous joint injury, inflammatory arthritis, metabolic disease (haemochromatosis), developmental abnormality (hip dysplasia), avascular necrosis
• Risk factors: age >45, female sex, obesity (strongest modifiable risk factor — 2-3× risk for knee OA), previous joint injury, occupational overuse, family history

Pathophysiology

• Progressive loss of articular cartilage with concurrent bone remodelling
• Chondrocyte-mediated degradation of cartilage matrix (collagen and proteoglycans)
• Subchondral bone sclerosis, osteophyte formation, synovial inflammation
• Whole joint disease: involves cartilage, bone, synovium, capsule, ligaments, and periarticular muscles
• Not purely 'wear and tear' — active inflammatory and metabolic processes contribute

Typical Features (NICE NG226)

• Age ≥45 years
• Activity-related joint pain (worse with use, better with rest)
• Morning stiffness lasting <30 minutes (or no morning stiffness)
• Intermittent symptoms with good and bad days
• Insidious onset over months to years

Common Joint Involvement

• Knee: medial compartment most common; varus deformity
• Hip: groin pain, reduced internal rotation
• Hand: DIP joints (Heberden nodes), PIP joints (Bouchard nodes), first CMC joint (thumb base)
• Spine: cervical and lumbar spondylosis

Examination Findings

• Bony enlargement of joint margins
• Crepitus on movement
• Restricted range of motion
• Joint effusion (particularly knee)
• Muscle wasting around affected joint
• Malalignment (varus/valgus)

Red Flags

• Hot, red, swollen joint — consider septic arthritis, gout, pseudogout
• Systemic symptoms (fever, weight loss) — consider infection or malignancy
• Prolonged morning stiffness >60 minutes — consider inflammatory arthritis (RA)
• Rapid onset or young patient — investigate for secondary causes
• Locked joint — loose body, meniscal tear

Bedside

• Clinical assessment is sufficient for diagnosis in typical presentations (NICE NG226)
• Assess functional impact and quality of life

Bloods

• Not required for diagnosis in typical OA
• If inflammatory arthritis suspected: ESR, CRP, RF, anti-CCP
• If gout suspected: serum urate (may be normal in acute attack)

Imaging

• Not required for diagnosis in typical clinical presentation (NICE NG226)
• X-ray features (when obtained): joint space narrowing, osteophytes, subchondral sclerosis, subchondral cysts
• X-ray may be useful if: atypical features, diagnostic uncertainty, pre-surgical planning
• MRI: rarely needed; may be useful for assessment of internal derangement

Special Tests

• Joint aspiration: if effusion present — to exclude septic arthritis, crystal arthropathy
• Synovial fluid in OA: clear, viscous, WCC <2,000/mm³

Non-pharmacological (NICE NG226 — core treatments for all patients)

• Exercise: combination of strengthening, aerobic fitness, and flexibility exercises (most important intervention; equivalent to NSAIDs in clinical trials)
• Weight loss: if BMI >25; every 1kg loss reduces knee joint load by 4kg; recommend 5-10% body weight reduction
• Education and self-management: understanding of condition, pacing activities, joint protection
• Walking aids: if mobility impaired
• Suitable footwear: shock-absorbing, supportive
• Occupational therapy: for hand OA (splinting, aids)
• Thermotherapy: heat or cold packs for symptom relief

Pharmacological

Topical treatments (first-line for knee and hand OA):

• Topical NSAIDs: diclofenac gel (Voltarol) or ibuprofen gel — apply TDS-QDS
• Topical capsaicin 0.025%: for hand and knee OA (takes 2-4 weeks for effect)

Oral analgesics:

• Paracetamol 1g QDS: limited evidence of benefit but still used; NICE NG226 does not recommend as first-line
• Oral NSAIDs (ibuprofen 400mg TDS, naproxen 250-500mg BD): at lowest effective dose for shortest duration; always co-prescribe PPI (omeprazole 20mg OD); assess CV, GI, renal risk first
• Avoid long-term opioids: NICE NG226 advises against for OA
• Duloxetine 30-60mg OD may be considered for persistent pain (off-label)

Intra-articular injections:

• Corticosteroid injection (triamcinolone 40mg + lidocaine 1%): for acute flare; benefit lasts 4-8 weeks; avoid repeated injections (limit to 3-4/year)
• Hyaluronic acid injections: not recommended by NICE

NOT recommended by NICE NG226:

• Glucosamine, chondroitin
• Acupuncture, TENS (insufficient evidence for OA)
• Rubefacients

Surgical

• Total joint replacement (knee/hip): consider referral when conservative management fails and OA significantly impacts quality of life and function
• Arthroscopic washout/debridement: not recommended (no benefit; NICE NG226)

Referral Criteria

• Persistent symptoms despite optimised conservative management: orthopaedic referral for joint replacement assessment
• Diagnostic uncertainty: rheumatology referral
• Younger patients (<50) with significant OA: specialist assessment for secondary causes

• OA is a chronic, progressive condition; rate of progression varies considerably
• Knee replacement: >90% patient satisfaction at 1 year; 95% implant survival at 15 years
• Hip replacement: >95% implant survival at 15 years
• Weight loss of 5-10% can reduce pain scores by 25-50% in knee OA
• Exercise programmes reduce pain by 25-30% (comparable to NSAIDs)
• OA increases cardiovascular mortality risk by 20-30% (partly due to physical inactivity and NSAID use)
• Not all OA is progressive: 33-50% of patients with knee OA may stabilise or improve over time

X-ray Changes in OA (LOSS Mnemonic)

NICE NG226 Management Summary