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Osteoarthritis

SNOMED: 160414002952 wordsUpdated 03/03/2026
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Exam Tips

  • In UK exams, OA is usually a clinical diagnosis in patients aged 45+ with activity-related pain and morning stiffness <=30 minutes; routine X-ray is not mandatory.
  • Differentiate from inflammatory arthritis: prolonged morning stiffness, marked synovitis, and systemic features suggest an alternative diagnosis.
  • Knee OA pain pattern helps localisation: medial tibiofemoral (anteromedial), lateral tibiofemoral (anterolateral), patellofemoral (anterior pain on stairs/descending).
  • Hip OA classically causes groin pain and painful loss of internal rotation before flexion loss.
  • Hand OA signs to spot in OSCEs: Heberden nodes (DIP), Bouchard nodes (PIP), and thumb CMC squaring (see hand-joint surface anatomy/radiograph figure reference).
  • Always mention NSAID safety (GI, renal, cardiovascular risk) and co-prescribing a PPI when using oral NSAIDs.

Definition

Osteoarthritis is a chronic disorder of synovial joints in which mechanically and biologically driven joint tissue damage triggers an imperfect repair response. This leads to progressive structural change (cartilage loss, subchondral bone remodelling, osteophyte formation, and variable synovitis) with activity-related pain, short-lived morning stiffness, and functional limitation; any synovial joint can be affected, most commonly knee, hip, and hand.

Pathophysiology

OA is a whole-joint disease rather than isolated 'wear and tear' of cartilage. Repetitive mechanical stress and genetic susceptibility alter chondrocyte behaviour, increasing catabolic mediators (for example IL-1beta/TNF-alpha signalling, matrix metalloproteinases, and aggrecanases) and reducing effective matrix repair, causing cartilage fibrillation and joint-space loss. Subchondral bone then undergoes sclerosis and cyst formation, marginal osteophytes develop at joint edges, and low-grade synovitis contributes to pain flares. Pain arises mainly from innervated structures (synovium, capsule, subchondral bone, periarticular muscle), which explains discordance between radiographic severity and symptoms.

Risk Factors

  • Increasing age (especially over 45 years)
  • Female sex
  • Overweight and obesity
  • Previous joint injury (for example ligament injury, fracture, meniscal injury)
  • Repetitive occupational loading (kneeling, squatting, heavy lifting, prolonged standing)
  • High-load sports exposure or repetitive microtrauma
  • Muscle weakness and joint laxity
  • Joint malalignment (varus/valgus knee, leg length discrepancy, developmental hip morphology)
  • Family history/genetic predisposition
  • Coexisting inflammatory arthropathy or prior joint disease

Clinical Features

Symptoms

  • Activity-related joint pain with gradual onset over months to years
  • Morning stiffness absent or typically less than or equal to 30 minutes
  • Intermittent flares: sudden worsening for at least 24 hours, often lasting several days
  • Functional limitation (stairs, walking distance, grip/pinch, dressing, driving)
  • Knee OA: anterior/anteromedial pain, worse on stairs or inclines, pain after prolonged sitting
  • Hip OA: deep groin pain with possible referral to thigh, buttock, knee, or occasionally ankle
  • Hand OA: thumb-base pain, pain with pinch/grip, reduced dexterity

Signs

  • Bony enlargement and deformity (including Heberden and Bouchard nodes; see hand OA figure reference)
  • Crepitus and painful restricted range of movement
  • Joint line tenderness; small to moderate effusion (especially knee)
  • Varus or valgus knee malalignment in advanced disease
  • Muscle wasting/weakness (for example quadriceps or gluteal weakness)
  • Antalgic or Trendelenburg gait in advanced lower-limb disease
  • Thumb CMC squaring/subluxation in advanced hand OA (see thumb-base OA figure reference)

Investigations

Clinical diagnosis (primary care):In people aged 45 years or over with typical activity-related pain and short morning stiffness, OA is usually diagnosed clinically without routine imaging.
Plain radiograph of affected joint (if atypical features, diagnostic doubt, or pre-operative planning):Non-uniform joint-space narrowing, marginal osteophytes, subchondral sclerosis, and subchondral cysts.
Inflammatory blood tests (ESR/CRP, +/- RF/anti-CCP if inflammatory arthritis suspected):Usually normal in uncomplicated OA; raised inflammatory markers suggest alternative diagnoses.
Joint aspiration (if hot swollen joint or acute severe flare):Used to exclude septic arthritis and crystal arthropathy (microscopy, Gram stain, culture, crystal analysis).

Management

Lifestyle Modifications

  • Explain OA as a treatable long-term condition with fluctuating symptoms; support self-management and flare plans.
  • Structured therapeutic exercise (strengthening + aerobic + range-of-motion) for all patients regardless of age.
  • Weight reduction when overweight/obese to reduce pain and load on weight-bearing joints.
  • Activity pacing, footwear advice, walking aids, and occupational therapy input for function.
  • Physiotherapy for muscle strengthening, gait training, and joint-specific rehabilitation.
  • Psychological and sleep support when chronic pain, low mood, or poor sleep coexist.

Pharmacological Treatment

Topical NSAIDs (first-line for localised peripheral OA, especially knee/hand)

  • Diclofenac 1.16% gel: apply 2-4 g to affected joint 3-4 times daily (maximum 32 g/day from all sites)
  • Ibuprofen 5% gel: apply thin layer up to three times daily (product-specific maximum daily amount)

Lower systemic risk than oral NSAIDs; still caution in NSAID hypersensitivity, aspirin-sensitive asthma, active skin lesions, and concurrent oral NSAID overuse.

Oral NSAIDs (if topical treatment insufficient)

  • Naproxen 250-500 mg twice daily with food
  • Ibuprofen 400 mg three times daily (max 2.4 g/day)

Use lowest effective dose for shortest duration and co-prescribe gastroprotection (for example omeprazole 20 mg once daily). Avoid/caution in CKD, heart failure, uncontrolled hypertension, established cardiovascular disease, peptic ulcer disease, anticoagulation, and late pregnancy.

Simple analgesic

  • Paracetamol 1 g up to four times daily (maximum 4 g/day)

May provide modest benefit; avoid unintentional overdose from combination products and reduce maximum dose in low body weight/frailty or liver disease.

Intra-articular corticosteroid (for painful flare or significant inflammatory component)

  • Triamcinolone acetonide 40 mg intra-articular single dose
  • Methylprednisolone acetate 40 mg intra-articular single dose

Provides short-term pain relief; exclude joint infection first. Use aseptic technique and caution in diabetes (transient hyperglycaemia) and in frequent repeat injections.

Opioids (reserve, short-term, when other options unsuitable)

  • Codeine phosphate 30-60 mg every 4-6 hours when required (maximum 240 mg/day)

Not routine long-term OA therapy. Counsel on constipation, sedation, falls risk, dependence, and driving impairment; avoid strong opioids unless specialist-led.

Surgical / Interventional

  • Total knee replacement for severe symptomatic knee OA refractory to optimal conservative treatment
  • Total hip replacement for severe symptomatic hip OA with major pain/disability
  • Unicompartmental knee replacement in selected unicompartment disease
  • Corrective osteotomy in selected younger patients with malalignment
  • Joint fusion or selected hand procedures in advanced painful hand OA when function is severely affected

Complications

  • Progressive pain and chronic pain sensitisation
  • Reduced mobility and physical deconditioning
  • Loss of independence in activities of daily living
  • Falls risk (especially knee/hip OA with weakness or instability)
  • Joint deformity (for example Heberden/Bouchard nodes, thumb-base deformity, varus knee)
  • Sleep disturbance, anxiety, depression, reduced quality of life
  • Work limitation and social participation restriction

Prognosis

OA is heterogeneous and not inevitably progressive; many patients have fluctuating symptoms with intermittent flares. Hand interphalangeal OA often settles symptomatically over time, while thumb-base and hip OA more often cause persistent disability, and a substantial subset with hip or knee disease eventually require joint replacement. Prognosis is influenced by joint site, obesity, biomechanics, pain severity, and comorbidity burden.

Sources & References

NICE Guidelines(1)

📖Textbook References(8)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1124)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1124)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 876)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 512)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 530)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 512, 513)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 511, 512)[context]
  • [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 529, 530)[context]

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