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Define osteoarthritis (OA).
Degenerative joint disease characterised by progressive loss of articular cartilage, subchondral bone remodelling, osteophyte formation, and synovial inflammation leading to pain and functional limitation.
Which joints are most commonly affected in OA?
Weight-bearing joints (knees, hips, spine), hands (DIP, PIP, 1st CMC), and feet (1st MTP). MCP joints are spared.
Pathophysiology of OA?
Mechanical stress + biochemical degradation → chondrocyte injury → ↑ matrix metalloproteinases (MMPs), ↓ type II collagen synthesis → cartilage loss + bone sclerosis + osteophytes.
List modifiable and non-modifiable risk factors for OA.
Modifiable: obesity, joint injury, occupational stress. Non-modifiable: age, female sex, genetics, congenital malalignment.
Describe radiographic features of OA.
Joint space narrowing (asymmetric), osteophyte formation, subchondral sclerosis, subchondral cysts. No periarticular osteopenia (cf. RA).
Clinical features of OA.
Pain worse with activity, relieved by rest; morning stiffness <30 min; bony swelling; crepitus; restricted ROM; Heberden (DIP) and Bouchard (PIP) nodes.
Differentiate OA from rheumatoid arthritis (RA).
OA: asymmetric, non-inflammatory, <30 min stiffness, DIP involved, negative RF/CCP. RA: symmetric, inflammatory, >60 min stiffness, MCP/PIP involved.
Role of MRI in OA.
Not routinely required. Used for differential diagnosis (AVN, meniscal tear, stress fracture) or early OA detection before radiographic changes.
Initial management of OA.
Education, weight loss, exercise (quad strengthening, aerobic), physiotherapy, simple analgesia (paracetamol), topical NSAIDs, heat/cold therapy.
Second-line pharmacologic therapy.
Oral NSAIDs ± PPI cover, intra-articular corticosteroids for flare, duloxetine (chronic pain), topical capsaicin. Avoid opioids long-term.
Surgical indications in OA.
Severe pain/disability despite maximal therapy, significant functional limitation, radiographic evidence of joint destruction.
Describe the role of joint replacement in OA.
Total joint arthroplasty relieves pain and restores function. Most effective for end-stage knee and hip OA; lifespan ~15–20 years.
Which pharmacologic agents are NOT recommended for OA?
Glucosamine/chondroitin (no consistent evidence), hyaluronic acid injections (minimal benefit), systemic steroids (no role).
What is erosive OA?
Inflammatory subset of hand OA affecting DIP/PIP joints with central erosions (‘gull-wing’ deformities). Middle-aged women; may respond to hydroxychloroquine.
Biochemical findings in OA.
Normal inflammatory markers (ESR, CRP). Synovial fluid: non-inflammatory (WCC <2000/mm³).
OA vs CPPD (pseudogout) overlap.
CPPD can mimic OA but often involves atypical joints (MCP, wrist). Radiograph: chondrocalcinosis. Synovial fluid: rhomboid, weakly positive birefringent crystals.
Explain knee OA subtypes.
Medial compartment → varus deformity; Lateral → valgus deformity; Patellofemoral → anterior knee pain, worse on stairs.
Practice-changing evidence for exercise therapy in OA.
2023 Cochrane review: structured exercise (≥12 weeks) improves pain/function equivalent to oral NSAIDs; cornerstone of long-term management.
Australian PBS nuance for OA pharmacotherapy.
No PBS subsidy for duloxetine unless major depressive disorder; intra-articular corticosteroids PBS-listed for large joints; biologics not indicated.
Key exam pearls.
Morning stiffness <30 min; asymmetrical; absence of systemic symptoms; no synovitis; DIP involvement; bony-hard swellings; x-ray features mnemonic: LOSS (Loss of space, Osteophytes, Sclerosis, Subchondral cysts).