Arthritis - osteoarthritis, generalised and regional
Description
- Whole-joint disease - cartilage, subchondral bone, synovium, capsule, ligament, periarticular muscle
- *Not "wear and tear"* - an active, low-grade inflammatory and metabolic process with failed repair
- Cardinal features: use-related pain, short-lived (<30 min) morning/inactivity stiffness, crepitus, bony enlargement, restricted movement
- Contrast inflammatory arthritis: >60 min stiffness, better with use, soft-tissue swelling
Patterns
- Nodal generalised OA - DIP (Heberden's nodes) and PIP (Bouchard's nodes), first carpometacarpal (thumb base), strongly female, familial
- Knee - medial tibiofemoral compartment most often -> varus deformity; patellofemoral
- Hip - superior pole most common; groin pain radiating to the knee
- Spine - facet joint OA, disc degeneration -> spinal stenosis
- Erosive (inflammatory) OA - interphalangeal joints, central "gull-wing" erosions, more pain and inflammation
- Secondary OA - the site is the clue
Joints characteristically SPARED in primary OA
- MCPs, wrists, elbows, shoulders, ankles
- *OA at these joints means look for a secondary cause*: haemochromatosis (MCP 2 and 3), CPPD, prior trauma, acromegaly, avascular necrosis, ochronosis, neuropathic joint
Epidemiology
- The commonest form of arthritis and the leading cause of chronic pain and disability in older Australians
- ~2.2 million Australians; radiographic OA in >50% over 65
- Commonest sites: knee > hand > hip
- Age is the dominant risk factor
- F>M, especially after menopause - women have ~2x the risk of bilateral knee OA
- Radiographic change correlates poorly with symptoms - ~50% of radiographic knee OA is asymptomatic, and symptomatic OA can have near-normal films
Aetiopathogenesis
Mechanism
- Chondrocyte phenotype shift -> inc MMPs and ADAMTS-5 (aggrecanase) -> proteoglycan and type II collagen loss
- IL-1beta, TNF-alpha from synovium and chondrocytes
- Cartilage fibrillation -> fissuring -> full-thickness loss -> eburnated bone
- Subchondral bone: sclerosis, cysts, bone marrow lesions (the MRI correlate of pain)
- Marginal osteophyte formation - attempted repair
- Low-grade synovitis and effusion
Risk factors
- Systemic
- Age - the strongest
- Female sex
- Obesity - OR ~2.4 (overweight ~1.35); each 2-unit BMI rise -> ~36% inc knee OA risk
- Metabolic as well as mechanical: obesity also increases hand OA risk
- Genetic - substantial for nodal hand OA and hip OA
- Inverse relationship with osteoporosis - high BMD increases OA risk
- Local / mechanical
- Prior joint injury - meniscal tear, ACL rupture, intra-articular fracture
- Malalignment - varus/valgus at the knee
- Quadriceps weakness and proprioceptive deficit
- Developmental hip dysplasia - the commonest cause of premature hip OA; also FAI, Perthes, SUFE
- Occupational
- Squatting >30 min/day OR ~6.9; kneeling >30 min/day OR ~3.4; >10 flights of stairs/day OR ~2.7
- Obesity + occupational bent-knee work: OR ~14.7
- Farming (hip), construction, heavy manual work
- Activity
- Repetitive high-impact exercise increases risk in a normal joint
- In an already abnormal joint, even low-impact recreational activity increases risk
Secondary causes
- Metabolic: haemochromatosis, ochronosis (alkaptonuria), Wilson disease, acromegaly, gout, CPPD
- Endocrine: hyperparathyroidism, hypothyroidism, diabetes
- Structural: dysplasia, prior fracture, meniscectomy, Paget disease
- Inflammatory: any prior inflammatory or septic arthritis
- Neuropathic (Charcot) joint
- Avascular necrosis, haemophilic arthropathy
Diagnosis
- Clinical diagnosis - no investigation is required in a typical older patient
Clinical criteria
- Age >=45, activity-related joint pain, morning stiffness <30 min or absent
- No systemic features, no prolonged stiffness, no warmth or soft-tissue swelling
Hand examination
- DIP > PIP > 1st CMC involvement, with MCP SPARING
- Heberden's (DIP) and Bouchard's (PIP) nodes - bony, not soft
- Squaring of the thumb base, crepitus, reduced ROM
- *Absent: erythema, warmth, rheumatoid nodules, tophi, psoriatic plaques* - the discriminators
Differential
| Discriminator | |
|---|---|
| Psoriatic arthritis | Also hits DIPs, but skin/nail psoriasis, dactylitis, pencil-in-cup erosions, enthesitis |
| Rheumatoid arthritis | MCP/PIP with DIP sparing, soft swelling, prolonged stiffness, RF/anti-CCP |
| Crystal arthritis | Usually monoarticular, acute, erythematous |
| Erosive OA | Central gull-wing erosions vs marginal in RA/PsA |
Radiographs - "LOSS"
- L - Loss of joint space (focal/asymmetrical - contrast the uniform loss of RA)
- O - Osteophytes
- S - Subchondral sclerosis
- S - Subchondral cysts (geodes)
- Also: bone attrition/altered contour, soft tissue swelling
- Weight-bearing views for knee and hip - non-weight-bearing films underestimate joint space loss
- X-ray is for excluding alternatives and planning surgery, not for diagnosis - severity correlates poorly with symptoms
Laboratory
- ESR, CRP, RF, ANA normal - order them only to exclude an inflammatory arthritis, not to diagnose OA
- Synovial fluid: non-inflammatory, WCC <2000/mm3, clear/viscous
- Screen for secondary causes if young, atypical distribution (MCP, wrist, shoulder, ankle), or rapidly progressive: ferritin/transferrin saturation, calcium, PTH, TSH, urate
MRI
- Not routine. Shows bone marrow lesions (correlate with pain and progression), cartilage loss, meniscal pathology
- Incidental meniscal tears are near-universal in OA knees and are not an indication for arthroscopy
Management
Axis: core therapy for everyone, then add pharmacological and interventional layers by response. No treatment alters structural progression.
A. Core therapy - offered to every patient
- Education and self-management - the natural history is not relentless deterioration; say so
- Exercise - the single most effective intervention
- Aerobic + resistance training; quadriceps strengthening for knee OA; tai chi; range-of-motion programmes
- Land-based exercise gives pain relief and functional improvement persisting 2-6 months after stopping
- Knee OA responds better than hip OA
- The type of exercise matters far less than adherence
- Weight loss if overweight
- Proven for knee OA; evidence lacking for hip OA
- ADAPT trial: exercise + diet (~5.7% weight loss) improved pain, function and physical performance beyond either alone
- Target >=5-10% loss
- Walking aid (stick in the contralateral hand), footwear, activity pacing, workplace modification
B. Pharmacological - for pain
- Topical NSAID - first-line drug for knee and hand OA; minimal systemic exposure, preferred in the elderly
- Oral NSAID - the most effective oral analgesic; lowest effective dose, shortest duration
- Choice by comorbidity: non-selective for isolated knee OA without comorbidity; COX-2 selective if GI risk; avoid in CKD, heart failure, established CVD
- PPI cover if GI risk factors
- *Paracetamol has little benefit as monotherapy* - effect size close to zero; may be used as an adjunct
- Duloxetine - for pain refractory to NSAIDs, or where NSAIDs are contraindicated
- Start 30 mg, titrate to 60-90 mg daily; ~1.5x the chance of a 30-50% pain reduction
- Particularly useful with widespread pain or centralised sensitisation
- Tramadol - small additional benefit; significant harms in the elderly - falls, delirium, hyponatraemia
- *Avoid strong opioids* - no meaningful benefit over NSAIDs in OA, substantial harm
- Intra-articular corticosteroid
- For hip/knee OA refractory to oral and topical therapy
- Moderate short- to medium-term relief only (weeks); a 2017 saline-controlled trial found no benefit over saline, and the placebo effect is large
- Repeated injections associated with cartilage loss - limit frequency
C. Not recommended
- Glucosamine and chondroitin - Cochrane 2015: statistically significant but clinically trivial effect in trials <6 months
- Intra-articular hyaluronate (viscosupplementation)
- Acupuncture
- Platelet-rich plasma, stem cell injection
- Arthroscopic lavage and debridement, and partial meniscectomy for degenerative tears - no benefit over sham or physiotherapy
- Bisphosphonates - oral risedronate: no effect on pain or radiographic progression; IV zoledronic acid reduces knee pain and bone marrow lesions at 12 months but does not prevent cartilage loss
D. Surgical
- Joint replacement - the definitive treatment
- Indication: persistent pain and functional limitation despite adequate non-surgical management, and pain affecting sleep or quality of life - not radiographic severity
- Do not defer to the point of severe deconditioning; pre-operative physiotherapy improves outcome
- Osteotomy in young patients with unicompartmental disease and malalignment
- Trapeziectomy for thumb base OA
- Joint fusion for ankle/wrist
E. Comorbidity
- Manage cardiovascular risk (OA limits exercise capacity and shares metabolic risk factors)
- Falls assessment, sleep, mood, chronic pain support
Associations
- Obesity and metabolic syndrome
- Type 2 diabetes, hypertension, dyslipidaemia
- Inverse association with osteoporosis - high BMD, low fracture risk at the hip
- CPPD - chondrocalcinosis frequently coexists, and CPPD produces OA in an atypical distribution
- Haemochromatosis (2nd and 3rd MCPs, hook-like osteophytes), acromegaly, ochronosis
- Depression, sleep disturbance, social isolation
- Falls and fragility fracture (from pain, weakness and analgesic side effects)
- Sarcopenia and deconditioning
Natural history & complications
- Slowly progressive but highly variable - many joints stabilise or improve symptomatically
- Pain fluctuates and correlates poorly with radiographic change
- Hip OA generally progresses faster than knee OA
- No disease-modifying therapy exists - all current treatment is symptomatic
Mortality
- Radiographic knee OA: ~3x cardiovascular mortality and ~2x all-cause mortality; effect greater when symptomatic
- Hand OA carries no such excess
- Mediated by reduced physical activity, obesity and NSAID exposure
Complications
- Chronic pain, functional dependence, work disability
- Muscle wasting and deconditioning -> falls
- NSAID toxicity: GI bleeding, AKI, hypertension, cardiovascular events - the commonest iatrogenic harm in this population
- Deformity (varus knee, fixed flexion), secondary lumbar and contralateral joint pain
- Perioperative complications, prosthetic infection and loosening after arthroplasty
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