Osteoarthritis

Degenerative joint disease characterized by progressive cartilage loss, subchondral bone remodeling, osteophyte formation, and low-grade synovial inflammation, resulting from an imbalance between cartilage breakdown and repair. Most common form of arthritis, leading cause of disability in older adults.

Risk factors: age, obesity (mechanical load + metabolic/inflammatory contribution), female sex, joint malalignment, previous joint injury/trauma, occupational/repetitive joint loading, genetic predisposition, prior inflammatory arthritis.

Classified by:

• Primary (idiopathic): no identifiable underlying cause, associated with aging/wear

• Secondary: due to identifiable cause ; post-traumatic, inflammatory arthritis sequelae, metabolic (hemochromatosis, ochronosis), congenital/developmental joint abnormality, avascular necrosis

• Commonly affected joints: knees, hips, hands (DIP/PIP joints, first CMC joint), spine (facet joints), first MTP joint

• Joint pain: mechanical pattern ; worse with activity/weight-bearing, relieved by rest (distinguishes from inflammatory arthritis where rest worsens/morning stiffness prolonged)

• Morning stiffness: typically brief, <30 minutes (contrast with rheumatoid arthritis where morning stiffness >1 hour is characteristic)

• Reduced range of motion, crepitus on joint movement

• Joint examination findings:

• Bony swelling/enlargement (not soft/boggy synovitis as in inflammatory arthritis)

• Heberden's nodes (DIP joints), Bouchard's nodes (PIP joints) ; hand OA

• Fixed flexion deformity, varus/valgus deformity (knee OA)

• Reduced internal rotation (early sign, hip OA)

• Mild joint effusion possible but marked warmth/erythema atypical (suggests alternative/superimposed inflammatory process, e.g., crystal arthropathy)

• Functional impact: difficulty with stairs, walking distance, rising from chairs, fine motor tasks (hand OA)

• Progressive course, though pain severity does not always correlate with radiographic severity

Primarily clinical for typical presentation (age >45, activity-related pain, no/brief morning stiffness); imaging not always required to confirm diagnosis in classic cases (per NICE clinical diagnosis criteria).

• Plain radiographs (weight-bearing views for knee/hip): joint space narrowing, osteophytes, subchondral sclerosis, subchondral cysts; classic findings but severity doesn't always correlate with symptoms; useful to exclude other pathology or when diagnosis uncertain, or pre-surgical planning

• Blood tests: NOT required for diagnosis, generally normal (ESR/CRP normal or mildly elevated) ; used to exclude inflammatory arthritis if diagnostic uncertainty (rheumatoid factor, anti-CCP, ANA if inflammatory features present)

• Joint aspiration: if effusion present and diagnostic uncertainty : synovial fluid analysis (non-inflammatory, WCC <2000/mm³ typical in OA) helps exclude septic arthritis, crystal arthropathy (gout, pseudogout)

• MRI: not routine, reserved for specific indications (suspected meniscal/ligamentous injury, avascular necrosis, atypical presentation)

Differentials: rheumatoid arthritis and other inflammatory arthropathies (prolonged morning stiffness, symmetric small joint involvement, systemic symptoms, elevated inflammatory markers), gout/pseudogout (acute, monoarticular, marked erythema/warmth), septic arthritis (acute, hot, systemically unwell — exclude urgently if acute monoarticular presentation), avascular necrosis, referred pain (hip OA can present as knee pain).

Core/first-line (all patients):

• Patient education: nature of condition, self-management expectations

• Weight loss if overweight/obese (significant impact on symptom burden and disease progression, especially weight-bearing joints)

• Exercise: strengthening (particularly quadriceps for knee OA) and aerobic exercise ; improves pain and function, does NOT accelerate joint damage (address common patient misconception)

• Physiotherapy referral for individualized exercise program, gait aids assessment (cane, walking aids)

Pharmacological (symptom control, does not modify disease progression):

• Topical NSAIDs (diclofenac gel); first-line for knee/hand OA, particularly favored in older patients (fewer systemic effects)

• Oral NSAIDs: first-line if topical insufficient ; use lowest effective dose, shortest duration, with gastroprotection (PPI co-prescription) if risk factors (age, GI history, concurrent anticoagulant/steroid); caution in cardiovascular disease, renal impairment

• Paracetamol: modest efficacy alone per current evidence, may be used as adjunct but no longer considered strongly effective as monotherapy in current guidelines

• Topical capsaicin: adjunct option for localized joint pain

• Intra-articular corticosteroid injection: short-term symptom relief (weeks-months) for flares, particularly knee OA ; avoid frequent repeated injections (cartilage toxicity concern with excessive use)

• Intra-articular hyaluronic acid: evidence mixed/weak, not routinely recommended by major guidelines (e.g., NICE, AAOS) though used in some practice

• Duloxetine: option for chronic OA pain, particularly with central sensitization component

• Opioids: NOT recommended for routine use given poor risk-benefit in chronic non-cancer pain ; reserved for short-term severe flares awaiting definitive treatment, avoid long-term use

Surgical management (for severe disease refractory to conservative management, significant functional limitation/quality of life impact):

• Joint replacement (arthroplasty) ; knee/hip most common, highly effective for pain relief and function restoration

• Osteotomy: selected younger patients with malalignment, joint-preserving option

• Arthroscopic debridement/meniscectomy: limited role, not recommended for pure OA management (evidence does not support benefit over sham/conservative management in absence of mechanical locking symptoms)

Referral: orthopedics for surgical assessment when conservative management fails and significant functional impairment/pain persists; rheumatology if diagnostic uncertainty or inflammatory features present.