Osteoarthritis (OA)
Non-inflammatory degenerative joint disease driven by progressive articular cartilage loss.
Also known as: OA, degenerative joint disease, DJD, osteoarthrosis
Overview
Chronic degenerative joint disease characterized by progressive loss of articular cartilage, subchondral bone remodeling, osteophyte formation, and mild synovitis. Most commonly affects weight-bearing joints (knee, hip), the hand DIP/PIP and first CMC joints, and the cervical and lumbar spine.
Epidemiology
Most prevalent form of arthritis worldwide. Prevalence rises sharply after age 50; women > men after menopause. Symptomatic knee OA affects ~10% of US adults over 60.
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Risk factors
- Age >50
- Female sex (especially hand and knee OA)
- Obesity (knee, hip)
- Prior joint injury, surgery, or intra-articular fracture (post-traumatic OA)
- Repetitive occupational or athletic loading
- Genetic predisposition (familial hand OA)
- Joint malalignment (varus/valgus), congenital hip dysplasia
- Metabolic/endocrine: hemochromatosis, acromegaly, alkaptonuria (secondary OA)
Pathophysiology
Imbalance between cartilage matrix synthesis and degradation, driven by matrix metalloproteinases and pro-inflammatory cytokines (IL-1, TNF). Cartilage softens, fibrillates, and erodes. The underlying subchondral bone responds with sclerosis, cyst formation, and marginal osteophytes. Low-grade synovial inflammation contributes to pain but is qualitatively different from autoimmune arthritis.
Clinical presentation
Symptoms
- Insidious joint pain worse with activity and improved by rest
- Brief morning stiffness (<30 minutes) and gel phenomenon after inactivity
- Reduced range of motion, crepitus, functional limitation
- Knee: medial joint-line pain, buckling, difficulty with stairs
- Hip: groin pain referred to thigh or buttock, limp
- Hand: pain and bony enlargement at DIP (Heberden) and PIP (Bouchard) nodes; first CMC squaring
Signs / physical exam
- Bony enlargement, crepitus, tenderness at joint line
- Cool joint without significant warmth or erythema
- Restricted ROM, antalgic gait
- Mild effusion possible but lacking the boggy synovitis of RA
Classic findings
Heberden nodes (DIP) and Bouchard nodes (PIP); squared first CMC joint; medial knee joint-line tenderness.
Differential diagnosis
- Rheumatoid arthritis — Symmetric MCP/PIP/wrist involvement, prolonged morning stiffness (>1 h), constitutional symptoms, positive RF/anti-CCP, elevated ESR/CRP
- Psoriatic arthritis — DIP involvement with psoriasis or nail pitting, dactylitis, enthesitis; can mimic hand OA
- Gout / pseudogout — Acute monoarticular attacks with warmth and erythema; crystals on arthrocentesis
- Septic arthritis — Acute monoarticular pain with fever and effusion; arthrocentesis with WBC >50,000 mandatory to exclude
- Hemochromatosis arthropathy — MCP 2/3 involvement (handshake sign), hook-like osteophytes, elevated ferritin/transferrin saturation
- Avascular necrosis (hip) — Groin pain with restricted internal rotation; crescent sign on plain film; MRI sensitive
- Bursitis / tendinopathy — Periarticular tenderness without true joint-line pain; preserved passive ROM
Diagnostic workup
Diagnostic criteria
ACR clinical criteria for knee OA: knee pain plus at least 3 of: age >50, stiffness <30 min, crepitus, bony tenderness, bony enlargement, no palpable warmth. Radiographic hallmarks (Kellgren-Lawrence): joint-space narrowing, subchondral sclerosis, subchondral cysts, marginal osteophytes.
Labs
- Generally not required for diagnosis when classic clinical and radiographic features present
- ESR, CRP, RF, anti-CCP, ANA only if inflammatory arthritis suspected (should be normal or negative in OA)
- Arthrocentesis only when effusion present and inflammatory or septic process must be excluded — OA fluid is non-inflammatory (WBC <2000, clear/straw-colored)
Imaging
- Weight-bearing plain radiographs of the affected joint — first-line
- MRI reserved for atypical presentations, suspected meniscal or ligamentous injury, or possible avascular necrosis
- Ultrasound can detect effusion and osteophytes but is not routinely needed
Diagnostic algorithm
| Feature | Osteoarthritis | Rheumatoid arthritis |
|---|---|---|
| Onset | Insidious, older age | Subacute, 30-50 yo (any age) |
| Joint pattern | DIP, PIP, 1st CMC, knees, hips, spine | MCP, PIP, wrists; symmetric |
| Morning stiffness | <30 min | >1 hour |
| Symptom pattern | Worse with activity, better with rest | Better with activity, worse after rest |
| Systemic symptoms | Absent | Fatigue, low-grade fever, weight loss |
| Inflammatory markers | Normal | Elevated ESR/CRP |
| Serology | Negative | RF and/or anti-CCP often positive |
| Synovial fluid WBC | <2000 (non-inflammatory) | 2000-50,000 (inflammatory) |
| Radiographs | Joint-space narrowing, osteophytes, subchondral sclerosis | Periarticular osteopenia, marginal erosions, symmetric joint-space loss |
Treatment
First-line
- Patient education and self-management programs
- Exercise: low-impact aerobic, strengthening (quadriceps for knee OA), aquatic therapy
- Weight loss (5-10% body weight) for knee or hip OA in overweight patients
- Topical NSAIDs (diclofenac gel) — preferred initial pharmacotherapy for hand and knee OA
- Acetaminophen up to 3 g/day (modest benefit, useful when NSAIDs contraindicated)
- Oral NSAIDs — ibuprofen, naproxen, meloxicam (lowest effective dose, shortest duration; add PPI if GI risk)
Second-line / adjunct
- Intra-articular corticosteroid injection (triamcinolone, methylprednisolone) — short-term relief for flares; limit to 3-4 per joint per year
- Duloxetine — adjunct for chronic knee OA pain, particularly with comorbid depression or widespread pain
- Topical capsaicin — adjunct for hand or knee OA
- Tramadol — limited role; reserve for patients who cannot tolerate NSAIDs and have failed other measures
- Intra-articular hyaluronic acid — conditional, not recommended by 2019 ACR for knee or hip
- Avoid chronic opioids — no long-term benefit and substantial harm
Complications
- Progressive functional decline, falls
- Sleep disturbance, depression, chronic opioid exposure (iatrogenic)
- Secondary muscle atrophy and deconditioning
- Joint deformity (varus knee, fixed flexion of hip)
- Perioperative complications of arthroplasty: infection, DVT/PE, periprosthetic fracture
PANCE pearls
- Morning stiffness <30 minutes and pain that worsens through the day with activity favor OA over RA.
- First CMC squaring and Heberden/Bouchard nodes are pathognomonic for primary hand OA.
- ACR conditionally recommends AGAINST glucosamine, chondroitin, hydroxychloroquine, methotrexate, TNF inhibitors, and stem cell injections for OA.
- If a patient with presumed OA develops a hot, swollen joint, perform arthrocentesis — superimposed gout, pseudogout, or septic arthritis can occur.
References
- ACR/AF 2019 — 2019 American College of Rheumatology/Arthritis Foundation Guideline for the Management of Osteoarthritis of the Hand, Hip, and Knee (Kolasinski et al., Arthritis Care Res 2020)
- OARSI 2019 — OARSI Guidelines for the Non-Surgical Management of Knee, Hip, and Polyarticular Osteoarthritis (Bannuru et al., Osteoarthritis Cartilage 2019)
- AAOS 2021 — AAOS Clinical Practice Guideline: Management of Osteoarthritis of the Knee (Non-Arthroplasty), 3rd ed.
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