Osteoarthritis

The most common joint disease worldwide is often dismissed as 'just aging' — but confusing it with rheumatoid arthritis on the NCLEX will cost you the question every time.

Osteoarthritis (OA) is a degenerative, non-inflammatory joint disease caused by progressive breakdown of articular cartilage. It is NOT autoimmune — it results from mechanical wear and tear, often worsened by obesity, repetitive joint stress, and aging. Weight-bearing joints (knees, hips) and the DIP joints of the hands are most commonly affected. Pain worsens with activity and improves with rest — the opposite pattern of inflammatory arthritis. Morning stiffness is brief, typically lasting less than 30 minutes, resolving once the joint is moved. On assessment, you find crepitus (a grating sensation with movement), Heberden nodes (bony enlargements at DIP joints), and Bouchard nodes (at PIP joints). Joint enlargement is bony and hard, not the boggy swelling of RA. Lab values are characteristically normal — ESR, CRP, and rheumatoid factor are not elevated because OA lacks systemic inflammation. X-rays show joint space narrowing and osteophyte (bone spur) formation. Management is primarily conservative: weight reduction is the single most impactful non-pharmacologic intervention for knee OA. Acetaminophen is first-line for mild pain; NSAIDs are used for moderate symptoms but require GI and renal monitoring. Joint replacement (arthroplasty) is considered when conservative measures fail.

Key Distinctions

Don't confuse OA stiffness (<30 minutes, improves with movement) with RA stiffness (>1 hour, worse in morning). OA affects DIP joints; RA targets MCP and PIP joints symmetrically. OA labs are normal — if ESR or RF is elevated, think RA or another inflammatory condition, not OA. OA pain increases with use; gout pain is sudden, acute, and often nocturnal.

Clinical Pearl

Heberden = DIP = farther from the Hand. Bouchard = PIP = closer to the Body. Normal labs + crepitus + activity pain = OA, not RA.