Musculoskeletal · PANCE / PANRE

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

Comparison of osteoarthritis vs rheumatoid arthritis — the highest-yield differentiation on PANCE.

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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Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants.