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RISK FACTORS	Age over 50, female sex, obesity, prior joint injury or surgery, repetitive occupational joint stress, family history, joint malalignment
ETIOLOGY	Progressive degeneration of articular cartilage with secondary bony remodeling; not primarily inflammatory
PATIENT PRESENTATION	Gradual onset of joint pain that worsens with activity and improves with rest; brief morning stiffness lasting less than 30 minutes
CLASSIC PHYSICAL EXAM	Heberden nodes (DIP joints), Bouchard nodes (PIP joints), bony enlargement, crepitus on passive motion, decreased range of motion; absence of warmth, erythema, or soft tissue swelling
KEY DIAGNOSTIC RESULTS	X-ray: asymmetric joint space narrowing, osteophytes, subchondral sclerosis, subchondral cysts; normal inflammatory markers (ESR, CRP); synovial fluid WBC below 2,000 cells per mm³
MANAGEMENT	Non-pharmacologic therapy first (exercise, weight loss); topical or oral NSAIDs; intra-articular corticosteroid injections for flares; total joint arthroplasty for refractory end-stage disease
KEYWORDS	"Pain worse with use," "improves with rest," "morning stiffness less than 30 minutes," "Heberden nodes," "Bouchard nodes," "osteophytes," "joint space narrowing," "crepitus," "bony enlargement"

1. Pathophysiology

Osteoarthritis is fundamentally a disease of progressive articular cartilage degradation combined with a failure of the chondrocyte repair response. It is the most common form of arthritis worldwide and the leading cause of chronic disability in older adults. Understanding its mechanism is essential because every symptom and exam finding tested on vignettes maps directly to the underlying cartilage and bone pathology.

Normal articular cartilage is composed of type II collagen and proteoglycans (primarily aggrecan), which trap water and provide a smooth, compressible surface for load-bearing. In osteoarthritis, the balance between cartilage synthesis and degradation shifts toward destruction. Matrix metalloproteinases (MMPs) and aggrecanases produced by chondrocytes and synovial cells break down the collagen-proteoglycan framework faster than it can be rebuilt. The cartilage loses its water content, becomes thin and fibrillated, and eventually erodes down to the subchondral bone.

Once the cartilage is lost, the subchondral bone is exposed to direct mechanical stress. The bone responds in two ways. First, it undergoes sclerosis (thickening and hardening) directly beneath the eroded cartilage surface, which accounts for the subchondral sclerosis seen on X-ray. Second, microfractures in the sclerotic bone allow synovial fluid to be forced into the marrow space, forming subchondral cysts. At the joint margins, new bone growth occurs as the body attempts to stabilize the joint and redistribute load. These bony outgrowths are called osteophytes and are the hallmark radiographic finding.

The clinical correlation is direct. Pain occurs because subchondral bone, periosteum, and the joint capsule are richly innervated, while cartilage itself has no nerve supply. This explains why pain worsens with activity (mechanical loading on exposed bone) and improves with rest. The brief morning stiffness (less than 30 minutes) reflects mild gelling of the joint during inactivity, as opposed to the prolonged stiffness of inflammatory arthritis caused by overnight accumulation of inflammatory cytokines. Crepitus on exam is the sound and sensation of roughened cartilage and bone surfaces grinding against each other. Heberden nodes (DIP) and Bouchard nodes (PIP) are palpable osteophytes at the joint margins of the hands.

A critical point for exam purposes: osteoarthritis is not primarily an inflammatory process. While low-grade synovial inflammation can occur as cartilage debris triggers innate immune responses, the disease is driven by mechanical wear and failed repair. This distinction separates it from rheumatoid arthritis and other inflammatory arthropathies both clinically and on laboratory testing.

2. Classification and Clinical Manifestation

CLASSIFICATION	DESCRIPTION	JOINTS INVOLVED
Primary (Idiopathic)	No identifiable underlying cause; attributed to age-related cartilage degeneration and cumulative mechanical stress	DIP, PIP, first CMC, knees, hips, cervical and lumbar spine
Secondary	Results from a known predisposing condition or event	Same joints as primary, plus atypical joints depending on the underlying cause

Common causes of secondary osteoarthritis:

CAUSE	MECHANISM	NOTABLE JOINT PATTERN
Post-traumatic	Prior fracture, meniscal tear, ligament injury disrupts normal joint mechanics	Knee (ACL tear), ankle (fracture)
Obesity	Excess mechanical load accelerates cartilage loss	Knees (bilateral), hips
Hemochromatosis	Iron deposition in cartilage causes chondrocyte toxicity	Second and third MCP joints (distinctive)
Calcium pyrophosphate deposition (CPPD)	Crystal-induced cartilage damage	Knees, wrists
Acromegaly	Excess growth hormone causes abnormal cartilage and bone growth	Generalized, including the spine
Neuropathic (Charcot joint)	Loss of proprioception and pain sensation leads to repetitive unrecognized trauma	Depends on neuropathy distribution; foot/ankle in diabetes, knee/hip in tabes dorsalis

Joint distribution and clinical features by location:

JOINT	CLINICAL FEATURES	EXAM PEARL
DIP joints	Heberden nodes; most classic hand OA finding	Distinguish from psoriatic arthritis, which also affects DIP but has nail pitting and dactylitis
PIP joints	Bouchard nodes	Less commonly tested than Heberden nodes
First CMC (thumb base)	Pain with pinch grip, difficulty opening jars; "squaring" of the thumb base	Very high yield; frequently the presenting complaint in hand OA vignettes
Knee	Pain ascending or descending stairs, crepitus, varus or valgus deformity in advanced disease	Most commonly affected weight-bearing joint overall
Hip	Groin pain (referred along the obturator nerve), decreased internal rotation on exam	Hip OA pain is felt in the groin, not the lateral hip (lateral hip pain suggests trochanteric bursitis)
Spine (cervical/lumbar)	Osteophyte compression of nerve roots or spinal cord; facet joint hypertrophy	Can cause radiculopathy or spinal stenosis; vignettes may describe neurogenic claudication

3. Diagnostic Workup

TEST	ROLE	EXPECTED FINDINGS
X-ray of the affected joint	Best initial test	Asymmetric joint space narrowing, osteophytes, subchondral sclerosis, subchondral cysts
ESR and CRP	Rule out inflammatory arthritis	Normal or minimally elevated
Rheumatoid factor and anti-CCP	Rule out rheumatoid arthritis	Negative
Synovial fluid analysis	Distinguish from inflammatory or septic arthritis when effusion is present	Non-inflammatory: clear, viscous; WBC below 2,000 per mm³; no crystals
MRI	Not routine; used when diagnosis is unclear or to evaluate for surgical planning	Early cartilage loss, bone marrow edema, meniscal tears; more sensitive than X-ray for early disease

Best Initial Test: Plain Radiograph (X-ray)

The diagnosis of osteoarthritis is fundamentally clinical and radiographic. When a patient older than 50 presents with gradual onset of use-related joint pain, brief morning stiffness, and bony enlargement on exam, the first step is to obtain a weight-bearing X-ray of the symptomatic joint. The four classic radiographic findings can be remembered as the mnemonic "LOSS": Loss of joint space (narrowing), Osteophytes, Subchondral sclerosis, and Subchondral cysts.

Joint space narrowing in osteoarthritis is characteristically asymmetric, affecting the portion of the joint under the greatest mechanical load. In the knee, medial compartment narrowing is most common. This contrasts with inflammatory arthritis (such as rheumatoid arthritis), where joint space narrowing tends to be symmetric and uniform.

Laboratory Tests: The Role of Ruling Out

There is no laboratory test that confirms osteoarthritis. Instead, labs are ordered to exclude other diagnoses. ESR, CRP, rheumatoid factor, anti-CCP antibodies, and ANA should all be normal. If any of these are abnormal, the examiner is redirecting you toward an inflammatory or autoimmune arthritis. This is a common testing strategy: the vignette describes what sounds like osteoarthritis, but an elevated ESR or positive rheumatoid factor should make you reconsider the diagnosis.

Synovial Fluid Analysis

When a joint effusion is present and the diagnosis is uncertain, arthrocentesis with synovial fluid analysis is the next step. Osteoarthritis produces a non-inflammatory fluid: clear or straw-colored, highly viscous (high hyaluronic acid content), and a WBC count below 2,000 cells per mm³. This distinguishes it from inflammatory arthritis (2,000 to 50,000 WBC), and septic arthritis (over 50,000 WBC, often over 100,000). Polarized light microscopy should show no crystals, ruling out gout and pseudogout.

When to Order MRI

MRI is not needed for routine diagnosis. It is indicated when the clinical picture is atypical, when you suspect an internal derangement (such as a meniscal tear) as a contributing factor, or for preoperative planning. For board purposes, if a vignette gives you a classic presentation and asks for the "best next step," the answer is X-ray, not MRI.

4. Management and Treatment

STEP	INTERVENTION	DETAILS
First line (all patients)	Non-pharmacologic therapy	Exercise (aerobic and strengthening), weight loss if BMI is elevated, physical or occupational therapy, assistive devices
Mild to moderate pain (hand/knee)	Topical NSAIDs	Diclofenac gel 1%, applied four times daily to the affected joint
Moderate pain (knee/hip)	Oral NSAIDs	Ibuprofen 400 to 800 mg three times daily, or naproxen 250 to 500 mg twice daily; use the lowest effective dose for the shortest duration
GI protection with oral NSAIDs	Proton pump inhibitor co-therapy	Omeprazole 20 mg daily if patient has GI risk factors (age over 65, history of peptic ulcer, concurrent anticoagulant or corticosteroid use)
Acute flare with effusion	Intra-articular corticosteroid injection	Triamcinolone 40 mg (large joint) or 10 mg (small joint); provides weeks to months of relief; limit to 3 to 4 injections per joint per year
Chronic pain adjunct (knee)	Duloxetine	60 mg daily; conditionally recommended for knee OA when NSAIDs are insufficient or contraindicated
Refractory end-stage disease	Total joint arthroplasty	Indicated when pain is severe, function is significantly impaired, and conservative measures have failed

Non-pharmacologic Management

Every exam question about osteoarthritis management begins here. Exercise and weight loss are the foundation of treatment and should be recommended to all patients regardless of disease severity. Weight reduction is particularly high yield for knee OA: even modest weight loss (5% of body weight) meaningfully reduces joint loading and pain. Physical therapy improves quadriceps strength and joint stability. These interventions are always the correct "first step" in a vignette asking about initial management.

Pharmacologic Therapy

For hand and knee osteoarthritis, topical NSAIDs (diclofenac gel) are preferred as the initial pharmacologic agent because they provide local relief with minimal systemic absorption and fewer gastrointestinal and cardiovascular side effects than oral formulations. For hip osteoarthritis, topical agents are impractical due to the depth of the joint, so oral NSAIDs are the first-line pharmacologic choice.

When prescribing oral NSAIDs, always consider the patient's comorbidities. In patients with cardiovascular disease, naproxen is the preferred NSAID due to its relatively lower cardiovascular risk. In patients with chronic kidney disease (GFR below 30), NSAIDs are contraindicated, and acetaminophen (up to 2 to 3 g per day) becomes the safer alternative despite its modest efficacy. In patients at risk for GI bleeding, co-prescribe a proton pump inhibitor or use a COX-2 selective inhibitor (celecoxib 200 mg daily).

Intra-articular Corticosteroid Injections

These are appropriate for patients who have an acute flare with a joint effusion or who have not responded adequately to oral therapy. The effect is temporary, typically lasting 4 to 8 weeks. Repeated injections (more than 3 to 4 per year in the same joint) may accelerate cartilage loss and are generally avoided.

Duloxetine

This serotonin-norepinephrine reuptake inhibitor (SNRI) is conditionally recommended as an adjunctive agent for chronic knee OA pain, particularly in patients who cannot tolerate NSAIDs or who have concomitant depression or neuropathic pain.

Surgical Management

Total joint arthroplasty (knee or hip replacement) is reserved for patients with end-stage disease: persistent pain despite maximal medical therapy, significant functional limitation, and radiographic evidence of advanced joint destruction. This is the definitive treatment and reliably improves quality of life. On the exam, the indication for surgery is a patient who has "failed all conservative measures" and has severe functional impairment.

Therapies to Avoid or Deprioritize

Intra-articular hyaluronic acid (viscosupplementation) is not recommended by current guidelines due to inconsistent evidence of benefit. Glucosamine and chondroitin sulfate have not demonstrated efficacy in rigorous trials and are not endorsed. Long-term opioid therapy is strongly discouraged due to the risks of dependence, tolerance, and lack of disease modification.

5. Differential Diagnosis and Distractors

DIFFERENTIAL	WHY IT IS SIMILAR	KEY DISCRIMINATOR
Rheumatoid arthritis	Both cause chronic joint pain and hand involvement	RA involves MCP and PIP joints (spares DIP), causes morning stiffness over 1 hour, has positive RF/anti-CCP, and shows periarticular erosions and symmetric joint space narrowing on X-ray
Psoriatic arthritis	Both can involve the DIP joints	Psoriatic arthritis presents with skin plaques, nail pitting, dactylitis ("sausage digits"), and pencil-in-cup deformity on X-ray
Gout	Both cause joint pain, often in older adults	Gout is acute and episodic with intense erythema and swelling; synovial fluid shows needle-shaped, negatively birefringent crystals; first MTP joint is classic
Pseudogout (CPPD)	Both affect the knee in elderly patients; CPPD can cause secondary OA	CPPD presents acutely; X-ray shows chondrocalcinosis (linear calcification in the meniscus or cartilage); synovial fluid shows rhomboid-shaped, positively birefringent crystals
Septic arthritis	Both can present with a single swollen, painful joint	Septic arthritis has fever, acute onset, warmth and erythema; synovial fluid WBC over 50,000 with over 75% neutrophils; this is an emergency requiring urgent drainage
Hemochromatosis arthropathy	Both cause degenerative joint changes	Hemochromatosis characteristically involves the second and third MCP joints (atypical for OA); look for elevated ferritin and transferrin saturation, bronze skin, diabetes, and hepatomegaly
Trochanteric bursitis	Both cause pain around the hip in older adults	Bursitis causes lateral hip and thigh pain with point tenderness over the greater trochanter; OA causes groin pain with decreased internal rotation

6. Traps and High-Yield Pearls

The single most common trap with osteoarthritis questions is confusing it with rheumatoid arthritis based on hand involvement. Both diseases affect the hands, but they affect different joints. Osteoarthritis targets the DIP joints (Heberden nodes), PIP joints (Bouchard nodes), and the first CMC joint. Rheumatoid arthritis targets the MCP and PIP joints while characteristically sparing the DIP joints. If a vignette describes DIP involvement with bony enlargement and brief morning stiffness, the answer is osteoarthritis, even if the hand involvement seems "arthritic." Conversely, if the vignette mentions MCP swelling with prolonged morning stiffness and elevated inflammatory markers, the answer is rheumatoid arthritis regardless of the patient's age.

A second common error is ordering the wrong test. When a vignette describes a classic presentation in a patient over 50 with use-related pain and crepitus, the next step is a plain X-ray, not MRI, not labs, and not synovial fluid analysis. MRI is more sensitive, but it is not the best initial test and is reserved for atypical presentations. Synovial fluid analysis is only indicated when there is an effusion and the differential includes infection or crystal disease.

A third trap involves management sequencing. Exam questions will test whether you know that non-pharmacologic therapy is always the first step before any medication. A vignette that asks for the "best initial management" in a newly diagnosed patient with mild knee OA is looking for "exercise and weight loss," not NSAIDs. Additionally, students frequently forget that topical NSAIDs are preferred over oral NSAIDs for hand and knee OA as the initial pharmacologic agent, due to their safer side effect profile.

Finally, watch for the patient with osteoarthritis of the second and third MCP joints. This is an unusual distribution for primary OA and should trigger consideration of hemochromatosis as the underlying cause. The vignette may include clues such as elevated liver enzymes, skin hyperpigmentation, or diabetes. Missing this pattern is a classic board trap that tests your ability to distinguish primary from secondary osteoarthritis.

The core competency being tested across all osteoarthritis questions is pattern recognition: identifying the non-inflammatory, degenerative joint pattern (DIP, first CMC, knees, hips, spine), distinguishing it from inflammatory arthritis through the history, exam, and labs, and applying a stepwise management approach that prioritizes non-pharmacologic therapy before medications and reserves surgery for end-stage disease.

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