Osteoarthritis of the Knee — Clinical Features

Epidemiology

Pathological Background (What Drives the Symptoms)

• Cartilage loss — focal fibrillation, erosions, and eventual full-thickness ulceration
• Subchondral bone sclerosis — thickening and eburnation (ivory-like polished surface where cartilage is lost)
• Osteophyte formation — bony outgrowths at joint margins
• Meniscal degeneration — integral to knee OA
• Synovitis — mild-to-moderate, with macrophage infiltration and cytokine release
• Subchondral cysts — formed by synovial fluid forced through microfractures (ball-valve mechanism)
• Capsular stretching and fibrosis
• Periarticular muscle weakness — especially quadriceps

Comparison of morphologic features of RA versus OA — note osteophytes, thinned/fibrillated cartilage, subchondral sclerosis/cysts, and loose bodies in OA vs. pannus and ankylosis in RA. — Robbins & Kumar Basic Pathology

Symptoms

1. Pain (cardinal feature)

• Mechanically driven: occurs with or just after joint use; typically worse toward the end of the day
• Activity-specific examples: stair climbing, arising from a chair (patellofemoral compartment, active >35° flexion), walking, prolonged standing
• Early disease: episodic — triggered by overuse, resolves with rest
• Advanced disease: continuous pain, present at rest, nocturnal pain
• Patellofemoral pain: predominates with knee bending activities; pain with squatting or descending stairs

2. Morning stiffness

• Usually brief: <15–30 minutes (contrast with RA where >1 hour is typical)
• Also present as "gelling" — stiffness after any period of inactivity that loosens with movement

3. Crepitus

• Audible and/or palpable grating or clicking during joint movement
• Most prominent under the patella on flexion and extension
• Results from irregular articular surfaces

4. Mechanical symptoms

• Buckling / giving way — from quadriceps weakness and/or ligamentous laxity; associated with falls
• Catching / locking — may reflect loose bodies (joint mice) or meniscal pathology; requires further evaluation only if arising after acute injury

5. Functional limitation

• Difficulty with stair climbing, rising from a chair, prolonged walking
• Progressive reduction in range of motion

Signs on Examination

X-ray and MRI Findings

X-ray (left): osteophytes at medial/lateral tibia and femur, medial joint space narrowing. MRI (right): denuded medial tibiofe­moral cartilage (arrows), severe medial meniscal extrusion (arrowhead), bone marrow lesions. — Harrison's 22E, Fig. 383-6

• L — Loss of joint space (asymmetric, medial > lateral in varus knee)
• O — Osteophyte formation at joint margins
• S — Subchondral sclerosis
• S — Subchondral cysts

Important: Radiographic severity correlates poorly with pain and disability. Many with advanced X-ray changes have no pain; some with severe pain show only mild X-ray changes. MRI is not routinely indicated diagnostically. — Harrison's 22E; Goldman-Cecil

Pain Sources in the Knee

Diagnosis

• Pain + brief morning stiffness (<30 min) + functional limitation
• Physical signs: crepitus, restricted/painful movement, joint tenderness, bony enlargement

Features suggesting an alternative diagnosis:

• Morning stiffness >30–60 minutes → consider RA
• Recent trauma → exclude fracture/internal derangement
• Hot, swollen joint → consider gout, pseudogout, septic arthritis
• Synovial fluid WBC >1,000/μL → inflammatory arthritis
• Prominent nocturnal pain in non-end-stage disease → distinct workup warranted

Clinical Phenotypes of Knee OA (Goldman-Cecil)

1. Chronic pain phenotype (central sensitization prominent)
2. Inflammatory phenotype (synovitis-driven)
3. Metabolic syndrome phenotype (obesity, diabetes, dyslipidaemia)
4. Bone and cartilage metabolism phenotype
5. Mechanical overload phenotype (malalignment, occupation-related)
6. Minimal joint disease phenotype (pain disproportionate to structural change)