Osteoarthritis of the Knee — Clinical Features

Overview

Knee OA is a degenerative joint disease characterized by articular cartilage loss, subchondral bone changes, osteophyte formation, and mild synovial inflammation. It typically presents in patients in their 50s and beyond, with an insidious onset evolving over years to decades. If a younger patient develops significant OA, an underlying secondary cause should be sought.

Symptoms

Pain

The dominant symptom and primary driver of clinical decision-making
Classically mechanical in nature — worse with activity (climbing stairs, rising from a chair), and often worse towards the end of the day
In early disease: pain occurs only with loading/activity
In advanced disease: pain may be present at rest or at night
Pain is nociceptive in nature but central sensitization/neuropathic mechanisms contribute in a substantial proportion of patients

Stiffness

Localized to the involved joint
Brief — typically lasts 15–30 minutes or less (contrast with RA, where stiffness lasts >1 hour)
Most noticeable on first mobilizing after inactivity ("gelling phenomenon")

Crepitus

Patients may feel and hear a grating or grinding sensation during joint movement
Most prominent under the patella on knee flexion/extension

Functional Limitation

Difficulty going up and down stairs
Difficulty rising from a chair
Catching or locking of the knee (associated with loose bodies or degenerative meniscal tears)
Can contribute to falls

Signs on Examination

Finding	Detail
Joint line tenderness	Palpable tenderness along the medial or lateral joint line
Crepitus	Palpable on passive/active movement; most prominent under patella
Effusion	Soft tissue swelling from synovial fluid accumulation
Bony swelling	Palpable osteophytes at joint margins
Reduced range of motion	Progressive loss of flexion/extension
Varus deformity	Most common; medial compartment narrowing causes "bow-leg" alignment
Fixed flexion deformity	Inability to fully extend the knee
Valgus deformity	Less common; lateral compartment involvement
Peri-articular tenderness	May involve surrounding soft tissues
Patellofemoral pain	Pain reproduced on patellofemoral compression
Ligamentous instability	May develop in advanced disease
Muscle wasting/weakness	Quadriceps atrophy from disuse and pain inhibition

In early disease, there may be very few visible signs. Signs accumulate as the disease progresses.

Radiographic Features (Investigations)

Plain weight-bearing AP, lateral, and sunrise views typically show:

Joint space narrowing (medial > lateral compartment; or patellofemoral)
Osteophytes at joint margins
Subchondral sclerosis (increased bone density beneath cartilage)
Subchondral cysts
Loose bodies (fragments of cartilage/bone — "joint mice")

Importantly, radiographic severity does not correlate well with pain or disability.

Pathological Basis of Findings

Comparison of OA (right) and RA (left) joint features. OA shows osteophytes, thinned/fibrillated cartilage, subchondral sclerosis, subchondral cysts, loose bodies, and mild synovial inflammation — but no ankylosis or pannus.

Pathological Change	Clinical Correlate
Cartilage fibrillation and thinning	Crepitus, pain
Osteophyte formation	Bony swelling, deformity, impingement
Subchondral cysts	Seen on X-ray
Bone eburnation (ivory-like surface)	Loss of cushioning → pain
Loose bodies ("joint mice")	Locking, catching sensation
Mild synovial inflammation	Effusion, warmth
Quadriceps atrophy	Instability, worsening pain

Diagnosis

Diagnosis is clinical, based on:

Symptoms: pain (mechanical), brief morning stiffness, functional limitation
Examination: crepitus, restricted/painful movement, joint tenderness, bony enlargement

Plain radiographs are not mandatory but are useful for atypical presentations or diagnostic clarity.

Red flags suggesting an alternative/additional diagnosis:

Morning stiffness >30 min → consider RA
Recent trauma → fracture
Hot, swollen joint → crystal arthropathy or septic arthritis

Sources: Goldman-Cecil Medicine, p. 2768–2769; Robbins & Kumar Basic Pathology, p. 791; Rosen's Emergency Medicine, Ch. 48

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