Overview

Knee osteoarthritis is a chronic, whole-joint disorder characterized by pain, stiffness, functional limitation and progressive structural change affecting cartilage, subchondral bone, synovium, menisci, ligaments and peri-articular muscles. Prevalence rises with age and obesity and contributes substantially to global disability; recent GBD analyses and reviews highlight knee OA as a leading cause of pain and years lived with disability worldwide. Clinically, diagnosis is often made without imaging using validated rules, and core first-line care is education + exercise + weight management.

Anatomy & Physiology

• Joint surfaces: femorotibial (medial/lateral) and patellofemoral compartments lined by hyaline cartilage; menisci distribute load and enhance stability; collateral and cruciate ligaments constrain translation/rotation.
• Synovium: regulates nutrient exchange and produces hyaluronan-rich fluid for lubrication; can mount inflammatory responses.
• Subchondral bone: shock absorption and load transfer; communicates with cartilage via osteochondral channels.
• Neuromuscular control: quadriceps, hip abductors and calf musculature modulate joint loading; alignment and gait mechanics determine compartmental stresses.

Aetiology and Risk Factors

Aetiology (multifactorial, interacting “whole-joint” mechanisms)

• Mechanical: abnormal joint loading (varus/valgus malalignment, meniscal loss) drives focal degeneration.
• Biological: low-grade synovitis, subchondral remodeling and BMLs; nociceptive and nociplastic pain contributions.
• Metabolic: obesity/adipokines and insulin resistance increase risk and symptom burden.

Risk factors

• Non-modifiable: age; female sex; genetics/family history.
• Modifiable: overweight/obesity; prior knee injury (e.g., ACL/meniscus); high occupational kneeling/squatting/lifting; malalignment; low muscle strength; physical inactivity.

Pathophysiology

• Joint load mismatch (demand > capacity) → focal cartilage matrix damage + meniscal stress.
• Synovial activation (cytokines, neuropeptides) → pain and effusion; central sensitization in some.
• Subchondral bone remodeling and BMLs → nociceptor ingrowth/angiogenesis → pain and structural progression.
• Malalignment/deconditioning perpetuate compartmental overload → osteophytes, joint-space loss, functional decline. 

Clinical Manifestations

• Activity-related knee pain (walking, stairs, squatting)
• Short morning stiffness (<30 min)
• “giving way”
• Crepitus and swelling
• Reduced function and confidence
• Flares after load spikes
• Nocturnal pain in advanced disease

Functional features

• Slower timed-up-and-go
• Difficulty rising from chair
• Reduced walking endurance
• Reduced balance.

Diagnosis

Diagnose clinically without imaging when all present—age ≥45, activity-related pain, no morning stiffness or stiffness ≤30 minutes; image if atypical features or red flags.

Imaging 

• Weight-bearing AP/lateral and skyline views to classify and plan
  • Radiograph severity by K-L grade
• MRI not routinely required—consider if alternative pathology suspected
• US can detect effusion/synovitis and guide injections

Classification 

• By compartment: medial/lateral tibiofemoral; patellofemoral; mixed.
• By radiograph: Kellgren–Lawrence 0–4 (0 normal → 4 severe with marked joint-space loss and deformity).
• By phenotype (useful clinically): biomechanical–malalignment/instability; inflammatory/synovitis-dominant; metabolic–obesity; bone-driven (BML-dominant); pain-sensitization predominant.

Treatment

• Education
• Structured exercise (strength—esp. quadriceps/hip; aerobic; neuromuscular/balance; tai chi)
• Weight loss if overweight/obese (goal ≥5–10%)
• Pacing and flare plan

Devices/adjuncts

• Cane in contralateral hand
• Knee taping
• Tibiofemoral unloader bracing for unicompartmental OA 

Pharmacologic (use lowest effective dose, shortest duration, alongside exercise)

• Topical NSAIDs (first-line)
• Oral NSAIDs + PPI if needed; acetaminophen limited benefit
• Duloxetine conditional for persistent pain
• Topical capsaicin optional
• Avoid routine opioids

Intra-articular therapies

• Corticosteroid: short-term relief for flares; avoid frequent repeat courses (signals of cartilage loss with repeated triamcinolone).
• Hyaluronic acid (no good evidence)
• PRP/stem cells: evidence inconsistent; many guidelines advise against outside research/specialist settings.

Interventional pain

• Radiofrequency ablation (genicular nerves): conditional option in refractory knee OA
  

Surgery

• Do not perform arthroscopy for primary degenerative knee disease (no meaningful long-term benefit).
• Consider realignment osteotomy (younger, unicompartmental malalignment) or unicompartmental/total knee arthroplasty for severe, function-limiting disease after optimal non-surgical care.

Complications and Prognosis

Complications

• Functional decline
• Falls/deconditioning
• Analgesic adverse effects (GI/CV with NSAIDs; dependence with opioids)
• Post-injection flare
• Accelerated progression in some with repeated IA steroids
• Surgical risks after arthroplasty

Prognosis

• Variable course; many stabilize/improve with sustained exercise and weight loss
• Poor prognostic factors
  • Obesity
  • Varus/valgus malalignment
  • Prior major knee injury
  • Severe baseline radiographic/structural damage
  • Depression/low self-efficacy

Acronym

• KNEE-OA = Kilos down (weight loss) + NSAIDs (topical → oral) + Exercise (strength/aerobic/balance) + Education/self-management + Offload (brace/tape/cane) + Adjuvants (IA steroid short-term; duloxetine) — escalate to surgery if refractory. (NICE, Arthritis Foundation)
  

References

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