Osteoarthritis

Introduction
Osteoarthritis (OA) is a chronic, progressive degenerative joint disease characterized by the breakdown of articular cartilage, subchondral bone changes, osteophyte formation, and varying degrees of synovial inflammation. It is the most common form of arthritis, leading to pain, stiffness, reduced range of motion, and functional disability. OA can affect any synovial joint but most frequently involves weight-bearing joints such as the knees, hips, and spine, as well as the hands.

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Epidemiology

• OA prevalence increases with age, affecting approximately 10–12% of the adult population and up to 50% of individuals over 65 years.

• More common in women after the age of 50.

• Leading cause of disability in older adults worldwide.

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Risk Factors

Non-modifiable:

• Age (risk rises significantly after 50).

• Female sex (especially postmenopausal).

• Genetic predisposition (family history, specific gene variants).

• Joint shape and alignment abnormalities.

Modifiable:

• Obesity (increases mechanical stress on weight-bearing joints).

• Joint injury or trauma.

• Repetitive occupational or sports-related stress.

• Muscle weakness.

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Pathophysiology

• Loss of cartilage homeostasis: chondrocytes produce less proteoglycan and collagen while increasing degradative enzymes.

• Cartilage softens, loses elasticity, and thins.

• Subchondral bone becomes sclerotic; cysts and osteophytes form.

• Synovial inflammation may develop, contributing to symptoms.

• The joint capsule and ligaments may become thickened, restricting movement.

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Classification

1. Primary (Idiopathic) OA:

• Localized: Involves 1–2 joints (e.g., knee OA).

• Generalized: Involves ≥3 joints.

2. Secondary OA:

• Results from predisposing factors such as trauma, congenital deformities, inflammatory arthritis, metabolic diseases (e.g., hemochromatosis), or endocrine disorders.

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Clinical Features

Symptoms:

• Gradual onset of joint pain, typically worsening with activity and improving with rest.

• Morning stiffness <30 minutes.

• Stiffness after periods of inactivity (“gelling”).

• Reduced joint function and mobility.

• Joint instability or buckling.

Signs:

• Bony enlargement (Heberden’s nodes at distal interphalangeal joints; Bouchard’s nodes at proximal interphalangeal joints).

• Crepitus on movement.

• Restricted range of motion.

• Joint tenderness and deformity in advanced stages.

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Commonly affected joints:

• Knees.

• Hips.

• Hands (DIP, PIP, first carpometacarpal joints).

• Spine (cervical and lumbar).

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Diagnosis

Clinical criteria:

• Based on characteristic symptoms and signs, supported by imaging.

Imaging:

• X-ray findings: Joint space narrowing, osteophyte formation, subchondral sclerosis, subchondral cysts.

• MRI: Not routinely required; useful for detecting early cartilage changes.

Laboratory tests:

• Usually normal; ESR and CRP are typically within normal range.

• Synovial fluid analysis: Non-inflammatory (clear, viscous, WBC <2000/mm³).

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Management

Goals:

• Relieve pain.

• Maintain and improve joint mobility.

• Minimize disability.

• Slow disease progression.

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1. Non-pharmacological Management

• Patient education on disease nature and joint protection.

• Weight loss to reduce stress on joints.

• Low-impact aerobic exercise (walking, swimming, cycling).

• Muscle strengthening and physiotherapy.

• Use of assistive devices (canes, braces, orthotics).

• Occupational therapy for activity modification.

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2. Pharmacological Management

a. First-line analgesia:

• Paracetamol (Acetaminophen): 500–1000 mg orally every 4–6 hours as needed (maximum 4 g/day).

b. Nonsteroidal anti-inflammatory drugs (NSAIDs) (for inadequate relief with paracetamol):

• Ibuprofen: 400–800 mg orally every 6–8 hours (maximum 3200 mg/day).

• Naproxen: 250–500 mg orally twice daily.

• Diclofenac: 50 mg orally two or three times daily.

• Topical NSAIDs (e.g., diclofenac gel) for localized pain.

• Consider gastroprotection (proton pump inhibitor) in high-risk patients.

c. COX-2 inhibitors (e.g., Celecoxib):

• 100–200 mg orally once or twice daily, with reduced GI risk compared to traditional NSAIDs.

d. Intra-articular therapies:

• Corticosteroid injections (e.g., Triamcinolone acetonide 20–40 mg per large joint) for acute flares; limited to 3–4 injections/year.

• Hyaluronic acid injections: Controversial benefit; used in selected patients.

e. Adjunctive analgesics:

• Duloxetine: 30–60 mg orally once daily for chronic pain not controlled by NSAIDs.

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3. Surgical Management

• Indications: Severe pain and functional limitation despite optimal medical therapy.

• Options:

  • Arthroscopy (for mechanical symptoms due to loose bodies, not for generalized OA).

  • Osteotomy (realignment procedures in younger patients with malalignment).

  • Joint replacement (total knee arthroplasty, total hip arthroplasty) in advanced disease.

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Prognosis

• OA is slowly progressive; rate varies by joint and patient factors.

• Early lifestyle interventions can significantly slow progression and improve quality of life.

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Complications

• Chronic pain and disability.

• Reduced mobility leading to muscle atrophy.

• Joint deformity.

• Secondary depression due to chronic illness.