Skip to Main Content

Source: Buys LM, Elliott ME. Osteoarthritis. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. Accessed June 22, 2012.

  • Degenerative joint disease
  • Osteoarthrosis

  • Progressive joint disorder caused by gradual loss of cartilage, resulting in development of osteophytes and cysts at joint margins.

  • Primary (idiopathic) osteoarthritis (OA) has no known cause.
  • Secondary OA may be associated with:
    • Rheumatoid arthritis
    • Trauma
    • Metabolic or endocrine disorders
    • Congenital factors

  • Damage to articular cartilage increases metabolic activity of chondrocytes resulting in cartilage swelling, destruction, and loss.
  • Aggrecan destruction increases activity of matrix metalloproteinase (MMP) 13, which destroys collagen.
  • Subchondral bone releases vasoactive peptides and MMPs. Neovascularization and increased permeability of adjacent cartilage contribute to further cartilage loss.
  • Joint space narrowing leads to painful, deformed joints.
  • Remaining cartilage softens and develops fibrillations, splitting, and exposure of underlying bone.
  • Brittle, stiffer bone develops sclerosis and microfractures and has decreased weight-bearing ability.
  • New bone formations (osteophytes) appear at joint margins.
  • Inflammation in joint capsule and synovium result in effusions and synovial thickening.

  • Prevalence and severity increase with age.
  • 15% of Americans affected, including 50% of those over age 65 and 85% of those age 75 or older.
  • Before age 50, men are more likely to have OA than women.
  • In older age groups, women have a higher prevalence of hip, knee, and hand OA than men.

  • Advancing age
  • Obesity
  • Repetitive use through work or leisure activities
  • History of joint trauma
  • Genetic predisposition

  • Depends on duration and severity of disease and number of joints affected.

Signs and Symptoms

  • Localized deep, aching joint pain; limitation of motion, stiffness, crepitus, and deformities.
  • Upon arising, joint stiffness lasts <30 minutes and resolves with motion.
  • Joints most commonly affected:
    • Distal interphalangeal (DIP) joints (Heberden’s nodes) and proximal interphalangeal (PIP) joints (Bouchard’s nodes) of hands
    • First carpometacarpal joints of wrist
    • Knees
    • Hips
    • Cervical and lumbar spine
    • First metatarsophalangeal joint of toes
  • Patients with lower extremity involvement may report weakness or instability.
  • Physical examination reveals tenderness, crepitus, and possibly joint enlargement; presence of warm, red, tender joints suggests inflammatory synovitis.

Means of Confirmation and Diagnosis

  • Patient history, examination of affected joint(s), radiologic findings, and laboratory testing.
  • Criteria for classification of OA of hips, knees, and hands include:
    • Presence of pain
    • Bony changes on examination
    • Normal erythrocyte sedimentation rate (ESR)
    • Radiographs showing characteristic osteophytes or joint space narrowing

Laboratory Tests

  • No specific clinical laboratory abnormalities
  • ESR may be elevated during inflammation.
  • Rheumatoid factor negative.
  • Synovial fluid analysis reveals high viscosity and mild leukocytosis (<2000 white blood cells/mm3 [<2 × 109/L]) with predominantly mononuclear cells.


  • Radiography
    • Changes often absent in early, mild OA.
    • With progression, potential joint space narrowing, subchrondral bone sclerosis, and marginal osteophytes.
    • In late OA, potential abnormal joint alignment and effusions.

Differential Diagnosis

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.