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Osteoarthritis
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Osteoarthritis

Osteoarthritis
Clinical Features
Joint pain
  • Joint pain, deformities (enlargement and possible twisting), and immobility
Limited morning stiffness
  • There is limited morning stiffness (less than 30 minutes) – which distinguishes it from rheumatoid arthritis
Worsening with activity
  • Symptoms worsen with activity.
pathogenesis
Degenerative
  • Degenerative disorder, due to so-called "wear and tear", with mild inflammation.
    • There is debate about the degree of inflammation in osteoarthritis and its role in the pathogenesis of the disease.
Thinning of articular cartilage
  • The foremost pathological finding is thinning/break-down of articular cartilage.
    • Note that articular cartilage is hyaline cartilage – it is avascular and devoid of lymphatics or nervous system structures.
Knee findings
Osteoarthritis
  • Cartilage degeneration.
    • There is thinning of the articular cartilage, degeneration of the fibrocartilaginous menisci, and resultant joint space narrowing.
    • Articular cartilage thinning is the foremost pathological finding in osteoarthritis (the cartilage swells and then ultimately softens and thins).
  • Bony deformation.
    • There is development of bone spurs (osteophytes) at the joint margins and subchondral sclerosis, which is hardening of the bone underneath the cartilaginous surface.
  • Synovial inflammation (synovitis).
    • Damaged cartilage initiates the release of cytokines and other inflammatory mediators that lead to synovial inflammation and further cartilage breakdown.
Predisposing factors
  • Age (roughly half of people over 65 years old have osteoarthritis)
  • Obesity
  • Joint trauma
    • Especially from excessive load bearing – think about obesity and excessive high impact loading as key causes of trauma
  • Female sex
    • Consider that chondrocytes, which are a key component of articular cartilage have estrogen receptors
Labwork
  • Synovial fluid (obtained via joint fluid aspiration) has less than 2,000 white blood cells (WBCs) per cubic millimeter (remember that the inflammation, if present, is mild).
  • Antibody testing (if no other systemic illness is present) is normal (negative).
Affected Joints
DIP joints & lower spine
  • As a generality, show that the distal interphalangeal (DIP) joints and lower spine are affected in OA but not RA.
    • Star the finding of DIP joint disease because it helps us distinguish OA from RA, in which the MCP joints are the primary site of disease.
  • Then, show that the proximal interphalangeal (PIP) joints, cervical spine, hips, and knees are affected in both OA and RA.
Finger Deformities
Now, let's look at key finger deformities in OA.
  • Draw a hand and show that OA at the DIP joint is called Heberden's node and at the PIP joint is called Bouchard's node.
    • Note that in a minority of patients, erosive osteoarthritis can lead to more rapid and more pronounced deformation of the joints with twisting and lateral deviation of the distal phalanges.

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