Osteoarthritis

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Basics

Description

  • Progressive loss of articular cartilage with reactive changes at joint margins and in subchondral bone
  • Primary osteoarthritis (OA)
    • Idiopathic: categorized by clinical features (localized, generalized, erosive)
  • Secondary OA
    • Posttraumatic
    • Childhood anatomic abnormalities (e.g., congenital hip dysplasia, slipped capital femoral epiphysis [SCFE], Legg-Calvé-Perthes disease)
    • Inheritable metabolic disorders (e.g., Wilson disease, alkaptonuria, hemochromatosis)
    • Neuropathic arthropathy (Charcot joints)
    • Hemophilic arthropathy
    • Endocrinopathies: acromegalic arthropathy, hyperparathyroidism, hypothyroidism
    • Paget disease
    • Noninfectious inflammatory arthritis (e.g., rheumatoid arthritis [RA], spondyloarthropathies)
    • Gout, calcium pyrophosphate deposition disease (pseudogout)
    • Septic or tuberculous arthritis
    • Femoral acetabular impingement (FAI)
  • System(s) affected: musculoskeletal
  • Synonym(s): osteoarthrosis; degenerative joint disease (DJD)

Epidemiology

  • Symptomatic OA most common in patients >40 years
  • Leading cause of disability in patients >65 years
  • Predominant sex: male = female
  • 90% of hip OA is primary.
  • Hip OA is more common in whites.

Prevalence
  • ~60 million patients
  • Increases with age; radiographic evidence of OA is present in many patients >65 years old.
  • Moderate to severe hip OA in 3–6% of whites; <1% in East Indians, blacks, Chinese, and Native Americans

Etiology and Pathophysiology

  • Failure of chondrocytes to maintain the balance between degradation and synthesis of extracellular collagen matrix. Collagen loss results in alteration of proteoglycan matrix and increased susceptibility to degenerative change.
  • Biomechanical, biochemical, inflammatory, and immunologic factors contribute to cartilage loss. Attempts at repair most commonly manifest as osteophyte formation.

Genetics
  • Up to 65% of OA may have a genetic component.
  • The heritability of end-stage hip OA is up to 27%.
  • Twin studies in women show 50% (hip, knee) to 65% (hip) heritability rates of OA.

Risk Factors

  • Increasing age: >50 years
  • Age as a risk factor is greatest for hip and knee OA.
  • Hand OA is most common in postmenopausal women.
  • Obesity (weight-bearing joints); BMI >35
  • Small critical shoulder angle (<30 degrees) can predispose to shoulder OA.
  • Trauma, infection, or inflammatory arthritis
  • Female gender (knee and hand)

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Basics

Description

  • Progressive loss of articular cartilage with reactive changes at joint margins and in subchondral bone
  • Primary osteoarthritis (OA)
    • Idiopathic: categorized by clinical features (localized, generalized, erosive)
  • Secondary OA
    • Posttraumatic
    • Childhood anatomic abnormalities (e.g., congenital hip dysplasia, slipped capital femoral epiphysis [SCFE], Legg-Calvé-Perthes disease)
    • Inheritable metabolic disorders (e.g., Wilson disease, alkaptonuria, hemochromatosis)
    • Neuropathic arthropathy (Charcot joints)
    • Hemophilic arthropathy
    • Endocrinopathies: acromegalic arthropathy, hyperparathyroidism, hypothyroidism
    • Paget disease
    • Noninfectious inflammatory arthritis (e.g., rheumatoid arthritis [RA], spondyloarthropathies)
    • Gout, calcium pyrophosphate deposition disease (pseudogout)
    • Septic or tuberculous arthritis
    • Femoral acetabular impingement (FAI)
  • System(s) affected: musculoskeletal
  • Synonym(s): osteoarthrosis; degenerative joint disease (DJD)

Epidemiology

  • Symptomatic OA most common in patients >40 years
  • Leading cause of disability in patients >65 years
  • Predominant sex: male = female
  • 90% of hip OA is primary.
  • Hip OA is more common in whites.

Prevalence
  • ~60 million patients
  • Increases with age; radiographic evidence of OA is present in many patients >65 years old.
  • Moderate to severe hip OA in 3–6% of whites; <1% in East Indians, blacks, Chinese, and Native Americans

Etiology and Pathophysiology

  • Failure of chondrocytes to maintain the balance between degradation and synthesis of extracellular collagen matrix. Collagen loss results in alteration of proteoglycan matrix and increased susceptibility to degenerative change.
  • Biomechanical, biochemical, inflammatory, and immunologic factors contribute to cartilage loss. Attempts at repair most commonly manifest as osteophyte formation.

Genetics
  • Up to 65% of OA may have a genetic component.
  • The heritability of end-stage hip OA is up to 27%.
  • Twin studies in women show 50% (hip, knee) to 65% (hip) heritability rates of OA.

Risk Factors

  • Increasing age: >50 years
  • Age as a risk factor is greatest for hip and knee OA.
  • Hand OA is most common in postmenopausal women.
  • Obesity (weight-bearing joints); BMI >35
  • Small critical shoulder angle (<30 degrees) can predispose to shoulder OA.
  • Trauma, infection, or inflammatory arthritis
  • Female gender (knee and hand)

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