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
- Most common joint disease in US.
- 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.
- Predominantly impacts weight-bearing joints
Prevalence
- >30 million patients affected in US
- 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)
General Prevention
Weight management; regular physical activity
-- To view the remaining sections of this topic, please log in or purchase a subscription --
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
- Most common joint disease in US.
- 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.
- Predominantly impacts weight-bearing joints
Prevalence
- >30 million patients affected in US
- 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)
General Prevention
Weight management; regular physical activity
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