- Definition
- Epidemiology
- Pathogenesis
- Clinical Manifestations
- Symptoms
- Physical Examination
- Evaluation
- Diagnosis
- Differential Diagnosis
Osteoarthritis (OA) is a disorder characterized by progressive joint failure in which all structures of the joint have undergone pathologic change. The pathologic sine qua non of OA is hyaline articular cartilage loss accompanied by increasing thickness and sclerosis of the subchondral bony plate, outgrowth of osteophytes at the joint margin, stretching of the articular capsule, and weakness of the muscles bridging the joint. There are numerous pathways that lead to OA, but the initial step is often joint injury in the setting of a failure of protective mechanisms.
OA is the most common type of arthritis. The prevalence of OA correlates strikingly with age, and it is much more common in women than in men. Joint vulnerability and joint loading are the two major risk factors contributing to OA. These are influenced by factors that include age, female sex, race, genetic factors, nutritional factors, joint trauma, previous damage, malalignment, proprioceptive deficiencies, and obesity.
The earliest changes of OA may begin in cartilage. The two major components of cartilage are type 2 collagen, which provides tensile strength, and aggrecan, a proteoglycan. OA cartilage is characterized by gradual depletion of aggrecan, unfurling of the collagen matrix, and loss of type 2 collagen, which leads to increased vulnerability.
OA can affect almost any joint but usually occurs in weight-bearing and frequently used joints such as the knee, hip, spine, and hands. The hand joints that are typically affected are the distal interphalangeal (DIP), proximal interphalangeal (PIP), or first carpometacarpal (thumb base); metacarpophalangeal joint involvement is rare.
- Use-related pain affecting one or a few joints (rest and nocturnal pain less common).
- Stiffness after rest or in morning may occur but is usually brief (<30 min).
- Loss of joint movement or functional limitation.
- Joint instability.
- Joint deformity.
- Joint crepitation (“crackling”).
- Chronic monarthritis or asymmetric oligo/polyarthritis.
- Firm enlargement of the joint margins, e.g., Heberden's nodes (hand DIP) or Bouchard's nodes (hand PIP).
- Mild synovitis with a cool effusion can occur but is uncommon.
- Crepitance-audible creaking or crackling of joint on passive or active movement.
- Deformity, e.g., OA of knee may involve medial, lateral, or patellofemoral compartments resulting in varus or valgus deformities.
- Restriction of movement, e.g., limitation of internal rotation of hip.
- Objective neurologic abnormalities may be seen with spine involvement (may affect intervertebral disks, apophyseal joints, and paraspinal ligaments).
- Routine lab work usually normal.
- ESR usually normal but may be elevated in pts who have synovitis.
- Rheumatoid factor, ANA studies negative.
- Joint fluid is straw-colored with good viscosity; fluid WBCs <1000/µL; of value in ruling out crystal-induced arthritis, inflammatory arthritis, or infection.
- Radiographs may be normal at first but as disease progresses may show joint space narrowing, subchondral bone sclerosis, subchondral cysts, and osteophytes. Erosions are distinct from those of rheumatoid and psoriatic arthritis as they occur subchondrally along the central portion of the joint surface.
Usually established on the basis of pattern of joint involvement. Radiographic features, normal laboratory tests, and synovial fluid findings can be helpful if signs suggest an inflammatory arthritis.
Osteonecrosis, Charcot joint, rheumatoid arthritis, psoriatic arthritis, crystal-induced arthritides.
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Osteoarthritis
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