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162 DEGENERATIVE JOINT DISEASE

162 DEGENERATIVE JOINT DISEASE
Harrison’s Manual of Medicine

162

DEGENERATIVE JOINT DISEASE

Definition
Pathogenesis
Clinical Manifestations
Evaluation
Diagnosis
Bibliography

Definition
Degenerative joint disease, or osteoarthritis (OA), is a disorder characterized by progressive deterioration and loss of articular cartilage accompanied by proliferation of new bone and soft tissue in and around involved joint.

Primary (idiopathic) OA: no underlying cause is apparent.

Secondary OA: a predisposing factor is present such as trauma, repetitive stress (occupation, sports), congenital abnormality, metabolic disorder, or other bone/joint disease.

Erosive OA: term often applied to pts who have hand DIP/PIP OA associated with synovitis and radiographic central erosions of the articular surface.
Pathogenesis
Initial changes begin in cartilage, with change in arrangement and size of collagen fibers. Proteases lead to loss of cartilage matrix. Proteoglycan synthesis initially undergoes a compensatory increase but eventually falls off, leading to full-thickness cartilage loss.
Clinical Manifestations
OA is the most common form of joint disease. It 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 DIP, PIP, or first CMC (thumb base); MCP involvement is rare.
SYMPTOMS

Use-related pain affecting one or a few joints (rest and nocturnal pain less common)

Stiffness after rest or in morning may occur but usually brief (< 30 min)

Loss of joint movement or functional limitation

Joint instability

Joint deformity

Joint crepitation (“crackling”)
PHYSICAL EXAMINATION

Chronic monarthritis or asymmetric oligo/polyarthritis

Firm or “bony” swellings 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)
Evaluation

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 <2000/µL; of value in ruling out crystal-induced 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.
Diagnosis
Usually established on basis of pattern of joint involvement, radiographic features, normal laboratory tests, and synovial fluid findings.
DIFFERENTIAL DIAGNOSIS   Osteonecrosis, Charcot joint, rheumatoid arthritis, psoriatic arthritis, crystal-induced arthritides.

TREATMENT

Pt education, weight reduction, appropriate use of cane and other supports, isometric exercises to strengthen muscles around affected joints.

Topical capsaicin cream may help relieve hand or knee pain.

Acetaminophen, salicylates, or NSAIDs; consider Cox-2-specific NSAIDs for those at risk of GI toxicity.

Tramadol—may be considered in pts whose symptoms are inadequately controlled with NSAIDs; as it is a synthetic opioid agonist, habituation is a potential concern.

Intraarticular glucocorticoids—may provide symptomatic relief but should be performed infrequently as cartilage breakdown may be accelerated if performed too often.

Intraarticular hyaluronin—indicated in pts who have not responded to nonpharmacologic therapy and analgesics; consider when NSAIDs contraindicated or ineffective.

Tidal irrigation—invasive modality; role in treatment remains unclear.

Glucosamine and chondroitin—proof of efficacy has not been established.

Systemic glucocorticoids have no place in the treatment of OA.

Surgery may be considered in pts with intractable pain and loss of function who are unresponsive to other measures.

Bibliography

For a more detailed discussion, see Brandt KD: Osteoarthritis, Chap. 321, p. 1987, in HPIM-15.

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