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الخميس، 5 فبراير 2009

Osteoarthritis

Introduction

Background

Osteoarthritis (OA) is the most common articular disease worldwide, affecting over 20 million individuals in the United States alone. Its high prevalence entails significant costs to society. Direct costs of osteoarthritis include clinician visits, medications, and surgical intervention. Indirect costs include such items as time lost from work. Costs associated with osteoarthritis can be particularly significant for elderly persons, who face potential loss of independence and who may need help with daily living activities. As the populations of developed nations age over the next few decades, the need for better understanding of osteoarthritis and for improved therapeutic alternatives will continue to grow.

Pathophysiology

Traditionally, osteoarthritis has been considered a disease of articular cartilage. The current concept holds that osteoarthritis involves the entire joint organ, including the subchondral bone and synovium.

Osteoarthritis has always been classified as a noninflammatory arthritis; however, increasing evidence has shown that inflammation occurs as cytokines and metalloproteinases are released into the joint. Therefore, the term degenerative joint disease is no longer appropriate when referring to osteoarthritis.

Osteoarthritis predominantly involves the weight-bearing joints, including the knees, hips, cervical and lumbosacral spine, and feet. Other commonly affected joints include the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints of the hands.

Cartilage is grossly affected. Focal ulcerations eventually lead to cartilage loss and eburnation. Subchondral bone formation also occurs, with development of bony osteophytes.

Frequency

United States

Osteoarthritis affects over 20 million individuals in the United States. Based on the radiologic definition of osteoarthritis, more than half of adults older than 65 years are affected.

International

Osteoarthritis is the most common articular disease. Estimates vary among different populations.

Mortality/Morbidity

  • The disease progression of osteoarthritis is characteristically slow, occurring over several years or decades.
  • Pain is usually the initial and principal source of morbidity in osteoarthritis. The patient can become progressively less active, leading to morbidities related to decreasing physical activity (including potential weight gain).

Race

The prevalence of osteoarthritis differs among different ethnic groups. Knee osteoarthritis appears to be more common in African American women than in other groups.

Sex

  • The likelihood of developing osteoarthritis increases with age. The disease is equally common among men and women aged 45-55 years. After age 55 years, the disease becomes more common in women.
  • DIP and PIP joint involvement that results in Heberden and Bouchard nodes is more common in women.

Age

  • Osteoarthritis can be defined epidemiologically (ie, using radiographic criteria) or clinically (eg, radiography findings plus clinical symptoms). Based on radiographic criteria, osteoarthritis occurs in 30% of affected individuals aged 45-65 years and in more than 80% by their eighth decade of life, although most are asymptomatic.

Clinical

History

  • Pain
    • Pain is the main reason persons with osteoarthritis (OA) seek medical attention.
    • Initially, symptomatic patients incur pain during activity, which can be relieved by rest and may respond to simple analgesics.
    • Morning joint stiffness usually lasts for less than 30 minutes.
    • Stiffness during rest (gelling) may develop.
    • Joints may become unstable as the osteoarthritis progresses; therefore, the pain may become more prominent (even during rest) and may not respond to medications.

Physical

  • Physical examination findings are mostly limited to the affected joints.
    • Malalignment with a bony enlargement (depending on the disease severity) may occur.
    • Most cases of osteoarthritis do not involve erythema or warmth over the affected joint(s); however, an effusion may be present.
    • Limitation of joint motion or muscle atrophy around a more severely affected joint may occur.
  • Sources of pain in osteoarthritis include the following:
    • Joint effusion and stretching of the joint capsule
    • Increased vascular pressure in subchondral bone
    • Torn menisci
    • Inflammation of periarticular bursae
    • Periarticular muscle spasm
    • Psychological factors
    • Crepitus (a rough or crunchy sensation) may be palpated during motion of an involved joint.

Causes

  • Risk factors of osteoarthritis include the following:
    • Increasing age
    • Obesity
    • Female sex
    • Trauma
    • Infection
    • Repetitive occupational trauma
    • Genetic factors
    • History of inflammatory arthritis
    • Neuromuscular disorder
    • Metabolic disorder
  • The etiopathogenesis of osteoarthritis has been divided into the following 3 stages:
    • Stage 1: Proteolytic breakdown of the cartilage matrix occurs. Chondrocyte metabolism is affected, leading to an increased production of enzymes, which includes metalloproteinases (eg, collagenase, stromelysin) that destroy the cartilage matrix. Chondrocytes also produce protease inhibitors, including tissue inhibitors of metalloproteinases (TIMP) 1 and 2 but in amounts insufficient to counteract the proteolytic effect.
    • Stage 2: This stage involves the fibrillation and erosion of the cartilage surface, with a subsequent release of proteoglycan and collagen fragments into the synovial fluid.
    • Stage 3: The breakdown products of cartilage induce a chronic inflammatory response in the synovium. Synovial macrophage production of cytokines, such as interleukin 1 (IL-1), tumor necrosis factor-alpha, and metalloproteinases, occurs. These can diffuse back into the cartilage and directly destroy tissue or stimulate chondrocytes to produce more metalloproteinases. Other pro-inflammatory molecules (eg, nitric oxide [NO], an inorganic free radical) may also be a factor. Eventually, these events alter the joint architecture, and compensatory bone overgrowth occurs in an attempt to stabilize the joint. As the joint architecture is changed and further mechanical and inflammatory stress occurs on the articular surfaces, the disease progresses unchecked.

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