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  • Image not available. Millions of Americans have osteoarthritis (OA). OA prevalence increases with age, with women more commonly affected than men.
  • Image not available. Contributors to OA are systemic (age, genetics, hormonal status, obesity, occupational, or recreational activity) and/or local (injury, overloading of joints, muscle weakness, or joint deformity).
  • Image not available. OA is primarily a disease of cartilage that reflects a failure of the chondrocyte to maintain proper balance between cartilage formation and destruction. This leads to loss of cartilage in the joint, local inflammation, pathologic changes in underlying bone, and further damage to cartilage triggered by the affected bone.
  • Image not available. Manifestations of OA are local, affecting one or a few joints; the knees are most commonly affected, as well as the hips and hands. Osteophytes (bony proliferation of affected joints) are often found, in contrast to the soft tissue swelling of rheumatoid arthritis.
  • Image not available. Nonpharmacologic therapy is the foundation of the treatment plan for all patients with OA. Nonpharmacologic therapy should be initiated before or concurrently with pharmacologic therapy.
  • Image not available. The most common symptom associated with OA is pain, which leads to decreased function and motion. Pain relief is the primary objective of medication therapy.
  • Image not available. Based on efficacy, safety, and cost considerations, scheduled acetaminophen, up to 4 g/day in divided doses, should be tried initially for pain relief in knee and hip OA. If this fails, topical or oral nonsteroidal antiinflammatory drugs (NSAIDs) are recommended, if there are no contraindications.
  • Image not available. Strategies to reduce NSAID-induced GI toxicity include the use of nonacetylated salicylates, COX-2 selective inhibitors, or the addition of misoprostol or a proton-pump inhibitor. COX-2 selective inhibitors vary in their ability to prevent GI toxicity, and concomitant use of aspirin largely negates their gastroprotective effects.
  • Image not available. COX-2 selective inhibitors can increase the risk of cardiovascular events. This may be a class effect, but the extent of this risk varies among COX-2 selective inhibitors, and traditional NSAIDs may also pose risks. This hazard, in addition to the GI toxicity possible with all NSAIDs, underscores the importance of using NSAIDs only as needed and after assessing the individual patient’s risk.
  • Image not available. NSAIDs are associated with GI, renal, cardiovascular, liver, and CNS toxicity. Monitoring with complete blood count, serum creatinine, and hepatic transaminase levels can be valuable in detecting potential toxicity.
  • Image not available. Topical NSAIDs are recommended for patients older than 75 years to decrease the risks of systemic toxicity.
  • Image not available. Other agents useful in treating knee OA include tramadol, intraarticular injections of corticosteroids, and duloxetine.

On completion of this chapter, the reader will be able to:

  1. Describe two physical and/or chemical characteristics of articular cartilage that make it suitable for its role in joint function.

  2. List three risk factors for the development of osteoarthritis (OA).

  3. Explain the basic pathophysiology of OA.

  4. Discuss the benefits and challenges associated with exercise as a treatment modality to decrease OA pain.

  5. Appropriately counsel an overweight patient with OA regarding the value of weight loss and exercise for the treatment of OA pain.

  6. Explain the mechanism of action of nonsteroidal antiinflammatory drugs (NSAIDs) ...

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