Upon completion of the chapter, the reader will be able to:
Explain the pathophysiologic mechanisms involved in the development of osteoarthritis (OA).
Identify risk factors associated with OA.
Recognize the clinical presentation of OA.
Determine the goals of therapy for individual patients with OA.
Formulate a rational nonpharmacologic plan for patients with OA.
Recommend a pharmacologic plan for treating OA, taking into consideration patient-specific factors.
Develop monitoring parameters to assess effectiveness and adverse effects of pharmacotherapy for OA.
Modify an unsuccessful treatment strategy for OA.
Deliver effective patient counseling, including lifestyle modifications and drug therapy, to facilitate effective and safe management of OA.
Osteoarthritis is the most common form of arthritis and is strongly related to age. Weight-bearing joints (eg, hips, knees) are most susceptible, but non–weight-bearing joints, especially hands, may be involved. OA causes tremendous morbidity and financial burden because of its high prevalence and effect on joints critical for daily functioning.1 OA is the leading cause of chronic mobility disability and the most common reason for total-hip and total-knee replacement.2
EPIDEMIOLOGY AND ETIOLOGY
Approximately 27 million Americans have signs and symptoms of OA.3 OA is more common in females and older persons, affecting an estimated 10% of men and 18% of women over age 60 years. Approximately 7% of Americans experience daily symptomatic hand OA, 6% experience daily symptomatic knee OA, and 3% experience daily symptomatic hip OA.3 Hip OA occurs more frequently in men.4 However, women tend to have more generalized disease and joint inflammation. Some patients can develop bony enlargements of the hands, called Bouchard nodes or Heberden nodes, in the absence of inflammation. The prevalence of OA in African Americans is similar to whites, but African Americans often experience more severe and disabling disease.
OA is characterized by damage to diarthrodial joints and joint structures (Figure 58–1). The pathophysiology is multifactorial and typified by progressive destruction of joint cartilage, erratic new bone formation, thickening of subchondral bone and the joint capsule, bony remodeling, development of osteophytes, variable degrees of mild synovitis, and other changes.5
Characteristics of osteoarthritis in the diarthrodial joint. (From DiPiro JT, Talbert RL, Yee GC, et al., [eds.] Pharmacotherapy: A Pathophysiologic Approach, 10th ed. New York: McGraw-Hill; 2017:1601, Fig. 90–2; with permission.)
The earliest stages of OA are characterized by increasing water content and softening of cartilage in weight-bearing joints. As the disease progresses, proteoglycan content of cartilage declines, and eventually, cartilage becomes hypocellular. Procatabolic and proinflammatory changes precede cartilage degradation and are thought to play important roles in OA development and progression.6
Subchondral bone undergoes metabolic changes, including increased bone turnover, that ...