The Burden of Osteoarthritis: Clinical and Quality-of-Life Issues
Published Online: October 06, 2009
Roland W. Moskowitz, MD
Osteoarthritis (OA) is the most common form of arthritis, affecting 27 million adults in the United States.1 OA typically occurs in the hands, knees, spine, and hips, although it may be seen in any of a variety of joints.2 Clinical diagnosis is based on observed symptoms, radiographic changes, or both, whereas differential diagnosis is normally supported through the use of laboratory studies. Although OA is often characterized as a degenerative disease, low-grade inflammation actually constitutes an important aspect of OA's pathologic process.3,4
OA is strongly correlated with aging: the risk of OA increases considerably with each decade after the age of about 45 years.1 Nevertheless, aging is not inevitably associated with OA. In fact, several pathophysiologic changes that occur in osteoarthritic cartilage differ notably from that associated with age-related changes in cartilage.5 That said, such age-related changes do play an important role in OA pathogenesis and, at a minimum, predispose individuals to the disease.6
Other than increasing age, there are a number of risk factors for OA, including comorbidities both related and unrelated to musculoskeletal conditions.7 The presence of other joint diseases is the most common musculoskeletal comorbid risk factor, whereas obesity is among the most common nonmusculoskeletal comorbidities associated with OA.7 Lifestyle variables, such as a history of manual labor and cigarette smoking, as well as sex- and phenotype-related conditions-such as age at menarche and joint hyperlaxity in men-can also play a role in conferring risk of OA.8 The genetic component of OA risk, while still being studied at present, has been partially elucidated in recent years as genome-wide scan studies have identified genetic variants associated with OA.9
Ultimately, it is the burden of suffering experienced by people with OA that is of primary concern, and that burden can be significant. Pain and functional impairment are the key domains of that burden, and taken together they often exert a significant reduction in quality of life (QOL).10-13 The present review will briefly describe the pathophysiology, prevalence, and typical outcomes of OA before addressing the issue of QOL in OA and the best means in which to measure it.
Pathophysiology of OA
Cartilage remodeling involves balanced interactions of synthesis and degradation to achieve homeostasis of the extracellular matrix (ECM).14 In OA this process becomes unbalanced, leading to pathologic changes in the affected joint.15 The articular cartilage cells, chrondocytes, are responsible for maintaining homeostasis of the ECM by producing its major components, collagen and proteoglycan, in response to deterioration. Changes in the chrondocytes are associated with abnormal anabolic and catabolic activities as well as abnormal proliferation and apoptosis.
In the early stages of OA, loosening of the collagen network as well as proteoglycan loss occur in the upper cartilage zones and may still, at that point, be reversible.15 Over time, these changes occur within deeper cartilage zones, reducing the elasticity of the cartilage and making a return to homeostasis increasingly difficult to achieve. Chrondocyte senescence-which is associated with increasing age-also appears to play a part in a reduced capacity for cartilage repair and contributes to OA progression.16
Recent data support the notion that changes in subchondral bone are also a factor in cartilage degradation.17 The subchondral bone, which is in immediate proximity of cartilage, may contribute to cytokines, growth factors, and prostaglandins escalating-perhaps initiating-the degenerative process.
Prevalence and Incidence of OA
Collecting prevalence data from multiple sources, including the Third National Health and Nutrition Examination Survey (NHANES III), the Framingham Osteoarthritis Study, and the Johnston County Osteoarthritis Project, the National Arthritis Data Workgroup arrived at a prevalence figure for 2005 of 26.9 million US adults (aged >25 years) with some form of OA.1 This constitutes a growth of approximately 6 million cases from 1995, more than a one-fourth increase in just 10 years. This likely reflects, in part, an aging of the US population, although increases in other related factors, such as obesity, as well as increases in methods of OA detection, may play a role in this observed prevalence.
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