Osteoarthritis: Its Course in Older Patients and Current Treatment Methods
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According to the Centers for Disease Control and Prevention (CDC), by the year 2020 about 60 million Americans will be affected by arthritis. It is a leading cause of disability in developed countries. It limits the physical capability and independence of affected individuals and causes high stress levels for caregivers.
Although the diagnosis of arthritis includes a wide spectrum of more than 100 disorders, osteoarthritis (OA) by definition is a failure of joint cartilage due to “wear and tear.” By age 75, nearly 85% of the U.S. population has clinical or radiographic features of OA.1 Once considered an inevitable part of aging, evidence now indicates that OA is a preventable late-life disease.
PATHOGENESIS
Articular cartilage is the primary tissue affected by OA. This cartilage absorbs shock and prevents stress concentration in the joint during use. Additionally, subchondral bone and periarticular muscles support the joint stricture. Osteoarthritis develops when an imbalance between the biologic properties of these structures and joint loading exists. Therefore, OA will ensue if either the cartilage is defective or an overuse injury occurs. In osteoarthritic cartilage, decreases in the levels of glycosaminoglycans, keratan sulfate, and hyaluronic acid cause diminished aggregation of proteoglycans and impaired function of the cartilage structure. Cartilage oligomeric matrix proteins (COMP), which play a role in organization of collagen fibrils, can be detected in the serum of patients with OA at higher levels, suggesting disruption of normal cartilage metabolism in the affected population.2
RISK FACTORS AND POSSIBLE CAUSES
Studies have identified several important risk factors for the development of OA (Table I). Age appears to be the strongest risk factor, affecting up to 97% of patients over age 65.3,4 Gender differences have been found in several studies, with women exhibiting a higher risk for developing OA.5 Multiple studies link obesity with osteoarthritis. Greater weight and body mass index (BMI) are associated with a higher incidence of hip arthritis.6 With the data from the Nurses Health Study, a prospective cohort study of 120,000 women, Karlson et al7 concluded that higher BMI coupled with older age were associated with increased risk of hip OA requiring surgical treatment.
Trauma and occupational injury has been studied extensively. Occupational activities have been linked to OA. Coggon et al8 compared 518 patients on OA surgical treatment list with controls matched for age and sex. In this study, persons with a BMI of 30 kg/m2 or higher whose work required prolonged squatting or kneeling had an odds ratio of 14.7 (95% CI, 7.2-30.2) of having OA compared with people with a BMI lower than 25 without such occupational hazard. In other studies, cumulative physical stress was linked to joint knee damage.9
Genetic factors such as vitamin D receptor inheritance, cartilage oligomeric protein, insulin-like growth factor, and human leukocyte antigen (HLA) subtypes may play a role in the development of classic OA.10,11 In women, a dominant gene may be responsible for OA associated with Heberden’s node formation, whereas in men this gene is recessive.12
Endocrine factors, particularly estrogen, may modulate the disease activity. Estrogen changes cell metabolism and may protect women against inflammatory diseases. Women on hormone replacement in the Framingham Osteoarthritis Study seemed to be less affected by OA,13 but this remains a controversial association.14
CLINICAL MANIFESTATIONS
The typical presentation of OA is joint pain, often described as a deep ache with use. At first, the pain is relieved by rest, but in severe disease it becomes continuous and interferes with sleep. Morning stiffness is typically brief but may last longer than 30 minutes. It also can occur after a period of inactivity.
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