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Osteoarthritis: 20 Clinical pearls

Osteoarthritis: 20 Clinical pearls

ABSTRACT: Osteoarthritis (OA) is the leading cause of chronic disability in older adults. A multitude of factors can contribute to the disease process. Only a portion of patients who have radiographic evidence of OA have associated pain. Several conditions can mimic OA. Laboratory tests often contribute little to the diagnosis. Treatment should be tailored to individual patients. Exercises and joint protection techniques are the mainstays of treatment. Patient education may be beneficial. Acetaminophen and NSAIDs are effective in many patients. Cyclooxygenase-2 inhibitors are associated with improved GI tolerability. Glucosamine and chondroitin sulfate may produce improvements in pain and function and may be associated with a decrease in the radiographic progression of OA. Corticosteroids can provide symptomatic relief. Surgery is an option for advanced
disease. (
J Musculoskel Med. 2008;25:476-480)
 

Osteoarthritis (OA), affecting more than 20 million persons in the United States alone, is by far the most common form of arthritis. Because of its high prevalence and its direct association with increasing age, OA is the leading cause of chronic disability in older adults. As the population continues to age in the coming years, OA will take on epidemic proportions.

Successful management of this disabling disease begins with an accurate diagnosis, which is usually based on the physical examination and appropriate joint testing. Treatment is tailored to the individual patient but usually includes exercise, joint protection, analgesic medications, and local corticosteroid injections. Newer treatments, such as ingestion of chondroitin sulfate and glucosamine and intraarticular injections of hyaluronic acid compounds, provide symptomatic relief in some patients, but efficacy in randomized trials has not been consistent. In this article, we review 20 pointers on the diagnosis and management of OA. 

DIAGNOSTIC PEARLS

1. A variety of possible factors underlie OA
OA is a multifactorial disease that often results in joint failure. Its development is related to a combination of aging changes within joint tissues and factors that affect joint structure or joint biomechanics. These factors, which vary among individual persons, can include obesity, previous joint injury, weakness in supporting muscles, congenital joint abnormalities (eg, hip dysplasia), joint use, joint alignment and laxity, genetic factors, bone density, and nutritional and metabolic factors.1 As OA develops, loss of cartilage; hypertrophic changes in neighboring bone and joint capsule; mild synovial inflammation; and degenerative changes in the menisci, ligaments, and tendons all contribute to pain and loss of joint function, resulting in joint failure.

2. Not simply "wear and tear"
The changes that occur in joint tissues as OA develops are the result of an active joint remodeling process in which the activity of catabolic pathways exceeds anabolic repair pathways.2 Unlike an inert automobile part that wears out over time because of repeated use, joint tissues are composed of living cells capable of both destroying and rebuilding tissue. Future treatments of patients with OA will target the imbalance in catabolic and anabolic activity within the joint.

3. Radiographic OA does not equal pain
The presence of radiographically perceived OA does not always correlate with symptoms of pain. Studies suggest that most persons older than 65 years will have radiographic evidence of OA, such as joint-space narrowing, subchondral sclerosis, and osteophytes, in at least 1 joint. However, only a portion of this population will have associated pain. For example, radiographic knee OA is present in about 30% of older adults, but symptomatic knee OA affects only about 7% of the same population.3 Thus, the majority of persons have asymptomatic radiographic disease.

Similarly, degenerative changes of the lumbar spine are found in up to 60% of asymptomatic patients older than 60 years.4 Therefore, it is often difficult to discern whether radiographic changes are incidental findings or are related to patient symptoms. The decision of whether the pain is the result of OA should be based on the clinical evaluation of the patient rather than on the radiographic findings.

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