Brian T. Easton, MD Lebanon, Virginia Submitted, revised, August 1, 2001. From the Department of Family Medicine, University of Virginia. Reprint requests should be addressed to Brian T. Easton, MD, PO Box 2377, 164 Carroll Street, Lebanon, VA 24266. E-mail: bte2w@virginia.edu
References
Osteoarthritis (OA) is a chronic and progressive disease in which damage is done to the joint and surrounding tissue. In the United States, OA is found in 6% of people older than 30 years and in 50% of those older than 60 years.1,2 It is the most common cause of disability in the United States and leads to considerable costs due to medical and surgical interventions and frequent absences from work.3-5 OA accounts for 2% of all visits to family physicians and is the 10th leading diagnosis encountered.6 Thus, a family physician can expect to have 2 or 3 patient encounters per week in which OA is one of the diagnoses. With the growing elderly population, this burden is likely to increase.
Pathophysiology
In OA, the smooth surface of hyaline cartilage develops irregularities because of alterations at the cellular level and gross mechanical forces.2 The role of inflammation has been debated in recent years, and its exact role is unknown. As OA progresses, the nearby bone remodels and forms further joint irregularities and osteophytes. These changes lead to narrowing of the joint space, and in some cases, chronic synovitis. Clinically, this causes pain, restricted movement, and periarticular muscle wasting. Treatment is aimed at these symptoms and structural abnormalities. The joints most commonly affected include the knees, hips, cervical and lumbosacral spine, distal interphalangeal (DIP) joints (producing Heberden nodes), proximal interphalangeal (PIP) joints (producing Bouchard nodes), and the first carpometacarpal joints of the hand. It is not known why these changes occur in some people and not in others. Epidemiologic studies and a recent sibling study raise the question of genetic influences in OA of the hip.7,8
Diagnosis
The diagnosis of OA is made on the basis of clinical and radiographic features. Few studies have compared a diagnostic test or strategy with a gold standard. Unfortunately, we do not have any good data about the usefulness of individual history and physical examination elements for diagnosing OA. Radiographs suggesting the diagnosis of OA (joint space narrowing, presence of osteophytes, irregular joint surfaces, sclerosis of subchondral bone, or bony cysts) must be closely correlated with clinical symptoms. According to epidemiologic surveys, only one half of patients with radiographic changes of OA of the knee complain of persistent pain.9 Classification criteria for OA of the knee, hip, and hands have been developed; they are outlined in Tables 1Table 2 through Table 3.10,13
Although these criteria have limitations, they are becoming the standard for defining these types of OA and have been adapted by the American College of Rheumatology.11-13 Currently, there are no criteria for diagnosing OA of the back. When evaluating a patient with joint pain, other diagnoses must be considered (ie, rheumatoid arthritis, gout, pseudogout, septic arthritis, bursitis, and tendonitis).
Treatment
Most of the treatments of OA address the symptoms rather than the cause of the disease. The short-term goal is to decrease pain; long-term goals are to improve functioning and slow progression of disease. Table 4 provides a summary of treatment options.
Exercise
A systematic review of 12 randomized controlled trials (RCTs) showed beneficial effects of exercise therapy in patients with mild to moderate OA of the knee and, to a lesser extent, the hip.14 Benefits included improvements in pain, self-reported disability, walking performance, and the patient’s global assessment of symptoms. Insufficient evidence was available to recommend one type of exercise program over another. Exercise interventions included aerobic exercises, strength training, range of motion exercises, and fitness walking. Exercise programs were conducted as individuals or groups, supervised or home-based. Although this review was limited by the small number of good studies, recommending exercise for OA may improve patients’ symptoms and add other health benefits.
Physical Therapy
A recent RCT compared 4 weeks of manual physical therapy plus a supervised knee exercise program with sham ultrasound for treatment of OA of the knee.15 By 8 weeks, 6-minute walk distances had improved by 13% in the treatment group compared with no change in the placebo group; osteoarthritis index scores had improved 56% over baseline compared with 15% in the placebo group. One year following therapy 5% of the treated group had undergone knee arthroplasty compared with 20% of the untreated group (number needed to treat = 7). Given these clinically important improvements, physical therapy should be an early choice in the treatment of OA.
A systematic review of transcutaneous electrical nerve stimulation (TENS) for treatment of OA of the knee found that this noninvasive modality offered significant pain relief.16 Both high-frequency and strong burst mode TENS showed significant improvement in pain relief when used for 4 weeks or more. Also, the acupuncture-like TENS improved pain relief, stiffness, and walking time in a 2-week placebo-controlled trial.