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ABSTRACT: Osteoarthritis (OA) is the leading cause of chronicdisability in older adults. A multitude of factors can contribute to thedisease process. Only a portion of patients who have radiographicevidence of OA have associated pain. Several conditions can mimicOA. Laboratory tests often contribute little to the diagnosis.Treatmentshould be tailored to individual patients. Exercises and joint protectiontechniques are the mainstays of treatment. Patient educationmay be beneficial. Acetaminophen and NSAIDs are effective in manypatients. Cyclooxygenase-2 inhibitors are associated with improvedGI tolerability. Glucosamine and chondroitin sulfate may produceimprovements in pain and function and may be associated with adecrease in the radiographic progression of OA. Corticosteroids canprovide symptomatic relief. Surgery is an option for advanceddisease. (J Musculoskel Med. 2008;25:476-480)
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.
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.
The physical examination should search for the presence of bone enlargement, crepitus, tenderness, and pain with both active and passive movement that suggests OA. Conditions that can mimic OA, such as bursitis and tendinitis, often present with pain more localized to the involved structure that worsens with active joint movement.
4. Is it knee OA or patellofemoral disease?
Anterior knee pain may be associated with patellofemoral disease. Younger patients with anterior knee pain may have mechanical dysfunction of the quadriceps and patellofemoral apparatus. The condition, sometimes referred to as "patellofemoral pain syndrome," is the leading cause of knee pain in patients younger than 45 years.5 The condition has a propensity to occur in women and may be self-limited.
Patients present with anterior knee pain that worsens with bending activities, such as climbing stairs. Prolonged sitting may worsen the pain. Often, patients also complain of instability, or "giving way," of the leg. On examination, pain can be elicited with compression of the patella and the patella may be "hypermobile. "Radiographs may show lateral subluxation of the patella. Patellofemoral disease is less responsive to pharmacological treatment. Thus, physical therapy, activity modification, and bracing are the mainstays of treatment.
5. Periarticular syndromes can mimic or add to OA pain
Syndromes such as bursitis and tendinitis can be associated with OA. In addition to being mimickers of OA pain, these periarticular conditions can at times arise from abnormal biomechanics related to OA pathology at the joint. The anserine bursa, located at the insertion of the medial collateral ligament at the knee, commonly becomes inflamed. Patients present with localized tenderness medially, about 2 to 3 cm below the joint line. A corticosteroid injection into the bursa can provide prompt symptom relief.
6. Lateral hip pain suggests bursitis, not OA
Trochanteric bursitis is a common cause of "hip" pain in older persons. Associated conditions include those that alter gait, such as lumbar spine disease, sacroiliac disease, leg length discrepancy, and OA of the large lower extremity joints.
The diagnosis can be made through the history and physical examination. Patients usually complain of pain localized to the lateral aspect of the upper thigh, unlike in hip OA, in which the pain is usually described as being localized to the groin.
Patients often comment on having difficulty in sleeping on the affected side. Unlike in hip OA, in which pain is elicited by internal rotation of the hip, the physical examination reveals pain with external rotation of the hip and localized tenderness with palpation over the greater trochanter. Injection of corticosteroids to the affected area is both diagnostic and therapeutic.
7. Laboratory testing usually not necessary
OA is a clinical diagnosis based on the patient's history, physical examination, and radiographic evaluation. Ordering rheumatoid factor (RF), antinuclear antibody (ANA) assays, and other tests is most often unnecessary and not cost-effective. RF is found in up to 10% of healthy patients,6 and ANA may be detected in up to 30% of healthy adults.7 Therefore, these tests have a low positive predictive value and do not provide clinical evidence of a systemic connective-tissue disorder.
8. Pain at base of thumb is a common complaint
The first carpometacarpal joint is a common site for OA. Women are affected more often than men. Patients present with pain at the base of the thumb that can be confused with wrist pain or de Quervain tenosynovitis. A classic "squaring" appearance of the base of the thumb may be present on both x-ray film and physical examinations. When traditional analgesics do not succeed, local injections of corticosteroids and splints or orthoses can help in management.
9. Erosions of hand OA differ from those of RA
Erosive, or inflammatory, OA affects the interphalangeal joints of the hands, more commonly in women than in men.8 At times, erosive OA may be confused with rheumatoid arthritis (RA). However, the erosions associated with OA are centrally located and associated with sclerosis; those of RA are generally periarticular and associated with juxta-articular osteopenia. In addition, the erosions of OA may affect the distal interphalangeal (DIP) joints, which are spared in RA.
10. Heberden node: Is it OA or gout?
Acute pain and swelling in a Heberden node (an area of bony enlargement and deformity seen with OA of the DIP joints) may suggest gout. These joint changes are most often asymptomatic. On occasion, these joints can be affected by gout, particularly in older women. A high frequency of diuretic use has been reported in such patients.
11. OA and hemochromatosis
OA changes seen at the second and third metacarpophalangeal (MCP) joints may be associated with hemochromatosis. Although OA can affect the MCPs, this is much less common than proximal interphalangeal and DIP joint disease. Therefore, sclerosis and classic "hooklike" osteophytes at the second and third MCPs should prompt suspicion of OA resulting from conditions that include hemochromatosis and calcium pyrophosphate deposition. Chondrocalcinosis may be noted on radiographs of the involved joints. Iron deposition in cartilage is involved in the pathogenesis. The arthropathy may be the initial presentation of the disease and may affect other joints.
12. Treatment needs to be individualized
Treatment varies depending on the patient's other medical conditions, severity of disability, lifestyle, and pattern and severity of disease. Patients who have a history of hypertension, renal insufficiency, or peptic ulcer disease probably are not candidates for treatment with NSAIDs and may require alternative analgesics, localized treatments, and physical therapy. Simple analgesics instead of NSAIDs should be considered as first-line therapy in patients who have a history of hypertension, renal insufficiency, or peptic ulcer disease. Those who have milder disease may obtain significant benefit from an exercise program. Obese patients can benefit from dietary counseling and exercise.
13. Exercise is a mainstay of therapy
Physical and occupational therapy are important modalities in the treatment of patients with OA. The exercises and joint protection techniques learned during such therapy should be mainstays of treatment throughout the course of the disease. Physical therapy includes targeted muscle strengthening and range of motion exercises as well as general aerobic conditioning. Studies support the benefits of exercise and physical therapy for OA in improving pain, muscle strength, and self-reported disability as well as in delaying the need for total joint replacement surgery.9 Occupational therapists can suggest canes or other assistive devices for advanced disease. Proper footwear, tailored orthoses, and splints can also help.
14. Patient education for long-term management
A comprehensive treatment approach is beneficial in the long-term management of OA; this includes provision of adequate social support and patient education. Independent, structured education programs for patients with OA and telephone-based interventions have been shown to benefit patients; resulting decreases in pain and visits to physicians are almost comparable to those with treatment using NSAIDs. Interestingly, office-based education during regularly scheduled patient visits does not achieve such benefits.10 Educating family members may improve their ability to provide adequate social support to the patient.
15. Acetaminophen is suggested as first-line pharmacological therapy for OA
Both the American College of Rheumatology and the Osteoarthritis Research Society International (OARSI) recommended acetaminophen as first-line pharmacological therapy for mild to moderate pain associated with OA of the hip or knee. The recommendations are based both on its efficacy and safety profile at a dose of 4 g/d.11 Short-term randomized, controlled trials comparing acetaminophen with NSAIDs showed that although the group of patients treated with NSAIDs reported decreased pain at rest compared with the acetaminophen group, the treatments provided similar improvements in quality-of-life measures.
Both NSAIDs and acetaminophen have been shown to decrease pain in OA by about 30%, but surveys have indicated that about 60% of patients prefer NSAIDs over acetaminophen.12 However, acetaminophen has a superior cost and safety profile compared with NSAIDs. The most common concern with acetaminophen use, hepatotoxicity, is usually relevant only in patients using excessive doses of medication, in those with underlying liver disease, and in those with significant alcohol consumption.
16. The use of NSAIDs should be individualized
Both the efficacy and adverse effects associated with various NSAIDs differ in individual patients, but there are general points to consider when using an NSAID. For example, in older patients, ibuprofen was associated with a lower risk of adverse effects compared with other NSAIDs and, therefore, is recommended as the first-line nonselective NSAID by some published guidelines.13 Nonacetylated salicylates, such as salsalate and choline magnesium trisalicylate, are suggested to have less renal toxicity and less antiplatelet activity than some of the other available agents.14
Indomethacin is not a preferred NSAID for management of OA pain in older patients. Some studies suggest that indomethacin may be associated with accelerated joint degeneration in patients with knee OA, and older patients appear to have more adverse effects from indomethacin than from other NSAIDs. Because of the multiple adverse events associated with NSAIDs, particularly in older patients, the lowest effective dose should be used and patients should be monitored at regular intervals.
17. COX-2 inhibitors and NSAIDs: Toxicities and precautions
The OARSI guidelines suggest that patients with increased GI risk factors should consider treatment with cyclooxygenase (COX)-2 inhibitors or traditional NSAIDs with the addition of misoprostol or a proton pump inhibitor. However, other potential toxicities with these agents, including renal and cardiovascular toxicity, need to be considered.
Although rofecoxib was removed from the market for an associated increased risk of adverse cardiovascular thrombotic events, recent meta-analyses with both celocoxib and nonselective agents showed no significant difference in cardiovascular events between the 2 groups. The increased risk of cardiovascular events in both groups was small (about 1% per year) and was largely nonsignificant, although it varied slightly with individual NSAIDs. However, both COX-2 inhibitors and nonselective NSAIDs carry a black-box warning about their potential cardiac toxicities; current recommendations are to use them with caution in patients with cardiac risk factors.
18. Glucosamine and chondroitin sulfate may be beneficial
Nutraceutical agents, such as glucosamine and chondroitin sulfate, have been subjects of continued controversy for the treatment of patients with OA. Several trials in Asia and Europe have suggested that glucosamine can produce modest improvements in pain and functional outcome compared with placebo, with efficacy similar to that of NSAIDs.15 These trials required that to achieve therapeutic benefit, a sufficient dosage of the agent (1500 mg/d) be used for a sufficient duration (minimum of 1 month).
One of the major problems with the numerous trials that have been performed with these agents is the heterogeneity of the preparations studied. In addition, because of lack of regulation in the United States, the formulation and dosage of glucosamine labeled in over-the counter preparations may not be reliable. It has been suggested that beneficial effects have been overestimated because of publication bias.
A recent multicenter study in the United States did not find any benefit of glucosamine or chondroitin sulfate when compared with placebo, but the combination of the 2 decreased pain in a subgroup analysis of the subjects reporting more pain at baseline.16 Some studies have suggested that these agents may have a disease-modifying effect.17,18 Considering that they are associated with minimal adverse effects, current recommendations include them in the treatment paradigm for OA, with suggestions to discontinue use if there is no improvement in 6 months.11
19. Intra-articular injections can relieve symptoms
Intra-articular corticosteroids, used sparingly, can provide symptomatic relief for patients who have OA. Studies suggest that intra-articular corticosteroid injections marginally improve OA-associated knee pain when compared with placebo. However, this effect usually lasts only a few weeks, and the long-term adverse effects of these injections are not completely known.
It has been suggested that corticosteroids may accelerate long-term joint damage. However, they are particularly useful in some circumstances, such as for an acutely inflamed or "flared" joint, as an adjunct to physical therapy, and as adjunctive management of patients who are not candidates for surgery. Depending on the joint and severity of disease, patients have varying responses to the injections. No more than 4 injections are recommended during a 1-year period.
Intra-articular viscosupplementation with hyaluronic acid–like compounds is now FDA-approved for the symptomatic management of knee OA. Studies show varying results, although most randomized, controlled trials suggest superior pain relief when compared with placebo.19,20 These injections are usually administered weekly for 3 to 5 weeks. It may take several weeks to achieve symptom relief, but the duration of action appears to be greater than with the use of corticosteroids. Patients who have not improved with simple analgesics or intra-articular corticosteroids and who have contraindications to the use of NSAIDs are candidates for treatment with these agents. However, the exact role of these agents in the management of OA and the cost-effectiveness of their use in clinical practice need to be better defined.
20. Surgery, as a last resort
Total joint replacement (TJR) is an effective treatment option for patients with end-stage OA when more conservative treatment options have not succeeded. OA is the most common indication for TJR of the hip and knee worldwide. Studies show a significant improvement in pain, function, and quality of life for years after such surgery. Pain and disability are the main indications for surgical treatment. Recent studies suggest that earlier surgery before the onset of severe disability leads to improved postoperative outcomes.21 However, one trial suggested that arthroscopic lavage and debridement were no better than placebo in relieving symptoms in patients with knee OA.22