26: Osteoarthritis

Osteoarthritis (OA) is the most common disease of the joints and is one of the leading causes of disability among older adults in the United States. Older age is the greatest risk factor for OA; the prevalence of symptomatic knee OA was 12.1% among adults age ≥60 years. OA is a complex disorder with multiple risk factors that range from genetic, demographic, metabolic, and biomechanical factors to congenital or developmental deformities of the joint. The diagnosis is based on history (ie, symptoms of joint pain, often with transient morning stiffness), physical examination (ie, crepitus, bony tenderness and bony enlargement) and characteristic radiographic features (ie, joint space narrowing with osteophytes). The multidisciplinary team approach used in geriatric medicine clearly applies to managing the OA patient. Nonpharmacologic measures are critically important in the management of OA in older adults and include aerobic, aquatic, and/or resistance exercises, as well as weight loss for overweight patients. Patient education and psychosocial support are as important as medical therapy, particularly in older adults. Pain relief is the primary indication for the use of pharmacologic agents in patients with OA who do not respond to nonpharmacologic interventions. Because of its efficacy–toxicity profile, acetaminophen is often the initial therapy, and nonsteroidal antiinflammatory drugs (NSAIDs) may be prescribed for those who have inadequate response to acetaminophen. Oral NSAIDs should be used with great caution in older adults given the increased risk of side effects, with topical NSAIDs offering a better efficacy–toxicity profile. Other pharmacologic modalities, including tramadol, intraarticular corticosteroid injections, intraarticular hyaluronate injections, duloxetine, and opioids, are conditionally recommended in patients who have had an inadequate response to initial therapy. Surgical interventions are generally reserved for those who have failed medical therapy, and thus have persistent pain and marked limitations in activities of daily living. The natural course and prognosis of OA largely depends on the joints involved, the underlying risk factors, the presence of symptoms, and the severity of the condition. Recent studies show an increased mortality among persons with OA compared with the general population. Therefore, management of older patients with OA should also focus on effective treatment of cardiovascular risk factors and comorbidities, as well as on increasing physical activity.

The best treatment for OA is prevention. However, OA is often diagnosed in its later stages, and there are no proven therapies that can prevent the progression of joint damage caused by OA. Advances in imaging modalities, especially MRI, and innovations in molecular biology have greatly advanced our knowledge of OA, and efforts are ongoing to identify preclinical biochemical and imaging biomarkers that will provide opportunities to diagnose and treat OA earlier so as to prevent further progression of the disease and increased disability.

Symptoms & Signs

Epidemiology of osteoarthritis—

OA is the most common type of arthritis that involves the entire joint, characterized by changes in articular cartilage (thinning and fissuring), and associated changes in subchondral bone, synovium, ligaments, joint capsule, and/or periarticular muscles. Symptomatic OA is defined by the presence of frequent pain and radiographic evidence of OA in that joint. The Kellgren-Lawrence scale is often used to characterize the radiographic severity of OA. Furthermore, prevalence of radiographic OA varies by the joint involved and differs considerably depending on the inclusion criteria for radiologic severity for OA. Table 26–1 summarizes the prevalence data from 3 recent U.S. population-based studies (the National Health and Nutritional Examination Surveys [NHANES] III, the Framingham Osteoarthritis Study, and the Johnston County Osteoarthritis Project). Hand and knee OA is more common among women, especially after age 50 years, and is also more common among African Americans. OA of the hip is more common in individuals of European descent compared to those of Asian or African descent.

Health impact—

OA is the reason for an estimated 30% of ambulatory care visits and is 1 of the leading causes of disability among older adults in the United States. OA disables approximately 10% of people who are older than age 60 years and compromises the quality of life of more than 20 million Americans. As such, OA costs the United States economy nearly $81 billion per year in direct medical care (eg, physician visits, laboratory tests, medications, surgical procedures), with indirect expenses (eg, lost wages, home care, lost wage-earning opportunities) of an estimated $47 billion per year. Given the aging of the population and increases in the prevalence of major OA risk factors (eg, obesity), the burden of OA is increasing exponentially in both human and economic terms.

Risk factors—

Epidemiologic studies have revealed several risk factors that may influence the development of OA and its subsequent progression. The influence of these risk factors upon the onset of OA differs considerably depending on the joint involved. As noted above, demographic characteristics, such as advancing age, sex, and race, are directly related to prevalence of OA. Genetic risk factors likely play a role as well, but they are probably polygenic and complex in nature. Potentially modifiable risk factors include obesity and biomechanical factors such as repetitive or isolated traumatic injury, malalignment (varus or valgus deformity), overload, joint instability caused by muscle weakness, and ligamentous laxity. These risk factors are particularly important in weight-bearing joints and may influence incidence more than radiographic progression. After age, obesity is the strongest risk factor for knee OA, particularly in women, and this risk applies across the age spectrum. A significantly elevated prevalence of knee OA from overuse has been demonstrated in farm workers, coal miners and construction workers. Long distance running or recreational activity itself is not related to the incidence of OA, barring the presence of joint injury. Age-related increase in obesity, varus/valgus laxity and decrease in muscle strength, and proprioception may also contribute to the development of OA with age.

Pathophysiology—

Given the strong relationship of OA to age, OA has long been considered a “wear and tear” degenerative disease, an inevitable consequence of aging. However, OA can be best defined as failed repair of joint damage that has been caused by abnormal intra- and extraarticular processes involving a combination of biomechanical, biochemical, and genetic factors mediated by a variety of pathways, rather than a degenerative process. Microinjury from excessive mechanical stress is likely to contribute to or trigger the cascade of events that results in the characteristic pathologic features of OA (Figure 26–1). Further damage of articular cartilage is mediated by proinflammatory cytokines and other catabolic factors, causing collagen and proteoglycan degradation. Age-related changes such as chondrocyte senescence and aging changes in the matrix may contribute to development of OA. There are also age-related periarticular changes such as sarcopenia, causing decreased ability of the bridging muscles to act as internal shock absorbers to absorb the forces transmitted to the subchondral bone and cartilage.

Clinical features of OA—

The most common symptom of OA is joint pain. Most patients complain of “mechanical” pain, which tends to worsen with activity and be relieved by rest. The onset of the symptoms of OA is usually insidious, beginning in only 1 or a few joints. Patients with hip or knee OA described 2 distinct types of pain: a dull, aching pain, which became more constant over time, and a less frequent but more intense, often unpredictable pain, which resulted in significant avoidance of social and recreational activities. Any episodic increases in pain and joint swelling should raise suspicion of synovitis caused by crystalline disease, such as gout or pseudogout. With more advanced disease, pain may be noted with progressively less activity, eventually occurring even at rest and at night. The origin of pain in OA is rarely clear and is likely to be heterogeneous. Etiology of pain can be attributed to anatomic changes in the joint, but there are also a number of patient-specific factors that may modify pain perception and pain reporting. Pain is not caused directly by cartilage damage as cartilage is aneural, but subchondral bone, the periosteum, osteophyte, periarticular ligaments, periarticular muscle, synovium, and the joint capsule can all be sources of nociceptive pain in OA as a result of the rich innervation around them. According to a recent systematic review of MRI findings of knee OA, only the presence of bone marrow lesions and synovitis/effusion were significantly associated with the presence of knee pain. Nociceptor pain can become persistent, and persistent pain is often associated with central neurogenic sensitization, thereby establishing a peripherally stimulated, but centrally mediated, chronic pain syndrome. OA can cause morning stiffness, but this typically resolves less than 30 minutes after a patient awakens. Joint stiffness may recur following periods of inactivity, a phenomenon termed gelling. Prolonged morning stiffness lasting more than an hour, nighttime pain that keeps the patient from sleeping, and persistent joint swelling should suggest other potential diagnoses such as an inflammatory arthritis. Patients may also report joint locking or joint instability. In addition to chronic pain and disability, sleep disturbance, fatigue and depression are also prominent features of OA in the older population. Physical examination of the patient with OA may reveal joint-line tenderness, crepitus or grating sensation, and osteophytes, particularly in the hands at the distal interphalangeal (DIP) joints and the proximal interphalangeal (PIP) joints. A varying amount of joint effusion and/or soft-tissue swelling can be present, but tends to be intermittent without warmth. As OA progresses, range of joint motion becomes diminished, and joint deformity and/or joint laxity may develop.

Classification of OA—

Although almost any joint can be involved, OA is often asymmetric and does not affect all joints equally. The joints most commonly affected are the hands, knees, hips, and spine; other joints, such as the shoulder, temporomandibular, sacroiliac, ankle, and elbow, are less commonly involved. OA has been classified as either primary (idiopathic) or secondary to known causes, but, as noted above, there has been much progress in the identification of risk factors for the development of OA. In the past, OA has been considered the prototype of noninflammatory arthritis; however, recent studies show that most types of OA have evidence of synovitis on MRI and/or in pathologic studies. For example, erosive hand OA has marked evidence of synovitis on gadolinium-enhanced MRI. OA has also been classified based on the site of involvement. The term nodal-generalized OA is characterized by polyarticular finger involvement (principally DIP and often PIP), OA of the first carpometacarpal (CMC), and a predisposition to OA of the knee, hip, and spine. It is most common in middle-aged women, typically with a strong family history among first-degree relatives and peak onset around the menopause. Patients complain of a symptomatic inflammatory component in the early stage and have mild functional disability in their hands. Their offspring have a significantly younger age of disease onset (both nodal and large joint OA) and often similar or more severe and extensive disease than their parents. Erosive hand OA shows marked subchondral change, a more florid and prolonged inflammatory component, and a tendency to intraarticular osseous fusion and prominent erosive, destructive changes, especially in the finger joints. It has a substantial impact on hand pain and disability. Systemic inflammatory signs and other typical features of rheumatoid arthritis (RA) (eg, nodules, extraarticular features, rheumatoid factor) are absent. Radiographically, central erosions and the “gull-wing” deformity characterize the disorder.

Certain systemic diseases are associated with the development of “secondary” OA. These include trauma, anatomical abnormalities, metabolic/endocrine disease, postinfectious arthritis, neuropathic disease, and abnormal structure and function of hyaline cartilage (Table 26–2).

Characteristics of specific joint involvement

Many of the characteristic clinical manifestations of OA are related to involvement of specific joints.

Hand OA—

The hands are commonly involved in OA in the population over 50 years of age. The DIP joints and the first CMC joint are commonly affected areas. Enlargement of the first CMC joint can result in a squared appearance to the hand. Prominent palpable osteophytes in the DIPs and the PIPs are known as Heberden nodes and Bouchard’s nodes, respectively. Among United States adults aged ≥60, 58% had DIP, 29.9% had PIP, and 18.2% had first carpal-metacarpal deformities. Symptomatic hand OA was associated with self-reported difficulty in lifting 10 lb, dressing and eating. Women and the very old (≥80 years) are especially vulnerable to the effect of hand problems on their daily activities.

Knee—

Nearly half of adults will develop symptomatic knee OA by age 85 years. Patients with chronic, frequent knee pain most often report localized (69%) knee pain followed by regional (14%) or diffuse (10%) knee pain. Patients with advanced knee OA often experience knee buckling or instability (“giving way”). Of those who experienced buckling, 12.6% fell during an episode. Persons with knee buckling had worse physical function than those without buckling. Common findings of knee OA include crepitus on active motion of the knee, bony tenderness, osteophytes, effusion without palpable warmth, and limitation of range of motion. A joint effusion can lead to flexion of the knee, and synovial fluid may migrate into the semimembranosus bursa posteriorly, creating a fluctuant swelling along the posterior aspect of the knee (ie, popliteal or “Baker’s” cyst).

Hip—

Although anterior or inguinal pain and tenderness typically indicate true involvement of the hip joint, pain from hip OA may be felt in the trochanter, referred to the knee, or along the tensor fascia lata (meralgia paresthetica). Pain around the hip may be caused by pain referred to the hip area from other structures, such as the trochanter bursae, lumbosacral spine, or damaged sciatic nerve. An assessment of the range of motion of the hip and knee joint, tenderness over the greater trochanter (for bursitis), pain in the posterior hip or buttocks (for sciatic nerve damage associated with lumbar radiculopathy) and lower lumbar spine will help determine whether hip pain is referred from these other joint areas. The pain from bursitis is felt laterally and usually does not limit motion. Patients may complain of difficulty walking stairs or lying on their side at night. By comparison, OA of the hip is associated with pain and limited range of motion, particularly with extension and internal rotation. The patient develops a characteristic gait in which they shift weight to the contralateral uninvolved hip (antalgic gait). The extremity shortens as the femoral head migrates superiorly in the acetabulum. Radiographic findings include osteophytes (femoral or acetabular) and joint space narrowing (superior, axial or medial).

Spine OA—

A continuum of clinical and radiologic findings including intervertebral disc narrowing, osteophytes arising from the margins of the vertebral body, and facet joint changes is often termed degenerative disease of the spine (“spondylosis”). Radiographic evidence of degenerative disease in the spine is almost universal in older people, but the correlation with the presence and severity of pain is very poor. Cervical spondylosis can cause neck pain, occipital headaches, upper extremity radicular pain, shoulder pain, and loss of dexterity of hands. In the cervical spine, although not common, large osteophytes may compromise the spinal canal, causing lower-extremity spasticity and gait disturbance. Anterior cervical osteophytes can impair movement, often related to diffuse idiopathic skeletal hyperostosis (DISH), and can cause pharyngeal stage dysphagia in older adults. Discogenic pain by disc herniation into the spinal canal or into the foramen is often characterized by low back and referred buttock/posterior thigh pain (radicular pain), aggravated by movement and sitting. Pain from facet joint OA is often aggravated by extension of the spine. Lumbar facet joint osteophytes can lead to lumbar canal stenosis from facet enlargement encroaching into the intervertebral foramina and/or spinal canal. The symptoms of spinal stenosis are often relieved by bending slightly forward, since the spinal canal dimensions increase in this position. Spinal stenosis can be related to neurogenic claudication, a pain in the legs or buttocks that worsens with prolonged standing and is relieved by sitting. Spondylolisthesis, a slipping of one vertebral body on another, is often associated with aching in the back and posterior thighs after standing. Nocturnal spine pain should raise concerns about a more ominous process, such as a malignancy. Osteoporosis-related compression fracture should be considered for the sudden onset of severe back pain.

The clinical diagnosis of OA is based on history, physical examination, and, sometimes, characteristic radiographic features. Before making a clinical diagnosis of OA in older adults, other disorders should be excluded, as physical or radiographic finding of OA is quite common in older adults without accompanying symptoms. When an older patient presents with less-typical features or has unusual joint involvement, confirming the presence of OA unequivocally can be particularly difficult. The physician must distinguish OA from referred pain, other inflammatory joint diseases such as RA, gout or pseudogout (ie, calcium pyrophosphate disease [CPPD]), and soft-tissue processes such as periarticular bursitis (eg, pes anserine bursitis mimicking knee OA, greater trochanteric bursitis simulating hip OA). Such patients will benefit from imaging studies of affected joints in combination with selected laboratory tests, although most patients do not need imaging studies for the diagnosis of OA. The characteristic radiographic features of OA include joint space narrowing, subchondral sclerosis, osteophytes, subchondral cysts, and altered bone contours. The presence of articular cartilage calcification (chondrocalcinosis) may be a clue to the presence of CPPD or secondary OA from an endocrine, metabolic, or heritable disorder that predisposes OA. Ultrasonography may be useful to demonstrate underlying inflammatory process such as synovitis or bursitis. Laboratory studies are not helpful in diagnosing OA, but may be required to help rule out other disorders (eg, gout, RA, or septic arthritis) or to diagnose an underlying disorder causing secondary OA, particularly among those with knee, hip, or atypical joint involvement. Inflammatory markers, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level, and immunologic tests, such as antinuclear antibodies and rheumatoid factor, should not be ordered routinely in older adults unless there are signs and symptoms of inflammatory arthritis or systemic autoimmune diseases. A uric acid level is recommended only if gout is suspected. Because these immunologic tests or serum urate levels often yield false-positive results in older adults, performing them may only add unnecessary diagnostic confusion when the pretest probability is low. When a patient presents with acute joint pain with synovial effusion, joint aspiration and synovial fluid analysis should be performed to rule out infectious etiology or crystalline disease. Synovial fluid findings in OA usually suggest a minimally inflammatory (white blood cell count <2000/mm³) or noninflammatory process. A number of biochemical markers are under investigation to help with diagnosis and to determine risk of progression or response to therapy.

Goals of Treatment

Patients with OA seek medical attention because of pain. In addition to pain, OA is accompanied by structural changes not only within the joint, including cartilage loss and formation of osteophytes, but also changes in muscle, bone, tendons, ligaments, menisci, synovium, and the joint capsule. These changes result in altered joint mechanics and muscle weakness, causing decreased physical function and disability. Therefore, functional improvement is as important as pain management in OA, particularly in the geriatric population. The multidisciplinary team approach often used in geriatric medicine clearly applies to managing the OA patient. The Osteoarthritis Research Society International (OARSI) and European League Against Rheumatism (EULAR) have developed guidelines for the management of OA of the hand, hip, or knee. Table 26–3 summarizes the most recent American College of Rheumatology (ACR) guidelines on the treatment of OA.

Nonpharmacologic Therapy

The nonpharmacologic program is critically important and needs to become a part of an OA patient’s lifestyle. It should be used prior to or in conjunction with pharmacologic treatments. Nonpharmacologic modalities strongly recommended for the management of knee OA include aerobic, aquatic, and/or resistance exercises, as well as weight loss for overweight patients.

Exercise—

Exercise is integral in reducing impairment, improving function, and preventing disability. A systematic review and meta-analysis for exercise therapy and OA of the hip or knee concluded that strength training or aerobic exercise regimens for patients with OA led to improved physical health and symptoms of OA. There was no significant difference in terms of reducing arthritis-related symptoms and disability in OA patients between aerobic and resistance training. For patients with advanced OA, range of motion and isometric strengthening exercise can initially be prescribed, and an exercise regimen may progress sequentially through isotonic strengthening, aerobic exercises, and, ultimately, to recreational exercise. Extra attention is needed for the older patient to enhance both safety and compliance with an exercise program; indeed, interventions such as supervised or individualized exercise therapy and self-management techniques may enhance exercise adherence. Tai Chi exercises specifically designed for patients with arthritis may also offer some symptomatic relief and are conditionally recommended by the ACR. Water exercises are of value for those with severe arthritis and marked deconditioning. In addition, elliptical training, cycling, and upper body exercise may help in such cases.

Weight loss—

A 2007 meta-analysis of weight reduction and knee OA showed that physical disability diminished after a moderate weight reduction regime, with weight loss of >5% from the baseline to be achieved within a 20-week period; that is, 0.25% per week. In addition, pain and physical disability were reduced if the patient lost more than 6 kg (13.2 lb). The combination of diet and modest exercise in older adults with knee OA has been known to be most effective in weight control. However, weight loss in the overweight, inactive older patient is a particular problem as weight loss without exercise can cause inadvertent decrease in muscle mass (sarcopenia).

Other nonpharmacologic modalities—

Other nonpharmacologic modalities conditionally recommended for knee OA include medial wedge insoles for valgus knee OA, subtalar strapped lateral insoles for varus knee OA, medially directed patellar taping, manual therapy, walking aids, thermal agents, self- management programs, and psychosocial interventions. Knee bracing was recommended by EULAR, but ACR has no recommendation because of conflicting data on efficacy. Patients may benefit from using a cane in one hand for OA of the contralateral hip or knee, but it needs to be properly fitted (ie, when standing, the elbow should be bent to approximately 20 degrees). When disability is more severe, a walker may be needed to maintain function. Physiotherapeutic measures include therapeutic ultrasound, manual therapy, application of heat and/or cold modalities, stretching/traction, and transcutaneous electrical nerve stimulation (TENS). Patient education and psychosocial support are as important as medical therapy, particularly in older adults. The patient needs to be educated on the nature of OA and its impact on their physical activity. Therapeutic options and the risks and benefits of the different approaches to management should be provided in depth. The initial patient evaluation should include an assessment of symptoms of depression and specific coping strategies that may limit future compliance to therapeutic recommendations. Lifestyle modifications are an integral part of the nonpharmacologic program. A patient with lumbar spine, hip, or knee OA should avoid deep chairs and recliners from which posture is poor and rising is difficult. Resting the affected joint can ease pain short-term, but prolonged rest may lead to muscle atrophy and decreased joint mobility.

Pharmacologic Therapy

Pharmacologic therapy is added when the nonpharmacologic program does not provide adequate relief of pain. Pharmacologic modalities conditionally recommended for the initial management of patients with knee OA include acetaminophen, oral and topical NSAIDs, tramadol, intraarticular corticosteroid injections, intraarticular hyaluronate injections, and duloxetine. Opioids were conditionally recommended in patients who had an inadequate response to initial therapy, but opioids should be used with caution in older adults.

Analgesics—

Acetaminophen is the initial therapy for mild OA because it is inexpensive, relatively safe, and effective. Although most patients have tried acetaminophen prior to visiting the physician, they rarely have tried the maximum recommended dose (4 g/day). It is important to review the patient’s medications exhaustively, including combination products with opioid analgesics and nonprescription medications, when the physician considers initiating acetaminophen in the full dosage. Hepatotoxicity can occur, but, at the therapeutic range, is primarily seen mainly in patients with concurrent alcohol abuse or in conjunction with other hepatotoxic medications. In OA subjects with moderate-to-severe levels of pain, NSAIDs appear to be more effective than acetaminophen. When acetaminophen fails to control symptoms, the use of NSAIDs or intraarticular corticosteroid injections is recommended. There is no convincing evidence that any of the available NSAIDs is more effective than any other for OA of the knee or hip, and patients’ responses to the different agents in terms of both efficacy and toxicity are unpredictable. Thus, low-cost products with a short half-life, such as ibuprofen or naproxen, may be an appropriate initial choice. If 2 to 4 weeks of low-dose therapy does not yield adequate control of pain, the dose should be gradually increased toward the maximum of that medication, taking into account the patient’s other comorbid conditions. Patients should be well informed of adverse effects, including peptic ulcer, gastrointestinal bleeding, renal dysfunction, edema, abnormal liver function tests, elevated blood pressure, and the potential cardiovascular risk when the therapy is initiated. Presence of multiple comorbidities and the risk of NSAID-associated gastrointestinal (GI) side effects limit their use in older patients, those on aspirin or anticoagulants, and those on concomitant use of glucocorticoids. The risk of GI side effects is greatest in the first month of use. Central nervous system dysfunction in older adults can occur even with the standard dosages, particularly with indomethacin. Nephrotoxicity is more likely to occur in patients with preexisting diabetes mellitus, congestive heart failure, liver cirrhosis, diuretic therapy, or chronic kidney disease while using an NSAID. The nonacetylated salicylates, sulindac, and nabumetone appear to be less toxic to the kidney. Short-acting NSAIDs, such as ibuprofen, interfere with the desirable antiplatelet effects of low-dose aspirin and should not be administered within 3 hours of aspirin. The risk of GI bleeding can be lessened by use of a cyclooxygenase-2 selective inhibitors (eg, celecoxib or meloxicam) or concomitant use of a proton pump inhibitor or misoprostol. However, gastroprotective agents are not protective below the ligament of Treitz and lower GI bleeding risk, which is common with NSAID use in older adults, remains high even with use of these agents. The potential reduction in GI risks cannot justify the use of cyclooxygenase inhibitors as an initial agent, given concerns about the increased risk of cardiovascular events and their cost. Furthermore, in the presence of low-dose aspirin, reduction of GI adverse effects may not be maintained. Topical NSAIDs use is also conditionally recommended for the hip or knee OA. Topical NSAIDs are safer but may be less efficacious than oral NSAIDs. Topical capsaicin or other salicylate-containing topical agents (eg, trolamine salicylate, hydroxyethylsalicylate, diethylamine salicylate) can relieve OA pain. ACR guidelines supports the use of topical capsaicin only for hand OA. Tramadol is a dual-acting weak mu-receptor inhibitor with serotonin reuptake inhibition. It has been shown to have an additive effect with acetaminophen. Side effects of tramadol include nausea, vomiting, lightheadedness, dizziness or headache. Because of frequent central nervous system-induced side effects in older people, the initial dose should be lowered, or avoided if possible, in the geriatric population. Although the ACR and EULAR guidelines on treatment of knee OA support the use of opioids when other treatments have failed or are not appropriate, they are poorly tolerated in older patients because of increased sensitivity to adverse side effects, particularly sedation, confusion, and constipation. The lowest dose of opioids should be used, whenever possible. Increased risk of falls from opioids use is of great concern for those who are already vulnerable to falls as a result of underlying joint failure. Opioid analgesics may be beneficial in older patients who were either not willing to undergo or had contraindications for total joint arthroplasty after having failed all other nonpharmacologic and pharmacologic therapies. Oral administration of a serotonin and norepinephrine reuptake inhibitor (eg, duloxetine) shows promise in the treatment of OA.

Intraarticular glucocorticoid injections help to relieve pain and increase joint flexibility for variable periods of time. They may be of greater value when synovial effusions or signs of inflammation are present and in patients with 1 or a few joints that are painful despite the use of an NSAID. Intraarticular glucocorticoid injections are recommended to be limited to less than 5 times a year in any given joint. With proper use of aseptic technique, septic arthritis is a very rare complication. Steroid injections should be used with caution in diabetic patients. Hip joint injection requires ultrasonographic or fluoroscopic guidance, and efficacy of glucocorticoid injections at sites other than the knee or hip is less certain. Hyaluronic acid is a simple, conserved long-chain high-molecular-weight disaccharide that is a natural secretion of the synovium in a normal joint. However, hyaluronic acid in the joints of OA patients is most often of low molecular weight, losing its biomechanical and antiinflammatory properties. Intraarticular injection of moderate to high-molecular-weight hyaluronan preparations, also known as viscosupplementation, are widely used to treat OA of the knee, but there is still some uncertainty about whether the injections are superior to placebo, oral NSAIDs, or intraarticular glucocorticoids. Significant pain reduction is often not achieved until weeks following the initial injection. The injections are generally well tolerated but there is a risk of postinjection reactive inflammatory synovitis and a small risk of joint infection.

Nutraceuticals—

Nutraceuticals are natural substances used to promote health and prevent disease. There are several nutraceuticals that are used for treatment of OA. The use of glucosamine and chondroitin for OA has been controversial, and results of randomized trials have varied. The balance of evidence from high-quality trials has shown little to no evidence of clinically meaningful benefit. ACR experts conditionally recommend that patients with knee or hip OA should not use the chondroitin sulfate or glucosamine. Other nutraceuticals that have been tried in the management of OA include flavocoxid, S-adenosylmethionine (SAM-e), Boswellia, collagen hydrolysate, Avocado-soybean, curcuma (tumeric), ginger, and evening primrose oil, but each of these have very limited evidence of efficacy.

Other agents—

Colchicine has been tried in patients who have inflammatory OA that is refractory to NSAIDs and/or intraarticular glucocorticoids and who have evidence of CPPD crystals. Hydroxychloroquine has also been tried anecdotally in patients with inflammatory or erosive OA that has been unresponsive to NSAIDs.

Complementary and Alternative Treatment

Acupuncture is conditionally recommended only for patients with refractory symptoms who desire nontraditional therapies or who cannot undergo surgical interventions. According to a recent meta-analysis on the effectiveness of acupuncture for OA of the knee, acupuncture seems to provide improvement in function and pain relief as an adjunctive therapy for OA of the knee when compared with credible sham acupuncture and education control groups.

Recommendations for hip OA are similar to those for the management of knee OA.

Modalities conditionally recommended for the management of hand OA include instruction in joint protection techniques, provision of assistive devices, use of thermal modalities and trapeziometacarpal joint splints, and use of oral and topical NSAIDs, tramadol, and topical capsaicin.

Surgery

Arthroscopic surgery—

Randomized trials have shown that arthroscopic surgery is no better than placebo for symptomatic benefit in knee OA. Recent epidemiologic studies have shown that meniscal damage is common in individuals with knee OA and may often be asymptomatic. Meniscectomy for traumatic injuries is associated with increased risk of developing knee OA. Therefore, the benefits of partial meniscectomy in knee OA is also unclear.

Total joint arthroplasty—

Although there are no clear criteria for surgical indication, surgical interventions are generally reserved for individuals with severe symptomatic OA who have marked limitations in function, such as performing the activities of daily living, and who have failed nonpharmacologic and pharmacologic therapies. Potential surgical candidates should have had an adequate trial of exercise and physical therapy. The primary goals of joint replacement are pain relief and functional improvement. Total joint arthroplasty is usually selected for OA of the hip, knee, and shoulder, and arthrodesis (fusion) is usually preferred for the wrist, ankle, and first metatarsophalangeal (MTP) joint. Hemiarthroplasty may be beneficial in joint replacement surgery for hip and knee OA and is successful in all age groups, showing excellent outcomes, even in the presence of obesity; however, there is an increased risk of mortality in older adults, and older age is related to worse function, particularly in women. In selected patients, corrective osteotomy and joint resurfacing can be considered instead of total arthroplasty. Various surgical interventions have been used to treat pain and dysfunction arising from OA at the base of the thumb (CMC or trapeziometacarpal joint OA). Patients who fail to respond to more conservative treatment may be candidates for trapeziectomy or CMC joint replacement.

The natural course and prognosis of OA largely depends on the joints involved, underlying risk factors, presence of symptoms, and the severity of the condition. OA is generally slowly progressive but stable, responding well to medical management. A subset of patients, however, follows a progressive trajectory and eventually requires surgical therapy. There are several factors associated with relatively rapid progression of disease, but risk factors for progression vary according to the joints involved. There are no FDA-approved disease-modifying drugs for OA, and current therapeutics mainly focus on relief of pain and functional improvement. Although a multidisciplinary approach and joint replacement surgery have altered the severity of OA’s impact, patients with OA still experience varying degrees of physical disability. A coping strategy of pain avoidance with limitation of activity may play a role in causing muscle weakness and joint instability and thus, contribute to physical disability. Therefore, patient education and psychosocial support are as important as medical therapy, particularly in older adults, to prevent disability. Recent studies have shown moderate evidence of increased mortality among persons with OA compared with the general population. History of diabetes, cancer, or cardiovascular disease, and the presence of walking disability were major risk factors for premature mortality. Possible explanations for the excess mortality include reduced levels of physical activity among persons with OA as a result of involvement of lower-limb joints and presence of comorbid conditions, as well as adverse effects of medications used to treat symptomatic OA, particularly NSAIDs. Therefore, management of patients with OA and walking disability should focus on effective treatment of cardiovascular risk factors and comorbidities, as well as on increasing physical activity.