Referensi OA

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Practice EssentialsOsteoarthritis is the most common type of joint disease, affecting more than 20 million individuals inthe United States alone. It can be thought of as a degenerative disorder arising from the biochemicalbreakdown of articular (hyaline) cartilage in the synovial joints. However, the current view holds thatosteoarthritis involves not only the articular cartilage but also the entire joint organ, including the

subchondral bone and synovium.

Essential update: New AAOS guideline for knee osteoarthritis treatment

In June 2013, the American Academy of Orthopaedic Surgeons (AAOS) released a revised clinicalpractice guideline (CPG) on the treatment of osteoarthritis of the knee. The 2 key changes from their2009 guideline are the following[1] :

The recommended dosage of acetaminophen was reduced from 4,000 mg to 3,000 mg a day; thischange is not specifically for osteoarthritis patients but reflects a change made by the FDA since2009 for all individuals who use acetaminophen

Intra-articular hyaluronic acid is no longer recommended as a treatment for patients withsymptomatic osteoarthritis of the knee

Other recommendations include the following[1] :

Patients with only symptoms of osteoarthritis and no other problems, such as loose bodies ormeniscus tears, should not be treated with arthroscopic lavage

Patients with a body mass index >25 should lose a minimum of 5% of their body weight

Patients should participate in low-impact aerobic exercise

Patients with symptomatic osteoarthritis of the knee can be treated with acetaminophen, intra-articular corticosteroids, or non-steroidal anti-inflammatory drugs (NSAIDs)

Custom-made lateral wedge insoles, glucosamine and/or chondroitin sulfate or hydrochloride,needle lavage, and acupuncture are not recommended

Signs and symptoms

Symptoms of osteoarthritis include the following:

Deep, achy joint pain exacerbated by extensive use - The diseases primary symptom Reduced range of motion and crepitus - Frequently present

Stiffness during rest (gelling) - May develop, with morning joint stiffness usually lasting for less than30 minutes

Osteoarthritis of the hand

Distal interphalangeal (DIP) joints are most often affected

Proximal interphalangeal (PIP) joints and the joints at the base of the thumb are also typicallyinvolved

Heberden nodes, which represent palpable osteophytes in the DIP joints, are more characteristic inwomen than in men

Inflammatory changes are typically absent or at least not pronouncedSeeClinical Presentationfor more detail.

Diagnosis

Osteoarthritis is typically diagnosed on the basis of clinical and radiographic evidence.[2, 3, 4, 5, 6] Nospecific laboratory abnormalities are associated with osteoarthritis.

Imaging studies

Plain radiography - The imaging method of choice because radiographs are cost-effective and canbe readily and quickly obtained[4, 7] ; in the load-bearing areas, radiographs can depict joint-spaceloss, as well as subchondral bony sclerosis and cyst formation

Computed tomography (CT) scanning - Rarely used in the diagnosis of primary osteoarthritis;however, it may be used in the diagnosis of malalignment of the patellofemoral joint or of the footand ankle joints
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Magnetic resonance imaging (MRI) - Not necessary in most patients with osteoarthritis unlessadditional pathology amenable to surgical repair is suspected; unlike radiography, MRI can directlyvisualize articular cartilage and other joint tissues (eg, meniscus, tendon, muscle, or effusion)

Ultrasonography - No role in the routine clinical assessment of patients with osteoarthritis; however,it is being investigated as a tool for monitoring cartilage degeneration, and it can be used for guidedinjections of joints not easily accessed without imaging

Bone scanning - May be helpful in the early diagnosis of osteoarthritis of the hand [8] ; bone scansalso can help differentiate osteoarthritis from osteomyelitis and bone metastases

Arthrocentesis

The presence of noninflammatory joint fluid helps distinguish osteoarthritis from other causes of jointpain. Other synovial fluid findings that aid in the differentiation of osteoarthritis from other conditionsare negative Gram stains and cultures, as well as the absence of crystals when fluid is viewed undera polarized microscope.

SeeWorkupfor more detail.

Management

Nonpharmacologic interventions

The cornerstones of osteoarthritis therapy, nonpharmacologic interventions include the following:

Patient education

Heat and cold

Weight loss[9]

Exercise

Physical therapy

Occupational therapy

Unloading in certain joints (eg, knee and hip)Pharmacologic therapy

For hand osteoarthritis, the American College of Rheumatology (ACR) conditionally recommends

using one or more of the following:

Topical capsaicin

Topical nonsteroidal anti-inflammatory drugs (NSAIDs) - Including trolamine salicylate

Oral NSAIDs

TramadolFor knee osteoarthritis, the ACR conditionally recommends using one of the following:

Acetaminophen

Oral NSAIDs

Topical NSAIDs

Tramadol

Intra-articular corticosteroid injections

For hip osteoarthritis, the ACR conditionally recommends using 1 or more of the following for initialmanagement:

Acetaminophen

Oral NSAIDs

Tramadol

Intra-articular corticosteroid injectionsSurgery

A referral to an orthopedic surgeon may be necessary if the osteoarthrit is fails to respond to a medicalmanagement plan. Surgical procedures for osteoarthritis include the following:

Arthroscopy

Osteotomy Arthroplasty - Particularly with knee or hip osteoarthritis
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FusionSeeTreatmentandMedicationfor more detail.

Image library

This radiograph demonstrates osteoarthritis of the right hip, including the findingof sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip is a bilateral finding, but it m ayoccur unilaterally in an individual who has a previous history of hip trauma that was confined to that one side.

BackgroundOsteoarthritis is the most common type of joint disease, affecting more than 20 million individuals in

the United States alone (see Epidemiology). It represents a heterogeneous group of conditionsresulting in common histopathologic and radiologic changes. It can be thought of as a degenerativedisorder arising from biochemical breakdown of articular (hyaline) cartilage in the synovial joints.However, the current view holds that osteoarthritis involves not only the articular cartilage but also theentire joint organ, including the subchondral bone and synovium.

Osteoarthritis predominantly involves the weight-bearing joints, including the knees, hips, cervical andlumbosacral spine, and feet. Other commonly affected joints include the distal interphalangeal (DIP),proximal interphalangeal (PIP), and carpometacarpal (CMC) joints. This article primarily focuses onosteoarthritis of the hand, knee, and hip joints (see Pathophysiology). For more information on arthritisin other joints, seeGlenohumeral ArthritisandWrist Arthritis.

Although osteoarthritis was previously thought to be caused largely by excessive wear and tear,

increasing evidence points to the contributions of abnormal mechanics and inflammation. Therefore,the term degenerative joint disease is no longer appropriate in referring to osteoarthritis. (SeePathophysiology.)

Historically, osteoarthritis has been divided into primary and secondary forms, though this division issomewhat artificial. Secondary osteoarthritis is conceptually easier to understand: It refers to diseaseof the synovial joints that results from some predisposing condition that has adversely altered the jointtissues (eg, trauma to articular cartilage or subchondral bone). Secondary osteoarthritis can occur inrelatively young individuals (see Etiology).[10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20]

The definition of primary osteoarthritis is more nebulous. Although this form of osteoarthritis is relatedto the aging process and typically occurs in older individuals, it is, in the broadest sense of the term,an idiopathic phenomenon, occurring in previously intact joints and having no apparent initiatingfactor.

Some clinicians limit the term primary osteoarthritis to the joints of the hands (specifically, the DIP andPIP joints and the joints at the base of the thumb). Others include the knees, hips, and spine(apophyseal articulations) as well.

As underlying causes of osteoarthritis are discovered, the term primary, or idiopathic, osteoarthritismay become obsolete. For instance, many investigators believe that most cases of primaryosteoarthritis of the hip may, in fact, be due to subtle or even unrecognizable congenital ordevelopmental defects.

No specific laboratory abnormalities are associated with osteoarthritis. Rather, it is typically diagnosedon the basis of clinical findings, with or without radiographic studies (see Workup).

The goals of osteoarthritis treatment include pain alleviation and improvement of functional status.Nonpharmacologic interventions are the cornerstones of osteoarthritis therapy and include thefollowing:
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Patient education

Application of heat and cold

Weight loss

Exercise

Physical therapy


Joint unloading, in certain joints (eg, knee and hip)Intra-articular pharmacologic therapy includes corticosteroid injection and viscosupplementation,which may provide pain relief and have an anti-inflammatory effect on the affected joint. (SeeTreatment.) Oral pharmacologic therapy begins with acetaminophen for mild or moderate pain withoutapparent inflammation.

If the clinical response to acetaminophen is not satisfactory or the clinical presentation isinflammatory, consider nonsteroidal anti-inflammatory drugs (NSAIDs). (See Medication.) If all othermodalities are ineffective and osteotomy is not viable, or if a patient cannot perform his or her dailyactivities despite maximal therapy, arthroplasty is indicated.

The high prevalence of osteoarthritis entails significant costs to society. Direct costs include clinicianvisits, medications, and surgical intervention. Indirect costs include such items as time lost from work.

Costs associated with osteoarthritis can be particularly significant for elderly persons, who facepotential loss of independence and who may need help with daily living activities. As the populationsof developed nations age over the coming decades, the need for better understanding of osteoarthritisand for improved therapeutic alternatives will continue to grow. (See Epidemiology.)

AnatomyJoints can be classified in either functional or structural terms. A functional classification, based on

movement, would categorize joints as follows:

Synarthroses (immovable)

Amphiarthroses (slightly moveable)

Diarthroses (freely moveable)A structural classification would categorize joints as follows:

Synovial

Fibrous

CartilaginousNormal synovial joints allow a significant amount of motion along their extremely smooth articularsurface. These joints are composed of the following:

Articular cartilage Subchondral bone

Synovial membrane

Synovial fluid

Joint capsuleThe normal articular surface of synovial joints consists of articular cartilage (composed ofchondrocytes) surrounded by an extracellular matrix that includes various macromolecules, mostimportantly proteoglycans and collagen. The cartilage facilitates joint function and protects theunderlying subchondral bone by distributing large loads, maintaining low contact stresses, andreducing friction at the joint.

Synovial fluid is formed through a serum ultrafiltration process by cells that form the synovialmembrane (synoviocytes). Synovial cells also manufacture hyaluronic acid (HA, also known as

hyaluronate), a glycosaminoglycan that is the major noncellular component of synovial fluid. Synovialfluid supplies nutrients to the avascular articular cartilage; it also provides the viscosity needed to


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absorb shock from slow movements, as well as the elasticity required to absorb shock from rapidmovements.

PathophysiologyPrimary and secondary osteoarthritis are not separable on a pathologic basis, though bilateralsymmetry is often seen in cases of primary osteoarthritis, particularly when the hands are affected. [2,21] Traditionally, osteoarthritis was thought to affect primarily the articular cartilage of synovial joints;however, pathophysiologic changes are also known to occur in the synovial fluid, as well as in theunderlying (subchondral) bone, the overlying joint capsule, and other joint tissues (see Workup).[22, 23,24, 25]

Although osteoarthritis has been classified as a noninflammatory arthritis, increasing evidence hasshown that inflammation occurs as cytokines and metalloproteinases are released into the joint.These agents are involved in the excessive matrix degradation that characterizes cartilagedegeneration in osteoarthritis.[26] Therefore, it is no longer appropriate to use the term degenerative

joint disease when referring to osteoarthritis.

In early osteoarthritis, swelling of the cartilage usually occurs, because of the increased synthesis ofproteoglycans; this reflects an effort by the chondrocytes to repair cartilage damage. This stage maylast for years or decades and is characterized by hypertrophic repair of the articular cartilage.

As osteoarthritis progresses, however, the level of proteoglycans eventually drops very low, causingthe cartilage to soften and lose elasticity and thereby further compromising joint surface integrity.Microscopically, flaking and fibrillations (vertical clefts) develop along the normally smooth articularcartilage on the surface of an osteoarthritic joint. Over time, the loss of cartilage results in loss of jointspace.

In major weight-bearing joints of persons with osteoarthritis, a greater loss of joint space occurs atthose areas experiencing the highest loads. This effect contrasts with that of inflammatory arthritides,in which uniform joint-space narrowing is the rule.

In the osteoarthritic knee, for example, the greatest loss of joint space is commonly seen in the medialfemorotibial compartment, though the lateral femorotibial compartment and patellofemoralcompartment may also be affected. Collapse of the medial or lateral compartments may result invarus or valgus deformities, respectively.

Erosion of the damaged cartilage in an osteoarthritic joint progresses until the underlying bone isexposed. Bone denuded of its protective cartilage continues to articulate with the opposing surface.Eventually, the increasing stresses exceed the biomechanical yield strength of the bone. Thesubchondral bone responds with vascular invasion and increased cellularity, becoming thickened anddense (a process known as eburnation) at areas of pressure.[27]

The traumatized subchondral bone may also undergo cystic degeneration, which is attributable eitherto osseous necrosis secondary to chronic impaction or to the intrusion of synovial fluid. Osteoarthritic

cysts are also referred to as subchondral cysts, pseudocysts, or geodes (the preferred Europeanterm) and may range from 2 to 20 mm in diameter. Osteoarthritic cysts in the acetabulum (see theimage below) are termed Egger cysts.

This radiograph demonstrates osteoarthritis of the right hip, including the findingof sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip is a bilateral finding, but it mayoccur unilaterally in an individual who has a previous history of hip trauma that was confined to that one side.
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At areas along the articular margin, vascularization of subchondral marrow, osseous metaplasia ofsynovial connective tissue, and ossifying cartilaginous protrusions lead to irregular outgrowth of newbone (osteophytes). Fragmentation of these osteophytes or of the articular cartilage itself results inthe presence of intra-articular loose bodies (joint mice).

Along with joint damage, osteoarthritis may also lead to pathophysiologic changes in associated

ligaments and the neuromuscular apparatus. For example, lateral collateral ligament complexabnormalities are common in knee osteoarthritis.

Pain mechanisms in osteoarthritis

Pain, the main presenting symptom of osteoarthritis, is presumed to arise from a combination ofmechanisms, including the following:

Osteophytic periosteal elevation

Vascular congestion of subchondral bone, leading to increased intraosseous pressure

Synovitis with activation of synovial membrane nociceptors

Fatigue in muscles that cross the joint

Overall joint contracture

Joint effusion and stretching of the joint capsule

Torn menisci

Inflammation of periarticular bursae

Periarticular muscle spasm

Psychological factors

Crepitus (a rough or crunchy sensation)

Central pain sensitizationWhen the spine is involved in osteoarthritis, especially the lumbar spine, the associated changes arevery commonly seen from L3 through L5. Symptoms include pain, stiffness, and occasional radicularpain from spinal stenosis. Foraminal narrowing is caused by facet arthritic changes that result incompression of the nerve roots. Acquired spondylolisthesis is a common complication of arthritis ofthe lumbar spine.

EtiologyThe daily stresses applied to the joints, especially the weight-bearing joints (eg, ankle, knee, and hip),play an important role in the development of osteoarthritis. Most investigators believe thatdegenerative alterations in osteoarthritis primarily begin in the articular cartilage, as a result of eitherexcessive loading of a healthy joint or relatively normal loading of a previously disturbed joint.External forces accelerate the catabolic effects of the chondrocytes and further disrupt thecartilaginous matrix.[28, 29, 30, 31]

Risk factors for osteoarthritis include the following [32, 33, 34, 35] :

Age

Obesity[36, 37, 38]

Trauma

Genetics (significant family history)

Reduced levels of sex hormones

Muscle weakness[39]

Repetitive use (ie, jobs requiring heavy labor and bending)[40]

Infection

Crystal deposition

Acromegaly

Previous inflammatory arthritis (eg, burnt-out rheumatoid arthritis)

Heritable metabolic causes (eg, alkaptonuria, hemochromatosis, and Wilson disease)

Hemoglobinopathies (eg, sickle cell disease and thalassemia)

Neuropathic disorders leading to a Charcot joint (eg, syringomyelia, tabes dorsalis, and diabetes)


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Underlying morphologic risk factors (eg, congenital hip dislocation and slipped femoral capitalepiphysis)

Disorders of bone (eg, Paget disease and avascular necrosis)

Previous surgical procedures (eg, meniscectomy)

Advancing age

With advancing age come reductions in cartilage volume, proteoglycan content, cartilagevascularization, and cartilage perfusion. These changes may result in certain characteristic radiologicfeatures, including a narrowed joint space and marginal osteophytes. However, biochemical andpathophysiologic findings support the notion that age alone is an insufficient cause of osteoarthritis.

Obesity

Obesity increases the mechanical stress in a weight-bearing joint. It has been strongly linked toosteoarthritis of the knees and, to a lesser extent, of the hips. A study that evaluated the associationsbetween body mass index (BMI) over 14 years and knee pain at year 15 in 594 women found that ahigher BMI at year 1 and a significant increase in BMI over 15 years were predictors of bilateral kneepain at year 15.[38] The association between BMI increase and knee pain was independent ofradiographic changes.

In addition to its mechanical effects, obesity may be an inflammatory risk factor for osteoarthritis.Obesity is associated with increased levels (both systemic and intra-articular) of adipokines (cytokinesderived from adipose tissue), which may promote chronic, low-grade inflammation in joints.[41]

Other causes

Trauma or surgery (including surgical repair of traumatic injury) involving the articular cartilage,ligaments, or menisci can lead to abnormal biomechanics in the joints and accelerate osteoarthritis.

Although repairs of ligament and meniscal injuries usually restore joint function, osteoarthritis hasbeen observed 5-15 years afterward in 50-60% of patients.[42]

Insults to the joints may occur even in the absence of obvious trauma. Microtrauma may also causedamage, especially in individuals whose occupation or lifestyle involves frequent squatting, stair-climbing, or kneeling.

Muscle dysfunction compromises the bodys neuromuscular protective mechanisms, leading toincreased joint motion and ultimately resulting in osteoarthritis. This effect underscores the need forcontinued muscle toning exercises as a means of preventing muscle dysfunction.

Valgus malalignment at the knee has been shown to increase the incidence and risk of radiographicprogression of knee osteoarthritis involving the lateral compartment.[43]

Genetics

A hereditary component, particularly in osteoarthritis presentations involving multiple joints, has longbeen recognized.[44, 45, 46] Several genes have been directly associated with osteoarthritis,[47] and manymore have been determined to be associated with contributing factors, such as excessiveinflammation and obesity.

Genes in the BMP (bone morphogenetic protein) and WNT (wingless-type) signaling cascades havebeen implicated in osteoarthritis. Two genes in particular,GDF5(growth and differentiation factor 5)and FRZB (frizzled related protein) have been identified in the articular cartilage in animal studies and

share a strong correlation with osteoarthritis.[48, 49, 50, 51]

Genome-wide association studies (GWAS) have identified an association between osteoarthritis oflarge joints and the MCF2L gene. This gene is key in neurotrophin-mediated regulation of peripheralnervous system cell motility.[52]

Genetic factors are also important in certain heritable developmental defects and skeletal anomaliesthat can cause congenital misalignment of joints. These may result in damage to cartilage and thestructure of the joint.


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Currently, clinical genetic testing is not offered to patients who have osteoarthritis unless they alsohave other anomalies that could be associated with a genetic condition. In the future, testing mayallow individualization of therapeutics.

EpidemiologyUnited States and international statistics

Osteoarthritis affects more than 20 million individuals in the United States, though statistical figuresare influenced by how the condition is definedthat is, by self-report, by radiographic or symptomaticcriteria, or by a combination of these.[53]On the basis of the radiographic criteria for osteoarthritis, more50% of adults older than 65 years are affected by the disease.

Internationally, osteoarthritis is the most common articular disease. Estimates of its frequency varyacross different populations.

Age-related demographics

Primary osteoarthritis is a common disorder of the elderly, and patients are often asymptomatic.Approximately 80-90% of individuals older than 65 years have evidence of radiographic primaryosteoarthritis.[54]

Symptoms typically do not become noticeable until after the age of 50 years. The prevalence of thedisease increases dramatically among persons older than 50 years, likely because of age-relatedalterations in collagen and proteoglycans that decrease the tensile strength of the joint cartilage andbecause of a diminished nutrient supply to the cartilage.[54]

Sex-related demographics

In individuals older than 55 years, the prevalence of osteoarthritis is higher among women thanamong men.[54] Women are especially susceptible to osteoarthritis in the DIP joints of the fingers.Women also have osteoarthritis of the knee joints more frequently than men do, with a female-to-male

incidence ratio of 1.7:1. Women are also more prone to erosive osteoarthritis, with a female-to-maleratio of about 12:1.

Race-related demographics

Interethnic differences in the prevalence of osteoarthritis have been noted.[55] The disorder is moreprevalent in Native Americans than in the general population. Disease of the hip is seen lessfrequently in Chinese patients from Hong Kong than in age-matched white populations. Symptomaticknee osteoarthritis is extremely common in China.[56]

In persons older than 65 years, osteoarthritis is more common in whites than in blacks. Kneeosteoarthritis appears to be more common in black women than in other groups. Jordan et al foundthat in comparison with whites, African American men and women had a slightly higher prevalence ofradiographic and symptomatic knee osteoarthritis but a significantly higher prevalence of severe

radiographic knee osteoarthritis.[57]

PrognosisThe prognosis in patients with osteoarthritis depends on the joints involved and on the severity of thecondition. No proven disease- or structure-modifying drugs for osteoarthritis are currently known;consequently, pharmacologic treatment is directed at symptom relief.

A systematic review found the following clinical features to be associated with more rapid progressionof knee osteoarthritis[58] :

Older age Higher BMI

Varus deformity


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Multiple involved jointsPatients with osteoarthritis who have undergone joint replacement have a good prognosis, withsuccess rates for hip and knee arthroplasty generally exceeding 90%. However, a joint prosthesismay have to be revised 10-15 years after its placement, depending on the patients activity level.Younger and more active patients are more likely to require revisions, whereas the majority of olderpatients will not. (See Treatment.)

Patient EducationEducate patients on the natural history of and management options for osteoarthritis, emphasizing thebenefits of exercise and weight loss. Explain the differences between osteoarthritis and more rapidlyprogressive arthritides, such as rheumatoid arthritis.

SeveralArthritis Foundationstudies have demonstrated that education in osteoarthritis benefits thepatient. Through education, patients can learn and implement strategies for reducing pain andimproving joint function. Emphasize the need for physician follow-up visits.

For patient education information, see theArthritis Center, as well asOsteoarthritis.

History

The progression of osteoarthritis is characteristically slow, occurring over several years or decades.Over this period, the patient can become less and less active and thus more susceptible to morbiditiesrelated to decreasing physical activity (including potential weight gain).

Early in the disease process, the joints may appear normal. However, the patients gait may beantalgic if weight-bearing joints are involved.

Pain is usually the initial source of morbidity in osteoarthritis, with the diseases primary symptombeing deep, achy joint pain exacerbated by extensive use. Also, reduced range of motion and crepitusare frequently present. Stiffness during rest (gelling) may develop, with morning joint stiffness usuallylasting for less than 30 minutes.

Initially, pain can be relieved by rest and may respond to simple analgesics. However, joints may

become unstable as the osteoarthritis progresses; therefore, the pain may become more prominent(even during rest) and may not respond to medications.

Physical Examination

Physical examination findings in patients with osteoarthritis are mostly limited to the affected joints.[59,60, 61] Reduced range of motion and crepitus are frequently present.

Malalignment with a bony enlargement may occur. Most cases of osteoarthritis do not involveerythema or warmth over the affected joint(s); however, a bland effusion may be present. Limitation of

joint motion or muscle atrophy around a more severely affected joint may occur.

Osteoarthritis of the hand most often affects the distal interphalangeal (DIP) joints but also typicallyinvolves the proximal interphalangeal (PIP) joints and the joints at the base of the thumb. Heberden

nodes, which represent palpable osteophytes in the DIP joints, are more characteristic in women thanin men. Inflammatory changes are typically absent or at least not pronounced.

Progression of Osteoarthritis

The etiopathogenesis of osteoarthritis has been divided into 3 stages as follows:

Stage 1 Proteolytic breakdown of the cartilage matrix occurs

Stage 2 Fibrillation and erosion of the cartilage surface develop, with subsequent release ofproteoglycan and collagen fragments into the synovial fluid

Stage 3 Breakdown products of cartilage induce a chronic inflammatory response in the synovium,which in turn contributes to further cartilage breakdown

Several systems have been advocated for use in the grading of focal cartilage change; however, a

simple description of the extent of disease (ie, surface, partial-thickness, or full-thickness irregularitywith or without underlying subchondral bone change) is generally sufficient and prevents the
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confusion that may occur with numeric grading systems. Such systems are in any case intended morefor research purposes than for clinical use.

Certain diseases are often categorized as subsets of primary osteoarthritis. These include primarygeneralized osteoarthritis (PGOA), erosive osteoarthritis, and chondromalacia patellae.

Diagnostic ConsiderationsThe initial diagnostic goal is to differentiate osteoarthritis from other arthritides, such as rheumatoidarthritis. The history and physical examination findings are usually sufficient to diagnose osteoarthritis.Radiographic findings confirm the initial impression (see Workup), and laboratory values are typicallywithin the reference range.

Rheumatoid arthritis

Rheumatoid arthritis predominantly affects the wrists, as well as the metacarpophalangeal (MCP) andproximal interphalangeal (PIP) joints. It rarely, if ever, involves the distal interphalangeal (DIP) jointsor the lumbosacral spine.

Rheumatoid arthritis is associated with prominent, prolonged (> 1 hour) morning stiffness and overtly

swollen, warm joints. Radiographic findings include bone erosion (eg, periarticular osteopenia ormarginal erosions of bone) rather than formation. Laboratory findings that further differentiaterheumatoid arthritis from osteoarthritis include the following:

Systemic inflammation (elevated erythrocyte sedimentation rate [ESR] or C-reactive protein [CRP]level)

Positive serologies (rheumatoid factor [RF] or anticyclic citrullinated peptide [anti-CCP] antibodies)

Inflammatory joint fluid with a predominance of polymorphonuclear leukocytes (PMNs)

Elevated white blood cell (WBC) countAdditional arthritides

Back pain may result from spondyloarthropathy or from osteoarthritis with sacroiliac and lumbosacralspine involvement. Clinical history and characteristic radiographic findings can be used to differentiate

these disorders.

Secondary osteoarthritis must be considered in individuals with any of the following:

Chondrocalcinosis

History of joint trauma

Metabolic bone disorders

Hypermobility syndromes

Neuropathic diseasesThe following disorders should also be considered in the differential diagnosis:

Crystalline arthropathies (ie, gout and pseudogout)

Inflammatory arthritis (eg, rheumatoid arthritis)

Seronegative spondyloarthropathies (eg, psoriatic arthritis and reactive arthritis)

Septic arthritis or postinfectious arthropathy

Fibromyalgia

TendonitisIn patients with knee pain, other disorders to consider in the differential diagnosis arepatellofemoralsyndromeandprepatellar bursitis.

Differential Diagnoses Ankylosing Spondylitis

Avascular Necrosis

Fibromyalgia

Gout and Pseudogout

Imaging in Neuropathic Arthropathy (Charcot Joint) Lyme Disease

Patellofemoral Arthritis
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Psoriatic Arthritis

Rheumatoid Arthritis

Approach Considerations

Osteoarthritis is typically diagnosed on the basis of clinical and radiographic evidence.[2, 3, 4, 5, 6] Nospecific laboratory abnormalities are associated with osteoarthritis.

Researchers have investigated the use of monoclonal antibodies, synovial fluid markers, and urinarypyridinium cross-links (ie, breakdown products of cartilage) as osteoarthritic indicators.[62] No singlebiomarker has proved reliable for diagnosis and monitoring, but combinations of cartilage-derived andbone-derived biomarkers have been used to identify osteoarthritis subtypes, with possible impact ontreatment.[63]

Levels of acute-phase reactants are typically within the reference range in patients with osteoarthritis.The erythrocyte sedimentation rate (ESR) is not usually elevated, though it may be slightly so in cases

of erosive inflammatory arthritis. The synovial fluid analysis usually shows a white blood cell (WBC)count below 2000/L, with a mononuclear predominance.

Plain Radiography

Plain radiography is the imaging method of choice because it is more cost-effective than othermodalities and because radiographs can be obtained more readily and quickly.[4, 7] One importantcharacteristic of primary osteoarthritis is that the abnormalities found in the load-bearing (ie, highlystressed) areas of the affected joint differ from those found in the nonload-bearing areas. In the load-bearing areas, radiographs can depict joint-space loss, as well as subchondral bony sclerosis andcyst formation (see the image below).

This radiograph demonstrates osteoarthritis of the right hip, including the findingof sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip is a bilateral finding, but it m ayoccur unilaterally in an individual who has a previous history of hip trauma that was confined to that one side.The elbow is not commonly affected in osteoarthritis. However, elbow arthritis (see the images below)can occur as a result of trauma.
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Osteoarthritis of the elbow is not commonly seen; however, it can occur with a

history of previous trauma. Osteoarthritis of the elbow is not commonly seen;

however, it can occur with a history of previous trauma. Osteoarthritis of theelbow is not commonly seen; however, it can occur with a history of previous trauma.

MRI, CT, and Ultrasonography

Magnetic resonance imaging (MRI) can depict many of the same characteristics of osteoarthritis thatplain radiography can, but it is not necessary in most patients with osteoarthritis, unless additionalpathology amenable to surgical repair is suspected. Pathology that can be seen on MRI includes jointnarrowing, subchondral osseous changes, and osteophytes. Unlike radiography, MRI can directlyvisualize articular cartilage and other joint tissues (eg, meniscus, tendon, muscle, or effusion).

Computed tomography (CT) is rarely used in the diagnosis of primary osteoarthritis. However, it maybe used in the diagnosis of malalignment of the patellofemoral joint or of the foot and ankle joints.

Currently, ultrasonography has no role in the routine clinical assessment of the patient withosteoarthritis. However, it is being investigated as a tool for monitoring cartilage degeneration, and itcan be used for guided injections of joints not easily accessed without imaging.

For more information, seeImaging in Osteoarthritis.

Bone Scanning

Bone scans may be helpful in the early diagnosis of osteoarthritis of the hand.[8]Bone scans inosteoarthritis typically yield a symmetrically patterned, very mild increased uptake. In contrast, bonescans are often negative in the early stages of multiple myeloma, a cause of bone pain in older adultsthat can be confused with osteoarthritis. Bone scans also can help to differentiate osteoarthritis fromosteomyelitis and bone metastases.

Arthrocentesis

A diagnostic joint aspiration for synovial fluid analysis can help exclude inflammatory arthritis,infection, or crystal arthropathy. The presence of noninflammatory joint fluid helps distinguish

osteoarthritis from other causes of joint pain. Other synovial fluid findings that aid in the differentiationof osteoarthritis from other conditions are negative Gram stains and cultures, as well as the absenceof crystals when fluid is viewed under a polarized microscope.
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For more information, see the following:

Knee Arthrocentesis

Metacarpophalangeal Arthrocentesis

Shoulder Arthrocentesis

Approach Considerations

The goals of osteoarthritis treatment include alleviation of pain and improvement of functionalstatus.[64] Optimally, patients should receive a combination of nonpharmacologic and pharmacologictreatment.[65]

Nonpharmacologic interventions, which are the cornerstones of osteoarthritis therapy, include thefollowing:

Patient education

Heat and cold

Weight loss[9]

Exercise

Physical therapy


Unloading in certain joints (eg, knee, hip)A physiatrist may help in formulating a nonpharmacologic management plan for the patient withosteoarthritis, and a nutritionist may help the patient to lose weight. A referral to an orthopedicsurgeon may be necessary if the osteoarthritis fails to respond to a medical management plan.Surgical procedures for osteoarthritis include arthroscopy, osteotomy, and (particularly with knee orhip osteoarthritis) arthroplasty.

Pharmacologic Treatment

American College of Rheumatology guidelines

The American College of Rheumatology (ACR) has issued guidelines for pharmacologic treatment ofosteoarthritis of the hand, hip, and knee.[57] For hand osteoarthritis, the ACR conditionally recommends

using 1 or more of the following:

Topical capsaicin

Topical nonsteroidal anti-inflammatory drugs (NSAIDs), including trolamine salicylate

Oral NSAIDs

TramadolThe ACR conditionally recommends against using intra-articular therapies or opioid analgesics forhand osteoarthritis. For patients 75 years and older, the ACR conditionally recommends the use oftopical rather than oral NSAIDs.

For knee osteoarthritis, the ACR conditionally recommends using 1 of the following:

Acetaminophen

Oral NSAIDs

Topical NSAIDs

Tramadol

Intra-articular corticosteroid injectionsThe ACR conditionally recommends against using chondroitin sulfate, glucosamine, or topicalcapsaicin for knee osteoarthritis. The ACR has no recommendations regarding the use of intra-articular hyaluronates, duloxetine, and opioid analgesics.

For hip osteoarthritis, the ACR conditionally recommends using 1 or more of the following for initialmanagement:

Acetaminophen

Oral NSAIDs

Tramadol

Intra-articular corticosteroid injections
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The ACR conditionally recommends against using chondroitin sulfate or glucosamine for hiposteoarthritis. The ACR has no recommendation regarding the use of topical NSAIDs, intra-articularhyaluronate injections, duloxetine, or opioid analgesics.

Agency for Healthcare Research and Quality findings

A comparison of analgesics for osteoarthritis carried out by theAgency for Healthcare Research and

Quality(AHRQ) found that no currently available analgesic reviewed in this report offers a clearoverall advantage compared with the others.[66] The choice of analgesic for an individual patientshould take into account the trade-off between benefits and adverse effects, which differs acrossanalgesics. Patient age, comorbid conditions, and concomitant medication are key considerations.

The AHRQ comparison found that acetaminophen was modestly inferior to NSAIDs in reducingosteoarthritic pain but was associated with a lower risk of GI adverse effects.[66] On the other hand,acetaminophen poses a higher risk of liver injury.

AHRQ findings on adverse effects included the following:

Selective NSAIDs as a class were associated with a lower risk of ulcer complications than were thenonselective NSAIDs naproxen, ibuprofen, and diclofenac

The partially selective NSAIDs meloxicam and etodolac were associated with a lower risk of ulcer-related complications and symptomatic ulcers than were various nonselective NSAIDs

The risk of serious GI adverse effects was found to be higher with naproxen than with ibuprofen

Celecoxib and the nonselective NSAIDs ibuprofen and diclofenac were associated with anincreased risk of cardiovascular adverse effects when compared with placebo

The nonselective NSAIDs ibuprofen and diclofenac, but not naproxen, were associated with anincreased risk of heart attack when compared with placebo

The AHRQ noted that topical diclofenac was found to have efficacy similar to that of oral NSAIDs inpatients with localized osteoarthritis. No head-to-head trials compared topical salicylates or capsaicinwith oral NSAIDs for osteoarthritis.[66]

All NSAIDs had deleterious effects on blood pressure, edema, and kidney function. However, theAHRQ found no consistent clinically relevant differences between celecoxib, partially selective

NSAIDs, and nonselective NSAIDs with regard to the risk of hypertension, heart failure, or impairedkidney function.[66]

Analgesics, NSAIDs, and COX-2 inhibitors

Begin treatment with acetaminophen for mild or moderate osteoarthritic pain without apparentinflammation. If the clinical response to acetaminophen is not satisfactory or if the clinical presentationof osteoarthritis is inflammatory, consider using an NSAID.

Use the lowest effective dose or intermittent dosing if symptoms are intermittent, then try full doses ifthe patients response is insufficient.

Topical NSAID preparations, particularly diclofenac, are available. These preparations can beparticularly useful in patients with symptomatic disease that is limited to a few sites or in patients who

are at increased risk for adverse events with systemic NSAIDs.

In patients with highly resistant pain, consider the analgesic tramadol. Options in patients at anelevated risk for GI toxicity from NSAIDs include the addition of a proton-pump inhibitor or misoprostolto the treatment regimen and the use of the selective cyclooxygenase (COX)-2 inhibitor celecoxibinstead of a nonselective NSAID.

Duloxetine

The selective serotonin-norepinephrine reuptake inhibitor duloxetine has been found to be effective intreating osteoarthritis pain.[67] For example, in patients with knee osteoarthritis who had persistentmoderate pain despite optimized NSAID therapy, a randomized, double-blind trial found significantadditional pain reduction and functional improvement with duloxetine as compared with placebo.[68]

However, duloxetine was also associated with significantly more nausea, dry mouth, constipation,fatigue, and decreased appetite than placebo was.[68] To date, trials of duloxetine in osteoarthritis have
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been short in duration (10-13 weeks), and studies comparing duloxetine directly with other therapieshave not been performed.

Intra-articular injections

Intra-articular pharmacologic therapy includes injection of a corticosteroid or sodium hyaluronate (ie,hyaluronic acid [HA] or hyaluronan), which may provide pain relief and have an anti-inflammatory

effect on the affected joint.[69, 70]Ultrasound guidance can facilitate arthrocentesis and injection and isincreasingly being adopted by physicians such as rheumatologists and physiatrists for this purpose.

Corticosteroid

After the introduction of the needle into the joint and before steroid administration, aspiration of asmuch synovial fluid as possible should be attempted. Aspiration often provides symptomatic relief forthe patient and allows laboratory evaluation of the fluid, if necessary. Infected joint fluid andbacteremia are contraindications to steroid injection.

In patients with osteoarthritic knee pain, steroid injections generally result in clinically and statisticallysignificant pain reduction as soon as 1 week after injection. The effect may last, on average,anywhere from 4 to 6 weeks per injection, but the benefit is unlikely to continue beyond that time

frame.[71]

For hip osteoarthritis, a randomized, placebo-controlled study confirmed the effectiveness ofcorticosteroid injection, with benefits often lasting as long as 3 months.[72]

Some controversial evidence exists regarding frequent steroid injections and subsequent damage tocartilage (chondrodegeneration). Accordingly, it is usually recommended that no more than 3injections per year be delivered to any individual osteoarthritic joint. Systemic glucocorticoids have norole in the management of osteoarthritis.

For more information, seeCorticosteroid Injections of Joints and Soft Tissues.

Sodium hyaluronate

Intra-articular injection of sodium hyaluronate, also referred to as viscosupplementation, has beenshown to be safe and possibly effective for symptomatic relief of knee osteoarthritis.[73, 74] In the United

States, intra-articular HAs are classified as medical devices rather than as drugs.[75]

Intra-articular HAs approved by the FDA for the treatment of osteoarthritic knee pain include thenaturally extracted, noncross-linked sodium hyaluronate products Hyalgan,[76] Supartz, Orthovisc,and Euflexxa, as well as the cross-linked sodium hyaluronate product known as hylan G-F 20(Synvisc).

Euflexxa is derived from a fermentation process (Streptococcus), whereas the source material for theother products listed is chicken combs. At present, no distinct advantage or disadvantage has beenassociated with any particular source of HA.

Some differences between the viscosupplements do exist in the FDA-approved prescribinginformation. For example, whereas Hyalgan and Synvisc have been established as safe for repeattreatment, the safety and efficacy of other products for repeat treatment have not been established.

The exact mechanisms of action through which HAs provide symptomatic relief are unknown.Possible mechanisms include direct binding to receptors (CD44 in particular) in the synovium andcartilage that can lead to several biologic activation pathways.[77, 78]

The HA class in general has demonstrated a very favorable safety profile for chronic painmanagement in knee osteoarthritis, with the most common adverse event being injection-site pain.

Although any intra-articular injection (whether of HAs or of steroids) may elicit an inflammatoryresponse and possible effusion, only the cross-linked hylan G-F 20 product has been associated witha clinically distinct acute inflammatory side effect (ie, severe acute inflammatory reaction [SAIR] orHA-associated intra-articular pseudosepsis).

Prolotherapy

In a randomized, controlled trial of 90 adults with painful knee osteoarthritis who were randomized toeither dextrose prolotherapy, saline injections, or at-home exercise, the patients on prolotherapy
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experienced significantly greater improvement in pain, function, and stiffness over the other 2 groups.Injections were administered at 1, 5, and 9 weeks, with additional injections provided as needed atweeks 13 and 17.[79]

Additional pharmacologic agents

Muscle relaxants may benefit patients with evidence of muscle spasm. Judicious use of narcotics (eg,

oxycodone and acetaminophen with codeine) is reserved for patients with severe osteoarthritis.

Glucosamine and chondroitin sulfate have been used in Europe for many years and continue to bepopular with patients worldwide. In the United States, however, the glucosamine/chondroitin arthritisintervention trial (GAIT) reported, at best, limited benefit from glucosamine (500 mg 3 times daily),chondroitin sulfate (400 mg 3 times daily), or the combination of the 2 in patients with kneeosteoarthritis.[80, 81]

In GAIT patients overall, glucosamine and chondroitin sulfate alone or in combination did not reducepain effectively at 24 weeks, but in patients with moderate-to-severe pain at baseline, the rate ofresponse was significantly higher with combined therapy than with placebo (79.2% vs. 54.3%). [81]At 2years, no treatment achieved a clinically important difference in loss of joint-space width, thoughtreatment effects on Kellgren-Lawrence grade 2 knees showed a trend toward improvement relative

to the placebo group.[80]

The AHRQ comparison found no clear difference between glucosamine or chondroitin and oralNSAIDs for relieving pain or improving function.[66] However, the AHRQ observed that most trialsshowing therapeutic benefits from glucosamine used pharmaceutical-grade glucosamine that is notavailable in the United States, noting that the trial findings may therefore be inapplicable to currentlyavailable over-the-counter preparations.

Another agent, S-adenosylmethionine (SAM-e), is a European supplement receiving significantattention in the United States. A systematic review of SAM-e found that the evidence wasinconclusive, with a number of small trials of questionable quality; the authors concluded that theeffects of SAM-e on pain and function may be potentially clinically relevant but are expected to besmall.[82]

Chondroprotective drugs (ie, matrix metalloproteinase [MMP] inhibitors and growth factors) are beingtested as disease-modifying drugs in the management of osteoarthritis. For example, MMP-13 isspecifically expressed in the cartilage of individuals with osteoarthritis but not in the cartilage ofnormal adults.[83] German researchers reported on the synthesis and biologic evaluation of an MMP-13selective inhibitor that has demonstrated efficacy as a disease-modifying intra-articular injection forosteoarthritis.[84]

Other investigational agents include monoclonal antibodies that inhibit nerve growth factor (NGF),such as tanezumab. Anti-NGF agents have been shown to reduce chronic pain in patients withosteoarthritis.

Lifestyle Modification, Physical/Occupational Therapy, and Other

Nonpharmacologic MeasuresLifestyle modification, particularly exercise and weight reduction, is a core component in themanagement of osteoarthritis.[85, 86] Guidelines from Osteoarthritis Research Society International(OARSI) advise that nonpharmacologic treatment of hip and knee osteoarthritis should initially focuson self-help and patient-driven modalities rather than on modalities delivered by healthprofessionals.[65]

The ACR strongly recommends the following nonpharmacologic measures for patients with knee orhip osteoarthritis[87] :

Cardiovascular or resistance land-based exercise

Aquatic exercise

Weight loss, for overweight patients

The ACR conditionally recommends the following measures for patients with knee or hiposteoarthritis:


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Self-management programs

Manual therapy in combination with supervised exercise

Psychosocial interventions

Thermal agents

Walking aids, as neededFor patients with knee osteoarthritis, the ACR also conditionally recommends the following measures:

Medially directed patellar taping

Medially wedged insoles for lateral-compartment osteoarthritis

Laterally wedged subtalar strapped insoles for medial-compartment osteoarthritis

Tai chiFor knee osteoarthritis, an American Academy of Orthopaedic Surgeons (AAOS) guideline suggestsencouraging patients to participate in self-management educational programs such as thoseconducted by theArthritis Foundationand to incorporate activity modifications into their lifestyle (eg,walking instead of running or engaging in alternative activities).

Instruct the patient to avoid aggravating stress to the affected joint. Implement corrective procedures ifthe patient has poor posture.

Weight reduction relieves stress on the affected knees or hips. The benefits of weight loss, whetherobtained through regular exercise and diet or through surgical intervention, may extend not only tosymptom relief but also to a slowing in cartilage loss in weight-bearing joints (eg, knees).[88] In addition,weight loss lowers levels of the inflammatory cytokines and adipokines that may play a role incartilage degradation.[89]

Some patients with osteoarthritis benefit from heat placed locally over the affected joint. A minority ofpatients report relief with ice.[90]

Physical activity

Although people with osteoarthritis tend to avoid activity, exercise is an effective treatment for thiscondition, producing improvements in pain, physical function, and walking distance. Long-termwalking and resistance-training programs have been shown to slow the functional decline seen in

many patients with osteoarthritis, including older patients.[89]

Osteoarthritis of the knee may result in disuse atrophy of the quadriceps. Because these muscleshelp protect the articular cartilage from further stress, quadriceps strengthening is likely to benefitpatients with knee osteoarthritis. Stretching exercises are also important in the treatment ofosteoarthritis because they increase range of motion.

In a study of patients with knee osteoarthritis, Jan et al found that in most respects, nonweight-bearing exercise was as therapeutically effective as weight-bearing exercise.[91]After an 8-weekexercise program, the 2 types of exercise resulted in equally significant improvements in function,walking speed, and muscle torque. However, patients in the weight-bearing group demonstratedgreater improvement in position sense, which may help patients with complex walking tasks, such aswalking on a spongy surface.

Chaipinyo and Karoonsupcharoen found no significant difference between home-based strengthtraining and home-based balance training for knee pain caused by osteoarthritis. However, greaterimprovement in knee-related quality of life was noted in the strength-training group.[92]

The importance of aerobic conditioning, particularly low-impact exercises (if osteoarthritis is affectingweight-bearing joints), should be stressed as well. Swimming, especially the aerobic aquatic programsdeveloped by the Arthritis Foundation, can be helpful.

The benefits of exercise have been found to decline over time, possibly because of poor adherence.Factors that determine adherence to exercise have not been carefully studied in patients withosteoarthritis. In a review of this topic, Marks and Allegrante concluded that interventions to enhanceself-efficacy, social support, and skills in the long-term monitoring of progress are necessary to fosterexercise adherence in people with osteoarthritis.[93]

Tai chi
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A prospective, single-blind, randomized, controlled study by Wang et al suggested that tai chi is apotentially effective treatment for pain associated with osteoarthritis of the knee.[94] In this trial, 40patients with symptomatic tibiofemoral osteoarthritis who performed 60 minutes of tai chi twice weeklyfor 12 weeks experienced significantly greater pain reduction than did control subjects who underwent12 weeks of wellness education and stretching.

The mean difference in Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC)pain scores was 118.80 mm.[94] The tai chi cohort also had significantly better WOMAC physicalfunction scores, patient and physician global visual analog scale scores, chair stand times, Center forEpidemiologic Studies Depression Scale scores, self-efficacy scores, and Short Form 36 physicalcomponent summaries.

Similarly, a systematic review and meta-analysis concluded that research results are encouraging andsuggest that tai chi may be effective in controlling pain and improving physical function in patients withknee osteoarthritis.[95] The researchers noted, however, that the strength of the evidence is limited bythe small number of randomized, controlled trials with a low risk of bias.

Assistive devices

The use of assistive devices for ambulation and for activities of daily living (ADLs) may be indicated

for patients with osteoarthritis. Braces and appropriate footwear may also be of some use. A cane canbe used in the contralateral hand for hip or knee osteoarthritis. The patient can be taught joint-protection and energy-conservation techniques.

For patients with hand osteoarthritis, the ACR conditionally recommends evaluating the patientsability to perform ADLs and providing assistive devices as needed. The ACR conditionallyrecommends splints for patients with trapeziometacarpal joint involvement.[87]

Occupational therapy and physical therapy

Occupational adjustments may be necessary for some patients with osteoarthritis. An occupationaltherapist can assist with evaluating how well the patient performs ADLs, as well as with retraining ofthe patient as necessary. Joint-protection techniques should be emphasized. Physical therapymodalities, especially those aimed at deconditioned patients, can be helpful, particularly in patients

with hip or knee involvement.

Electromagnetic field stimulation and TENS

A pulsed electromagnetic field stimulation device (Bionicare) has been approved by the US Food andDrug Administration (FDA) for use in patients with knee osteoarthritis. Pulsed electromagnetic fieldstimulation is believed to act at the level of articular cartilage by maintaining the proteoglycancomposition of chondrocytes through downregulation of its turnover.[96]

A multicenter, double-blind, randomized, placebo-controlled 4-week trial in 78 patients with kneeosteoarthritis found improved pain and function in those who were treated with the device.[97]A double-blind, placebo-controlled 3-month trial in 58 patients with moderate-to-severe knee osteoarthritisshowed that the use of a highly optimized, capacitively coupled, pulsed electrical stimulus deviceyielded significant symptomatic and functional improvement.[98]

Another randomized clinical trial demonstrated that pulsed short-wave treatment was effective inrelieving pain and improving function and quality of life in women with knee osteoarthritis on a short-term basis; additional studies are needed to validate the 12-month follow-up.[99]

Transcutaneous electrical nerve stimulation (TENS) may be another treatment option for pain relief.To date, however, there is only limited evidence that TENS is beneficial in this setting. A systematicreview could not confirm that TENS is effective for pain relief in knee osteoarthritis.[100]A randomizedcontrolled trial found that TENS applied in conjunction with therapeutic exercise and daily activitiesincreased quadriceps activation and function in patients with tibiofemoral osteoarthritis.[101]

Acupuncture

Acupuncture is becoming a more frequently used option for treatment of the pain and physicaldysfunction associated with osteoarthritis. Some evidence supports its use. For example, a review


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article of randomized, controlled trials reported that the level of pain persisting after acupuncture wassignificantly lower than the level of pain persisting after control treatments.[102]

Several groups have issued guidelines regarding acupuncture for knee osteoarthritis. The AAOSneither recommends nor opposes the use of acupuncture for pain relief in knee osteoarthritis, citinginconclusive evidence.[103]OARSI suggests that acupuncture may yield symptomatic benefit in these

patients.

[65]

The ACR recommends traditional Chinese acupuncture for patients with chronic moderate-to-severe pain who would be candidates for total knee arthroplasty but who either do not want it orhave contraindications to it.[87]

Arthroscopy

A procedure of low invasiveness and morbidity, arthroscopy will not interfere with future surgery.However, a randomized, controlled trial in patients with moderate-to-severe osteoarthritis found thatarthroscopic surgery for osteoarthritis of the knee provided no additional benefit beyond that affordedby optimized physical and medical therapy.[10]

Arthroscopy is indicated for removal of meniscal tears and loose bodies; less predictable arthroscopicprocedures include debridement of loose articular cartilage with a microfracture technique andcartilaginous implants in areas of eburnated subchondral bone (see the images below). These

treatments have varying success rates and should be performed only by surgeons experienced inarthroscopic surgical techniques.[10, 104, 105] Overall, arthroscopy is not recommended for nonspecificcleaning of the knee in osteoarthritis.

Arthroscopic view of a torn meniscus before (top) and after (bottom) removal of loose meniscal

fragments. Arthroscopic view of an arthritic knee.
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Arthroscopic view of a knee after the removal of loose fragments of articular and

meniscal cartilage. Arthroscopic view of the removal of cartilaginous loose body.Patients who undergo arthroscopy usually require a period of crutch use or exercise therapy. Thisperiod typically lasts days but sometimes extends for weeks.

Osteotomy

Osteotomy is used in active patients younger than 60 years who have a malaligned hip or knee jointand want to continue with reasonable physical activity.[106] The principle underlying this procedure is toshift weight from the damaged cartilage on the medial aspect of the knee to the healthy lateral aspectof the knee. Osteotomy is most beneficial for significant genu varum, or bowleg deformity. (Theeffectiveness of osteotomy for genu valgum is not highly predictable.)

Osteotomy often can help individuals avoid requiring a total knee replacement until they are older. Itcan lessen pain, but it can also lead to more challenging surgery if the patient later requiresarthroplasty.

Contraindications for osteotomy are as follows:

Knee flexion of less than 90

A flexion-extension contracture of more than 15

Varus over 15-20

Instability from previous trauma or surgery

Severe arterial insufficiency

Bicompartmental involvementPatients undergoing osteotomy require partial weight-bearing until bony healing occurs. Afterward,

exercise is indicated.

Arthroplasty

Arthroplasty consists of the surgical removal of joint surface and the insertion of a metal and plasticprosthesis (see the images below). The prosthesis is held in place by cement or by bone ingrowth intoa porous coating on the prosthesis. The use of cement results in faster pain relief, but bone ingrowthmay provide a more durable bond; accordingly, prostheses with a porous coating are used in youngerpatients.
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Anteroposterior radiograph shows knee replacement in 1 knee and arthritis in

the other, with medial joint-space narrowing and subchondral sclerosis.Anteroposterior radiograph of the pelvis and hips shows an arthritic hip not treated surgically and a total hip

replacement. Anteroposterior radiograph obtained after knee replacement.

Lateral radiograph obtained after knee replacement (same patient as in the above image).

Arthroplasty is performed if all other modalities are ineffective and osteotomy is not appropriate or if apatient cannot perform ADLs despite maximal therapy.[107, 108]This procedure alleviates pain and mayimprove function. At a minimum, 10-15 years of viability are expected from joint replacement in theabsence of complications.

Infection is a particular postoperative concern in cases of total joint replacement. This complication isnow rare, however, especially with the use of perioperative antibiotics.

Prevention of thrombophlebitis and resultant pulmonary embolism is important in patients whoundergo lower-extremity arthroplasty procedures for osteoarthritis. The surgeon must use all meansavailable to prevent these complications. Early motion and ambulation, when possible, are ofparticular importance. The use of low-molecular-weight heparin or warfarin is also indicated.

After joint replacement, patients require partial weight-bearing, which progresses to full weight-bearingin 1-3 months; range-of-motion and strengthening exercises are started within a few days after joint-replacement surgery and continued until the patient has good range of motion and strength. After
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resection arthroplasty of the hip, patients require instruction in the use of crutches or a walker, whichare usually needed permanently.

For more information, see the following articles:

Total Knee Arthroplasty

Unicompartmental Knee Arthroplasty Surgical Treatment of Interphalangeal Joint Arthritis

Minimally Invasive Total Hip Arthroplasty

Fusion and Joint Lavage

Fusion consists of the union of bones on either side of the joint. This procedure relieves pain butprevents motion and puts more stress on surrounding joints. Fusion is sometimes used after kneereplacements fail or as a primary procedure for ankle or foot arthritis.

Observational studies suggested a benefit for joint lavage. However, sham-controlled trials yieldedconflicting results, and a meta-analysis concluded that joint lavage does not result in pain relief orimprovement of function in patients with knee osteoarthritis.[109]

Prevention

Overweight patients who have early signs of osteoarthritis or who are at high risk should beencouraged to lose weight. Recommend quadriceps-strengthening exercises in patients withosteoarthritis of the knees, except in those with pronounced valgus or varus deformity at the knees.(See Lifestyle Modification, Physical/Occupational Therapy, and Other Nonpharmacologic Measures.)

It has been proposed that low vitamin D levels may play a role in the development and progression ofosteoarthritis; however, studies of vitamin D status and osteoarthritis have produced conflictingresults.[110, 111]

A systematic review found no convincing evidence that selenium, vitamin A, or vitamin C is effectivefor the treatment of osteoarthritis.[112]A prospective cohort study also found no evidence that vitamin Csupplementation slowed the progression of knee osteoarthritis; however, it did find that patients whoreported taking vitamin C were 11% less likely to develop knee osteoarthritis.[113]

Medication Summary

The goals of pharmacotherapy in osteoarthritis are to reduce morbidity and to prevent complications.To date, no disease-modifying or structure-modifying intervention has been proved effective inosteoarthritis. Pay careful attention to a particular pharmacologic regimens adverse-event profile.

Pharmacologic agents used in the treatment of osteoarthritis include the following:

Acetaminophen Nonsteroidal anti-inflammatory drugs (NSAIDs), oral and topical

Intra-articular corticosteroids

Intra-articular sodium hyaluronate

Opioids

Duloxetine

Muscle relaxants

Nutriceuticals (eg, glucosamine/chondroitin sulfate)

Analgesics, Other

Class Summary

Pain control is essential to the management of osteoarthritis. The goals of treatment include painalleviation and improvement of functional status.

View full drug information
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Acetaminophen (Tylenol, Panadol, Aspirin-Free Anacin)

An initial trial with acetaminophen is warranted in patients with mild-to-moderate osteoarthritissymptoms who do not derive sufficient relief from nonpharmacologic measures. Acetaminophen is thedrug of choice for patients who have a documented hypersensitivity to aspirin or NSAIDs, who have ahistory of upper gastrointestinal (GI) tract disease, or who are on anticoagulants.

NSAIDs

Class Summary

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. They are used to relieveosteoarthritis pain when the clinical response to acetaminophen is unsatisfactory. The mechanism ofaction is nonselective inhibition of cyclooxygenase (COX)-1 and COX-2, resulting in reducedsynthesis of prostaglandins and thromboxanes. Other mechanisms may also exist, such as inhibitionof leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation,and various cell-membrane functions.

In more inflammatory presentations of osteoarthritis, such as knee involvement with effusion, theseagents may be used as first-line pharmacologic therapy. Use the lowest effective dose or intermittenttherapy if symptoms are intermittent. All of these medications increase the risk for GI ulcers and havebeen associated with increased risk of cardiovascular disease. Patients at high risk for GI toxicity mayconsider adding misoprostol or a proton-pump inhibitor to the regimen or substituting a COX-2specific inhibitor for the NSAID.


Ketoprofen (Orudis, Oruvail)

Ketoprofen is indicated for relief of mild-to-moderate pain and inflammation. Small dosages areinitially indicated in small and elderly patients and in those with renal or liver disease. Doses higherthan 75 mg do not increase therapeutic effects. Administer high doses with caution, and closelyobserve the patient for response.


Piroxicam (Feldene)Piroxicam decreases the activity of cyclooxygenase, which in turn inhibits prostaglandin synthesis.These effects decrease formation of inflammatory mediators.


Ibuprofen (Ibuprin, Advil, Motrin)

Ibuprofen relieves pain and inflammation. It is widely available and is relatively inexpensive as ageneric drug. After the very early stages of osteoarthritis, inflammation begins to play a role in thedisease. Thus, medications with a combination of analgesic and anti-inflammatory properties becomemore desirable, at least in theory.


Meloxicam (Mobic)

To some extent, meloxicam is more selective for COX-2 receptors than traditional NSAIDs are. Itdecreases the activity of cyclooxygenase, thereby, in turn, inhibiting prostaglandin synthesis. Theseeffects decrease the formation of inflammatory mediators.


Diclofenac (Voltaren, Arthrotec, Cataflam)

Diclofenac is one of a series of phenylacetic acids that have demonstrated anti-inflammatory andanalgesic properties in pharmacologic studies. It is believed to inhibit cyclooxygenase, which isessential in the biosynthesis of prostaglandins. Diclofenac can cause hepatotoxicity; hence, liverenzymes should be monitored in the first 8 weeks of treatment.

Diclofenac is rapidly absorbed; metabolism occurs in the liver by demethylation, deacetylation, andglucuronide conjugation. The delayed-release, enteric-coated form is diclofenac sodium, and theimmediate-release form is diclofenac potassium. It poses a relatively low risk for bleeding GI ulcers.
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Naproxen (Aleve, Anaprox, Anaprox DS, Naprelan, Naprosyn)

Naproxen is used for relief of mild to moderate pain. It inhibits inflammatory reactions and pain bydecreasing the activity of cyclooxygenase, which is responsible for prostaglandin synthesis. NSAIDsdecrease intraglomerular pressure and decrease proteinuria.

View full drug informationCelecoxib (Celebrex)

Celecoxib is a COX-2specific inhibitor. At therapeutic concentrations, COX-2 (inducible by cytokinesat sites of inflammation, such as the joints) is inhibited, and COX-1 isoenzyme (present in plateletsand the GI tract) is spared; therefore, in nonaspirin users, the incidence of GI toxicity (eg, endoscopicpeptic ulcers, bleeding ulcers, perforations, and obstructions) is decreased in comparison with thatseen in patients taking nonselective NSAIDs.

COX-2 is expressed in the kidney; however, the renal safety profile of celecoxib is not significantlysuperior to that of nonselective NSAIDs. Selective COX-2 inhibitors may increase the risk of cardiacdisease; 1 drug in this class, rofecoxib, has already been removed from the market for this reason.Celecoxib is currently under investigation for a possible associated risk of accelerated cardiac

disease.

Antidepressants, SNRIs

Class Summary

The selective serotonin-norepinephrine reuptake inhibitor (SNRI) duloxetine may be effective forreducing osteoarthritis pain.


Duloxetine (Cymbalta)

Potent inhibitor of neuronal serotonin and norepinephrine reuptake. Indicated for chronicmusculoskeletal pain, including discomfort from osteoarthritis and chronic lower back pain.

Analgesic, TopicalClass Summary

Topical analgesics are used for osteoarthritis involving relatively superficial joints, such as the kneejoint and the joints of the hands. They are much less effective for deeper joints, such as the hip joint.


Capsaicin (Dolorac, Capsin, Zostrix, Civamide)

Capsaicin is a topical analgesic of choice in osteoarthritis. Derived from plants of the Solanaceaefamily, it may render skin and joints insensitive to pain by depleting substance P in peripheral sensoryneurons. Capsaicin must be used for at least 2 weeks for the full effects to be appreciated.

Opioid AnalgesicsClass Summary

Opioid analgesics are used in patients whose pain has not been controlled with weaker analgesicmedications. They are a particularly reasonable choice in patients who do not want joint-replacementsurgery, are too medically ill for joint replacement, are not candidates for joint replacement for otherreasons, or are trying to buy time for subsequent joint-replacement surgery.

Elderly patients (aged 65 years and older) with arthritis are more likely to incur a fracture wheninitiating opioid therapy as opposed to NSAID therapy. A higher opioid dose is associated with agreater risk of fracture; this risk is due to an increased risk of falls. During the first 2 weeks afterinitiation of opioid treatment, short-acting opioids are associated with a greater fracture risk than long-acting opioids are.[114]


Tramadol (Ultram, Ultram ER)
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Tramadol inhibits ascending pain pathways, altering perception of and response to pain. This agentalso inhibits the reuptake of norepinephrine and serotonin.


Oxycodone (OxyContin, Roxicodone)

Pure narcotic analgesics, such as oxycodone, might be the initial drug of choice. Eventually, thisshort-acting narcotic can be replaced with a long-acting transdermal preparation, such as fentanyl(Duragesic patch).

Corticosteroids

Class Summary

Intra-articular pharmacologic therapy includes corticosteroid injection and viscosupplementation.Steroid injections generally result in a clinically and statistically significant reduction in osteoarthriticknee pain as soon as 1 week after injection. The effect may last, on average, anywhere from 4 to 6weeks per injection, but the benefit is unlikely to continue beyond that time frame.


Methylprednisolone (Depo-Medrol, Medrol, Solu-Medrol)

Methylprednisolone decreases inflammation by suppressing migration of polymorphonuclearleukocytes (PMNs) and reversing increased capillary permeability.


Betamethasone (Celestone Soluspan)

Betamethasone decreases inflammation by suppressing migration of PMNs and reversing increasedcapillary permeability. It affects the production of lymphokines and has an inhibitory effect onLangerhans cells.


Triamcinolone (Aristospan Intra-Articular)

Triamcinolone decreases inflammation by suppressing migration of PMNs and reversing capillarypermeability.

Intra-articular Agents

Class Summary

Intra-articular injections of these agents are used to treat patients with osteoarthritic knee pain that isunresponsive to conservative nonpharmacologic therapy and simple analgesics (eg, acetaminophen).


Sodium hyaluronate (Euflexxa, Hyalgan, Orthovisc, Supartz, Synvisc, Synvisc-One)

Sodium hyaluronate is a hyaluronic acid derivative that supports the lubricating and shock-absorbingproperties of articular cartilage.

1. American Academy of Orthopaedic Surgeons. Treatment of Osteoarthritis (OA) of the Knee.AAOS: American Academy of Orthopaedic Surgeons. Availablea

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