Osteoarthritis

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[edit] Osteoarthritis

Eric W. Jacobson

Osteoarthritis (OA, also known as osteoarthrosis or degenerative joint disease) is the most common rheumatic disease, affecting more than 50 million people in the United States.The cost to society for treatment and lost earnings is staggering.Recent advances in the understanding of the pathophysiology of OA have altered the conception of this disease.Once viewed as a slowly advancing disease with limited possibilities for medical intervention, OA is now seen as a disease that can be modified in regard to immediate treatment and long-term outcome.^[1]

[edit] EPIDEMIOLOGY

Osteoarthritis is a prevalent disease of cartilage that increases steadily with age.Up to 85% of the general population has radiographic evidence of OA by age 65.^[2] OA is equally distributed among men and women when all age groups are considered.In people over age 55, however, women are more often affected and tend to have more severe disease because of body habitus or genetic predisposition.Prevalence patterns of OA may be subtly different among races, but this may relate more to differences in occupations and lifestyles than directly to race.^[3] Genetic predisposition involves mainly OA of the distal interphalangeal (DIP) joints of the hands, which seems to follow an autosomal dominant pattern of inheritance with variable expression.Expression is gender linked and dominant in women.

[edit] ETIOLOGY

The etiology of OA is multifactorial (Box 132-1).Although a strong association exists between OA and aging, OA is not a natural consequence of aging.Biochemical changes in the matrix molecules of cartilage occur with age but are different from the biochemical changes that occur in osteoarthritic cartilage.^[4] Aging cartilage, however, may be more prone to OA if other etiologic factors (e.g., genetic predisposition) are present.

Joints that have sustained serious trauma (e.g., fractures, ligamentous injuries) are prone to OA in later years.Joints exposed to repetitive trauma also are associated with OA, often related to occupation.Ballet dancers have an increased incidence of OA in the ankles and feet because of repetitive trauma across these joints; American football players are prone to knee OA.An exception is long-distance runners, in whom studies have failed to show an increased incidence of OA in lower extremity joints despite repetitive stress.^[5] Self-selected body habitus in runners at baseline may be associated with protection against development of OA.

Obesity is also associated with OA, although studies show conflicting results.A statistically significant increase of knee OA was shown in obese women but not in obese men.^[6]

Any alteration of normal joint anatomy or of joint stability is associated with an increased risk of OA in that joint, as in congenital abnormalities (e.g., congenital hip dislocation) and acquired abnormalities (e.g., chronic dislocation resulting from trauma).Altered joint anatomy leads to a change in the distribution of force across that joint.In a normal joint, force is distributed uniformly across the cartilaginous surface.If the anatomy is altered, forces across the joint may localize to one area of cartilage, leading to focal damage.This initiates the osteoarthritic process.Therefore any process leading to joint destruction predisposes to secondary OA.This includes inflammatory arthropathies (e.g., rheumatoid arthritis [RA], gout, pseudogout), metabolic conditions affecting joints (hemochromatosis, ochronosis), bleeding diatheses (e.g., hemophilia) in which recurrent hemarthrosis occurs, avascular necrosis with subsequent alteration of normal bony contour, and neurologic disorders associated with altered sensation of proprioception around a joint.Alterations in the molecular composition of cartilage and secondary inflammatory processes are also important in the development of OA.

[edit] PATHOPHYSIOLOGY

Normal articular cartilage is composed of interstitial fluid, cellular elements, and matrix molecules (Box 132-2).Approximately 70% of cartilage is water; this percentage increases with advancing stages of OA.Cellular elements may be stationary (e.g., chondrocytes) or circulatory (e.g., lymphocytes, other mononuclear cells).The chondrocyte synthesizes matrix molecules, thus possessing reparative capabilities.The major matrix molecules consist of proteins (collagen, mainly type II; elastin; fibronectin) and complex polysaccharides (proteoglycans).The proteoglycan molecule is made up of a hyaluronic acid backbone with glycosaminoglycan derivatives attached at about 90-degree angles.This composition gives cartilage strength and elasticity.Its function is to absorb impact loading across the joint and to allow smooth gliding of juxtaposed articular surfaces.

The pathogenesis of OA involves a dual process of catabolism and repair.Remodeling is ongoing in normal cartilage; matrix molecules are regularly degraded by autolytic enzymes and then replaced through production by chondrocytes.In OA this process is altered and causes an overall loss of matrix molecules despite attempts at repair.The newly synthesized matrix molecules are considered mechanically inferior to the original molecules and therefore may be more prone to injury and further damage.The process may be initiated by local trauma that leads to chondrocyte injury.Chondrocytes release proteolytic enzymes (e.g., neutral proteases, acid cathepsins, collagenase, metalloproteases), which degrade matrix molecules, including the proteoglycan aggregate, producing smaller, nonaggregating molecules.This leads to thinner, mechanically inferior cartilage.The rate of release of these enzymes and the subsequent rate of matrix molecule destruction are significantly more rapid in osteoarthritic cartilage than in normal cartilage.^[7] Loss of tensile strength for load support leads to transmission of greater force to chondrocytes and subchondral bone.Chondrocytes sustain greater injury, leading to further release of degrading enzymes.Subchondral bone sustains microfractures, causing stiffening and loss of compressibility.Some of the breakdown products from cartilage and proteoglycans may stimulate a secondary inflammatory response involving polymorphonuclear leukocytes, synovial cells, and macrophages.The whole process is perpetuated in a continuous destructive cycle (Fig.132-1).

Figure 132-1 Pathogenesis of osteoarthritis.

[edit] PATIENT EVALUATION

[edit] History

Osteoarthritis is the prototype of a noninflammatory arthritis.From the history the physician should begin to differentiate OA from inflammatory arthropathies (e.g., RA).OA typically begins in the later decades of life and has a slow, insidious onset that is gradually progressive over many years.The joint distribution is distinctive, mainly involving the weight- bearing joints, the spine, and the hands.Unless the patient has a history of trauma or other predisposing factors, OA typically spares the wrists, elbows, and shoulders.Involvement of any of these joints without a history of trauma should suggest other causes of the arthritis.

The patient describes classic mechanical joint pain.The pain is typically aching in quality and is brought on by use of the joint.Early in the disease the pain is relieved by rest.In advanced disease, pain occurs at rest and with exertion.This is in contrast to inflammatory arthritis, in which pain frequently improves with activity.In classic OA, patients complain of pain, but there is no obvious swelling, redness, or warmth.With time the patient may describe progressive bony enlargement of joints and restricted joint motion.The patient describes short-term stiffness after inactivity and less than 30 minutes of stiffness in the morning.This is in contrast to the inflammatory arthritides, in which morning stiffness can be very prolonged and may correlate with disease activity.Patients may also describe a creaking or cracking of joints with motion that may worsen with progressive loss of cartilage (Box 132-3).

OA may involve the cervical and the lumbosacral spine, unlike RA, which typically involves the cervical spine but spares the lumbosacral spine.Nerve root compression may occur with spinal involvement.The patient may then complain of radiating pain down an extremity, associated with paresthesias and focal weakness.These symptoms should present in a dermatomal distribution.Osteoarthritic involvement of the lumbar spine can also lead to spinal stenosis.The classic history of spinal stenosis is leg claudication.Pain occurs with ambulation, persists with stopping and standing, but is relieved with sitting or bending forward.Vascular claudication, on the other hand, is relieved with stopping and standing still.

Inflammatory or erosive OA involves the hands, affecting proximal interphalangeal (PIP) and DIP joints, and is associated with swelling, redness, and warmth.True erosions occur, leading to joint destruction and occasionally bony ankylosis.This arthropathy may be confused with psoriatic arthritis, another erosive arthropathy often affecting DIP joints.

[edit] Physical Examination

Examination of a patient with OA requires consideration of the typical joint distribution (Box 132-4).OA tends to involve the weight-bearing joints, the spine, and the hands.Hips and knees are often affected, usually somewhat symmetrically.In the hands the classic joint involvement includes the first carpometacarpal (CMC) joint at the base of the thumb, the PIP joints, and the DIP joints.This is in contrast to RA, which involves the metacarpophalangeal joints and PIP joints but spares the DIP joints.OA also involves the first metatarsophalangeal (MTP) joints of the feet.

Joint examination in OA depends on the area being examined.In general, there is pain with motion and sometimes with palpation, limited range of motion of the joint (related to loss of articular cartilage), and bony enlargement of the joint (related to the proliferative spurs).The capsule may appear thickened.Typical OA shows no signs of active inflammation (warmth, erythema, trueeffusions).Lack of these signs helps distinguish OA from the inflammatory arthritides.Examination of the spine may reveal loss of range of motion, depending on the stage of the disease.When spinal involvement is present, a thorough neurologic examination of the extremities should be performed to screen for nerve root impingement syndromes.Hip examination reveals loss of range of motion and pain.Knee examination shows loss of motion and frequently crepitus (a feeling of crunching when the joint is moved).Effusions are generally absent.Bony enlargement of PIP and DIP joints leads to a knobby appearance.These changes are referred to as Bouchard's nodes in the PIP joints and Heberden's nodes in the DIP joints.CMC involvement is associated with a squaring at the base of the thumb, usually accompanied by marked pain with squeezing.MTP involvement is often associated with bunion formation.

As OA progresses, loss of articular cartilage becomes more prominent, and normal anatomy is altered.This changes the distribution of force across the joint, sometimes leading to strain across tendons, bursae, and other periarticular structures.The physician must therefore check for the presence of soft tissue rheumatism in areas in proximity toosteoarthritic joints.Trochanteric bursitis of the hip and anserine bursitis of the knee are common causes of pain, in addition to the pain caused by the OA (see Chapters 128 and 129 ).

[edit] LABORATORY STUDIES AND DIAGNOSTIC PROCEDURES

Laboratory studies in OA are generally unrevealing.Tests checking for systemic inflammation (e.g., erythrocyte sedimentation rate, C-reactive protein), blood counts, and general chemistries are normal.Ordering rheumatology profiles is not indicated when the history and physical examination are consistent with OA.Routine x-ray films confirm the presence of OA and are helpful in establishing extent of disease (Fig.132-2).Radiographic findings include joint space narrowing, subchondral bony sclerosis, subchondral cysts, and osteophytes (proliferative spurs) (Box 132-5; see Chapter 123 ).Erosions are not seen in general OA but may be seen in the inflammatory form.Computed tomography (CT) or magnetic resonance imaging (MRI) scans of the spine may be indicated if the patient has signs or symptoms suggesting a nerve impingement syndrome.These studies rule out neuroforaminal encroachment or disk herniation leading to nerve impingement.CT and MRI also are used to assess for associated spinal stenosis.

Figure 132-2 Severe osteoarthritis of hip (A) compared with normal hip (B). (Courtesy American Rheumatism Association.)

[edit] MANAGEMENT

As with any arthritis, treatment should begin with education so the patient understands the diagnosis, prognosis, and treatment options (Box 132-6).In OA it is important to preserve joint cartilage and thus range of motion.The patient is taught joint protection and avoids activities that lead to repetitive trauma to the joint; jogging, for example, results in repetitive stress across the knee joints and may predispose cartilage to more rapid deterioration.Similarly, weight loss is an appropriate goal for patients with OA involving lower extremities and the lumbar spine.

Physical therapy and occupational therapy are useful modalities for patients with OA.Basic physical therapy should include education regarding range of motion exercises, which may preserve joint mobility.Physical therapists teach patients appropriate strengthening exercises to preserve the strength of muscle groups surrounding involved joints.This helps maintain stability of the joints, reduce pain, and prevent injury.Heat, ultrasound, and massage techniques may also reduce pain.For chronic pain unresponsive to other measures, a transcutaneous electric nerve stimulation (TENS) trial may be appropriate; the patient can wear the unit throughout the day.The TENS unit can be adjusted to maximize electric output when pain increases.This is helpful for some patients with chronic low back, hip, and knee pain related to OA.An occupational therapy evaluation is useful in assessing the patient's functional limitations.Occupational therapists provide assistive devices that allow patients to perform home or work tasks that would otherwise be difficult or impossible.Patients are also taught the principles of joint protection and energy conservation.

The main medications used for the treatment of OA are analgesics and NSAIDs; both reduce pain.NSAIDs have the added advantage of reducing any secondary inflammation.Both types of medications are comparable for short-term pain control in symptomatic OA of the knee.^[8] Further studies are required to assess benefit risk of these medications for OA in general.In early disease, analgesics may be tried on an as-needed basis.As the disease progresses, regular use of analgesics or NSAIDs may be required to control symptoms.Patients taking NSAIDs chronically must be monitored closely for toxicity, especially gastrointestinal (GI) complications (e.g., gastritis, peptic ulcer disease) and renal insufficiency.

The mechanism of action of NSAIDs is to inhibit prostaglandin production by blocking a specific enzyme, cyclooxygenase.Prostaglandins are mediators of pain and inflammation but also play important roles in GI mucosal protection, maintenance of renal blood flow, and platelet aggregation.Blocking prostaglandin production is antiinflammatory, but patients are at risk for serious side effects, including GI complications.Cyclooxygenase I (COX-I) is found in all tissues and mediates the GI, renal, and platelet functions of prostaglandins.Cyclooxygenase II (COX-II) is induced mainly in areas of inflammation.^[9] Thus selectively blocking COX-II over COX-I should diminish inflammation without altering the protective benefits of prostaglandins in the GI tract and other tissues.Two selective COX-II inhibitors, celecoxib (Celebrex) and rofecoxib (Vioxx), have antiinflammatory benefits similar to other NSAIDs and a better GI toxicity profile.^[10]

Topical capsaicin also may be useful in the treatment of OA.^[11] Capsaicin can deplete and prevent reaccumulation of substance P at the sensory nerve terminals, thus reducing pain.It is usually applied four times per day.Local burning may occur initially, but this side effect generally ceases with continued use.

Use of hyaluronic acid (viscosupplementation) for OA is a relatively new treatment option.Both hyaluronin (Hyalgan) and hylan G-F 20 (Synvisc) have been approved for treatment of knee OA.^[12] Hyaluronic acid, a major component of synovial fluid, lubricates and protects the joint.In OA the amount of hyaluronic acid is reduced.Injecting hyaluronic acid–like substances into joints should restore the protective and lubricating properties.Patients receive either a five-dose (hyaluronin) or three-dose (hylan G-F 20) weekly series of injections into their affected knee.Studies comparing these compounds to placebo, intraarticular steroids, and NSAIDs have shown variable results, with improvement in pain and functional ability but uncertain long-term benefit.Benefit may be most pronounced in patients with milder disease.Currently, many rheumatologists consider viscosupplementation only for patients who have failed other treatment options.

Patients can now buy cartilage components such as glucosamine sulfate and chondroitin sulfate over the counter.These components are taken orally in various dosage regimens.Their long-term benefit is unclear, and large-scale studies are needed.

Judicial use of intraarticular corticosteroid injections can provide temporary relief of pain in some patients with OA.A long-acting corticosteroid preparation (triamcinolone hexacetonide or methylprednisolone acetate) mixed with a local anesthetic (1% lidocaine) is generally used.Patients are instructed to rest the joint for 2 to 3 days after an injection.Complications include infection (less than 0.001%), bleeding, skin atrophy, and postinjection flare.Frequent injections with corticosteroids may accelerate cartilage deterioration.For this reason the same joint should not be injected more frequently than every 3 months.If a joint is injected at this rate for more than 1 year, alternate treatment options should be explored.

The final treatment option for OA is surgery.Surgical procedures may include osteotomy, joint debridement, arthrodesis (fusion), and arthroplasty (replacement).Joint replacement should be considered for patients who have significant disability related to the OA and for whom medical treatment options have failed.

[edit] REFERENCES