AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Background

Osteoarthritis (OA) is a chronic disease process affecting synovial joints, particularly large weight-bearing joints. OA is particularly common in older patients but can occur in younger patients either through a genetic mechanism or, more commonly, because of previous joint trauma.

Related eMedicine topics:
Interphalangeal Joint Arthritis
Osteoarthritis [Orthopedic Surgery]
Osteoarthritis [Rheumatology]
Osteoarthritis, Primary
Wrist Arthritis

Related Medscape topics:
Resource Center Arthritis
Resource Center Joint Disorders

Pathophysiology

Joints can be classified as synovial, fibrous, or combination joints, based on the presence or absence of a synovial membrane and the amount of motion that occurs in the joint. Normal synovial joints allow a significant amount of motion along their extremely smooth articular surface. These joints are composed of a synovial membrane, articular or hyaline cartilage, subchondral bone, synovial fluid, and a joint capsule.

Although traditional teaching prescribes that osteoarthritis (OA) affects primarily the articular cartilage of synovial joints, pathophysiologic changes also occur in the synovial fluid, as well as in the underlying (subchondral) bone and the overlying joint capsule. The affected cartilage initially develops small tears, known as fibrillations, at the articular surface, followed by larger tears; the cartilage eventually fragments off into joints. The cartilage-forming cells (ie, chondrocytes) replicate in an attempt to keep up with the cartilage loss; however, they eventually are unable to do so, and the underlying bone becomes exposed as gross areas of the bone become denuded of cartilage.

In the early degenerative process, increased expression and content of various metalloproteinases occur. These proteinases are very much involved in the excessive matrix degradation that characterizes cartilage degeneration in OA.¹ Bone along the periphery of the joint replicates to form osteophytes, while the subchondral bone along the midportion of the joint becomes sclerotic, and areas within it may eventually undergo cystic degeneration because of focal resorption. Synovial fluid is formed through an ultrafiltration process of serum by cells that form the synovial membrane (synoviocytes). Synovial cells also manufacture the major protein component of synovial fluid, hyaluronic acid (also known as hyaluronate). Synovial fluid supplies nutrients to the avascular articular cartilage; it also provides the viscosity needed to absorb shock from slow movements, as well as the elasticity required to absorb shock from rapid movements.

The osteoarthritic joint is characterized by decreased concentration of hyaluronic acid because of reduced production by synoviocytes and increased water content because of inflammation, particularly during later stages of the disease.

The onset of pain is usually insidious, is generally described as aching or throbbing, and may be the result of changes that have occurred over the previous 15-20 years of the patient's life. Most often, the pain worsens with activity involving the affected joint and is initially relieved with rest; eventually, however, pain occurs even at rest. Since cartilage itself is not innervated, the pain is presumed to arise from a combination of mechanisms, 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

In addition to the underlying pathophysiologic changes described above, overall, the joint may undergo mechanical deformation, with resultant malalignment and instability. Alternatively, the joint can ankylose.

Related eMedicine topic:
The Approach to the Painful Joint

Related Medscape topic:
CME Management of Shoulder Osteoarthritis Reviewed

Frequency

United States

Osteoarthritis (OA) is the most prevalent musculoskeletal condition that causes joint pain. The incidence of OA increases with age, with estimates based on radiologic evidence indicating the following incidence patterns:

• At age 18-24 years, 7% of men and 2% of women show signs of OA in the hands.
• At age 55-64 years, 28% of men and women show signs of OA in the knee, and 23% show signs of OA in the hip.
• At age 65-74 years, 39% of men and women show signs of OA in the knee and 23% show signs of OA in the hip.
• At age 75-79 years, approximately 100% of men and women show some signs of OA.

Mortality/Morbidity

• Mortality does not occur directly from osteoarthritis (OA), but it can result indirectly from complications associated with immobility and deconditioning, medications used to relieve pain associated with OA, or from joint-related surgery.
• Morbidity can take the form of pain or loss of function.

Race

No significant correlation exists between the incidence of osteoarthritis (OA) and race, with the exception of the Chinese population, which demonstrates a decreased incidence of OA. Different prevalences are cited for different ethnic groups.

Sex

Osteoarthritis (OA) is equally prevalent in men and women aged 45-55 years. After age 55 years, the prevalence of OA increases in women in comparison with men. The primary differences in incidence between males and females are related to the sites affected by OA. The most common sites affected in females are distal interphalangeal joints, proximal interphalangeal joints, first carpometacarpal joints, metatarsophalangeal joints, hips (in those aged 55-64 y), and knees (in those aged 65-74 y). In males aged 65-74 years, the hips and knees are affected more frequently than they are in females.

Age

Most adults older than 55 years show radiographic evidence of osteoarthritis (OA).² Males develop OA before age 45 years, possibly because of a higher incidence of posttraumatic OA. After age 55 years, women are affected more frequently by OA and tend to have more severe disease than do men.

CLINICAL

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

History

Patients with osteoarthritis (OA) generally complain of insidious throbbing arthralgias with activity. Although initially, resting relieves the pain, the patient eventually begins to suffer pain even when he/she is at rest. Morning stiffness, which usually lasts less than 30 minutes, may also be experienced in the joint. Intermittent joint swelling and give-way weakness in the knees (ie, quadriceps pain inhibition) are noted.

Physical

• Early in the disease process of osteoarthritis, physical examination findings include the following:
• • Joints may appear normal.
  • Gait may be antalgic if weight-bearing joints are involved.
• Later in the disease process, physical examination findings include the following:
• • Visible osteophytes may be noted.
  • Joints may be warm to palpation.
  • Palpable osteophytes frequently are noted.
  • Joint effusion frequently is evidenced in superficial joints.
  • Range-of-motion limitations, because of bony restrictions and/or soft tissue contractures, are characteristic.
  • Crepitus with range of motion is not uncommon.

Causes

• Primary osteoarthritis (OA), which can be either localized or generalized, is most often idiopathic, except in rare cases in which a defective gene has been found to cause a familial form of OA.
• Secondary OA can be caused by the following:
• • Obesity (increases mechanical stress)^{3, 4}
  • Repetitive use (ie, jobs requiring heavy labor and bending)⁵
  • Previous trauma (ie, posttraumatic OA)
  • Infection
  • Crystal deposition
  • Acromegaly
  • Previous rheumatoid arthritis (ie, burnt-out rheumatoid arthritis)
  • Heritable metabolic causes (eg, alkaptonuria, hemochromatosis, Wilson disease)
  • Hemoglobinopathies (eg, sickle cell disease, thalassemia)
  • Neuropathic disorder leading to a Charcot joint (eg, syringomyelia, tabes dorsalis, diabetes)
  • Underlying orthopedic disorders (eg, congenital hip dislocation, slipped femoral capital epiphysis)
  • Disorders of bone (eg, Paget disease, avascular necrosis)

Related eMedicine topics:
Obesity [Endocrinology]
Obesity [Pediatrics: General Medicine]

Related Medscape topic:
Resource Center Obesity

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Other Problems to Be Considered

Crystal deposition disease
Pseudogout
Inflammatory arthritis
Seronegative spondyloarthropathies
Infected joint
Underlying mechanical pain

WORKUP

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Lab Studies

• Research has not yet produced a clinically useful diagnostic test for osteoarthritis (OA), so no laboratory studies can assist in the condition's diagnosis per se.
• Researchers have looked at monoclonal antibodies, synovial fluid markers, and urinary pyridinium cross-links (ie, breakdown products of cartilage).⁶ Erythrocyte sedimentation rate (ESR) is not usually elevated, but it may be slightly elevated in cases of erosive inflammatory arthritis.

Imaging Studies

• Studies on the diagnostic use of magnetic resonance imaging (MRI) in osteoarthritis (OA) of the knee are currently being conducted.⁷ A study attempted to correlate the clinical features of OA with MRI findings in patients with the condition. A large joint effusion was associated with pain and stiffness. The presence of an osteophyte in the patellofemoral compartment was associated with pain. All other imaging findings, including focal or diffuse cartilaginous abnormalities, subchondral cysts, bone marrow edema, subluxation of the meniscus, meniscal tears, and Baker cysts, were not associated with symptoms.^{8, 9}
• Bone scans¹⁰ may be helpful in the early diagnosis of OA of the hand. Bone scans also can help to differentiate joint pain due to OA from pain associated with other disease processes. For example, bone scans typically yield a symmetrical pattern of a very mild increased uptake in a symmetrical manner in OA. In contrast, bone scans are often negative in the early stages of multiple myeloma, a cause of bone pain in older adults that can be confused with OA. Bone scans also can help to differentiate OA from osteomyelitis and bone metastases. Single-photon emission computed tomography scanning (SPECT) helps to differentiate back pain due to degenerative disk disease from back pain due to spondylolysis.
• Plain radiographs are often negative early in the disease.
• The Kellgren-Lawrence Grading System, which is the most universally accepted method of classifying radiographic osteoarthritis, uses the following 4 radiographic features:
• • Joint space narrowing
  • Osteophytes
  • Subchondral sclerosis
  • Subchondral cysts

Other Tests

• Perform diagnostic joint aspiration for synovial fluid analysis to help rule out conditions other than osteoarthritis. The presence of noninflammatory joint fluid helps to distinguish OA from other causes of joint pain. Other findings that aid in the differentiation of OA from other conditions are negative Gram stains and cultures, as well as the absence of crystals when fluid is viewed under a polarized microscope.

Histologic Findings

Cartilage biopsy generally is not performed in the diagnosis of osteoarthritis.

TREATMENT

Section 6 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Rehabilitation Program

Physical Therapy

Lifestyle modification, particularly exercise and weight reduction, is a core component of the management of osteoarthritis (OA).^{11, 12} A program of physical therapy should emphasize the importance of strengthening all muscles that cross the given joint affected by OA.

Most research focuses on quadriceps strengthening in knee OA. Also important are stretching exercises, which increase range of motion. The importance of aerobic conditioning, particularly low-impact exercises (if OA affects weight-bearing joints), should be stressed. Swimming, especially aerobic aquatic programs through the Arthritis Foundation, can be helpful. Certain studies also indicate that a home exercise program for patients with OA of the knee provides an important benefit.

In a review on patient adherence to exercise, Marks and Allegrante concluded that interventions to enhance self-efficacy, social support, and skills in the long-term monitoring of progress are necessary to foster exercise adherence in people with OA.¹³

Use of assistive devices for ambulation and for activities of daily living may be indicated. Braces and appropriate footwear may also be of some use. A cane can be used in the opposite hand for OA of the hip, and a cane in the hand of comfort may be helpful for OA of the knee. The patient can be taught joint-protection and energy conservation techniques. Other physical therapy modalities include electrotherapy and thermotherapy.

Related Medscape topic:
CME Therapeutic Exercise May Be Effective for Hip Osteoarthritis

Occupational Therapy

Evaluation of how well the patient performs his/her activities of daily living, as well as retraining of the patient, can be assisted by the occupational therapist. Emphasize joint-protection techniques. Hand splinting, especially of the first carpometacarpal joint, may be indicated.

Recreational Therapy

A home exercise program that incorporates all of the above treatment principles could be designed and implemented to help the patient with osteoarthritis retain mobility.

Medical Issues/Complications

Osteophyte formation in the spine can lead to radiculopathy and/or myelopathy. Osteophyte formation in the cervical spine near the vertebral arteries can lead to vertebral artery compression.

Surgical Intervention

Surgical intervention for osteoarthritis (OA) may be indicated. Types of procedures vary according to the site and the degree of involvement. The types of surgical interventions that can be employed include the following:

• Surgical interventions for OA of the knee
• • Arthroscopic lavage - Using a saline lavage to wash out the joint
  • Joint realignment (realignment osteotomy)
  • Joint fusion (arthrodesis) - Surgically fusing the joint to eliminate motion
  • Joint replacement (arthroplasty)
• Surgical interventions for OA of the hip
• • Joint realignment (realignment osteotomy)
  • Joint fusion (arthrodesis) - Surgically fusing the joint to eliminate motion
  • Joint replacement (arthroplasty)
  • • Hip replacements generally are classified as either hemiarthroplasty (ie, replacement of the femoral side of the hip joint, while leaving the patient's acetabulum intact) or total hip arthroplasty (replacement of the femoral side of the hip joint and the acetabulum).
    • Further classification often involves specification of the specific hardware used (eg, unipolar prosthesis, bipolar prosthesis) and whether or not cement is used to hold the hardware in place.

Related eMedicine topics:
Acetabular Wear in Total Hip Arthroplasty
Complications of Total Knee Arthroplasty
Hip Replacement
Total Knee Arthroplasty
Unicompartmental Knee Arthroplasty

Related Medscape topic:
CME Arthroscopic Surgery May Not Be Helpful for Knee Osteoarthritis

Consultations

Consultation with an orthopedic surgeon may sometimes be needed. Rheumatology consultation is indicated if an alternative diagnosis (eg, rheumatoid arthritis) is suggested.

Related Medscape topic:
Resource Center Rheumatoid Arthritis

Other Treatment

Intra-articular steroid injections may provide pain relief and have an anti-inflammatory effect on the affected joint in osteoarthritis (OA). Such injections generally result in a clinically and statistically significant reduction in osteoarthritic knee pain as soon as 1 week after injection. The effect may last, on average, anywhere from 4-6 weeks per injection, but this benefit is unlikely to continue beyond that time frame.¹⁴ One randomized, placebo-controlled study confirmed the effectiveness of corticosteroid injection in the treatment of hip OA, with benefits often lasting up to 3 months.¹⁵ Some controversial evidence exists regarding frequent steroid injections and subsequent damage to cartilage (chondrodegeneration). Therefore, usually no more than 3 injections are recommended per year in any 1 osteoarthritic joint.

Intra-articular injection of sodium hyaluronate (ie, hyaluronic acid [HA], hyaluronan), also referred to as viscosupplementation, has been shown to be safe and effective for the symptomatic relief of knee OA. This topic has been reviewed in depth elsewhere.¹⁶ The largest meta-analysis of intra-articular HA injection, using 76 controlled clinical studies (and subsequently updated by the Cochrane Collaboration), concluded that this therapy is safe and effective in patients with knee OA.¹⁷

To date, the US Food and Drug Administration (FDA) has approved 5 intra-articular HAs for the treatment of pain associated with knee OA. These include naturally extracted, non–cross-linked sodium hyaluronate products (Hyalgan,¹⁸ Supartz, Orthovisc, Euflexxa) and 1 cross-linked sodium hyaluronate product known as hylan G-F 20 (Synvisc). Euflexxa is the only product derived from a fermentation process (Streptococcus), while the source material for the other 4 products is chicken combs. At present, no distinct advantage or disadvantage has been associated with either source of HA production.

Some differences between the viscosupplements do exist in the FDA-approved prescribing information. For example, Hyalgan and Synvisc have labeling that establishes their safety for repeat treatment, while other products have the precautionary statement that "the safety and efficacy of repeat treatment has not been established."

The HA class in general has demonstrated a very favorable safety profile for the chronic pain management of knee OA, with the most common adverse event being injection site pain. While any intra-articular injection (all HA products and steroids) may elicit an inflammatory response and possible effusion, a clinically distinct acute inflammatory side effect (ie, severe acute inflammatory reaction [SAIR] or HA–associated intra-articular pseudosepsis) has been described. However, preclinical and clinical data provide compelling evidence that this reaction is limited only to the cross-linked hylan G-F 20 product and may have an immunologic mechanism of action. Molecular weight per se has not been found to correlate with efficacy (eg, higher or lower viscosity does not equate with better or worse clinical outcomes).

Interestingly, the duration of residence of an intra-articular injection (days) cannot explain the prolonged clinical benefit (months), and accordingly, subsequent biological mechanisms have also been proposed that may play an important role in the clinical benefit. The combination of quadriceps strengthening and HAs may have a synergistic effect on pain.¹⁹

In the United States, HAs are classified as medical devices rather than as drugs. Although the exact mechanisms of action through which they provide symptomatic relief are unknown, several possibilities exist, including direct binding to receptors (CD44 in particular) in the synovium and cartilage that can lead to several biologic activation pathways.

These mechanisms of action can include the increased endogenous production of hyaluronate and aggrecan by the joint, a mechanical barrier to the activation of nociceptors, the inhibition of pain mediators (eg, PGE, bradykinin), an anti-inflammatory effect (eg, inhibition of proinflammatory cytokine activity, inhibition of inflammatory cell function), a beneficial effect on immune cells, an antioxidant effect, and the restoration of the synovial fluid's physical characteristics (viscoelasticity). Viscosity can help to facilitate the cushioning and lubricating characteristics of the joint during slow movements, while elasticity blunts deforming forces (compression and resistance to shear forces) during rapid motions.

A study Waddell and colleagues hypothesized that hyaluronan inhibits interleukin-1beta–induced metalloproteinase production from osteoarthritic synovial tissue.²⁰

As reviewed by Goldberg and Buckwalter, preclinical support is available for most of the HAs, as well as clinical evidence (particularly for Hyalgan) using arthroscopy, microscopy, and blinded morphologic assessments and weight-bearing radiographs for assessing joint space narrowing.²¹ Intra-articular HAs may also possibly be chondroprotective early in the development of OA. However, additional studies would seem to be warranted to further explore the ability of HAs to intervene in the disease processes associated with OA. Certainly, a single product with symptomatic and disease-modifying characteristics, even if only in some patient populations, would be a valuable option in the management of knee OA.

A pulsed electromagnetic field stimulation device (Bionicare) has also been FDA-approved for use in patients with knee OA. Pulsed electromagnetic field stimulation is believed to act at the level of hyaline cartilage by maintaining proteoglycan composition of chondrocytes via down-regulation of its turnover.²² One published multicenter, double-blind, randomized, placebo controlled, 4-week trial (n = 78 knee OA) found improved pain and function in patients who were treated with the device.²³

Transcutaneous electrical nerve stimulation (TENS) may be another treatment option for pain relief, but so far, there is limited evidence suggesting that this method would be beneficial for some patients.²⁴

Acupuncture is becoming a more frequently utilized option in treating pain and physical dysfunction associated with osteoarthritis. There is some support in the literature for its use. For example, a review article of randomized, controlled trials found a significant decrease in pain after acupuncture in comparison with the amount of pain persisting after control treatments.²⁵

Related Medscape topics:
CME/CE Use of Corticosteroid Injections for Musculoskeletal Disease Reviewed
CME Viscosupplementation for Osteoarthritis of the Knee: Strategies to Improve Patient Outcomes

MEDICATION

Section 7 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The American College of Rheumatology issued the following pharmacologic guidelines for the treatment of osteoarthritis of the hip and knee:

• Arthrocentesis with corticosteroid injection can be used only for knee OA if effusion is present.
• Up to 4 grams per day of acetaminophen can be administered. This is the preferred initial treatment for patients with OA.
• Topical anti-inflammatory medications or capsaicin can be administered only for knee OA.
• Low-dose nonsteroidal anti-inflammatory drugs (NSAIDs) (ie, analgesic doses) or nonacetylated salicylates may be indicated.
• Administer full-dose NSAIDs with misoprostol if risk factors for upper gastrointestinal bleeding are present.
• Narcotic analgesic use may be indicated in cases of severe pain.

Other medications have been investigated in OA (eg, Tramadol, cyclooxygenase (COX)-2 inhibitors, dietary supplements). Many medications have been tried and are in use, but research on their effectiveness is lacking. Glucosamine and chondroitin sulfate, currently being studied by National Institutes of Health (NIH) in double-blind trials, have been used in Europe for many years. S-adenosylmethionine (SAM-e [pronounced "sammy"]) is a European supplement receiving a lot of attention in the United States. Chondroprotective drugs (ie, matrix metalloproteinase [MMP] inhibitors, growth factors) are being tested as disease-modifying drugs in the management of OA. Although a number of agents are currently under study, no agent has been shown to have a disease-modifying effect in humans.²⁶

Related Medscape topic:
CME/CE Chondroitin and Glucosamine: Hype or Hope for Osteoarthritis?

Drug Category: Simple analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have osteoarthritis.

Drug Category: Topical analgesics

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

Drug Category: Nonsteroidal anti-inflammatory drugs

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit COX activity and prostaglandin synthesis. Other mechanisms may exist as well, such as the inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Drug Category: Cyclooxygenase-2 inhibitors

This class of medications can be particularly useful in the OA population, because patients in this group tend to be older and are therefore at increased risk for adverse GI effects due to NSAIDs. Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs.

Drug Category: Opioid analgesics

These agents are used in patients whose pain has not been controlled with weaker analgesic medications. They are a particularly reasonable choice in patients who do not want joint replacement surgery, are too medically ill for joint replacement, are not candidates for joint replacement for other reasons, or are trying to buy time for subsequent joint replacement surgery.

FOLLOW-UP

Section 8 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Further Inpatient Care

• Further inpatient care pertains to patients who have undergone a surgical procedure, such as joint replacement. Surgery generally takes place in the acute care setting. After surgery, transfer is arranged to a subacute unit or freestanding rehabilitation hospital, or the patient is discharged directly to home.

Further Outpatient Care

• Provide outpatient care in support of a patient with osteoarthritis who has undergone a surgical procedure. Provide outpatient physical therapy as well.

In/Out Patient Meds

• Analgesics may be prescribed for a patient with osteoarthritis who has undergone surgery. Prescribe anticoagulants/antiplatelet agents as indicated.

Deterrence

• The prevention of osteoarthritis (OA) is a controversial topic; however, it is believed that maintaining ideal body weight lessens the probability of developing OA. This appears to be particularly true for weight-bearing joints (ie, hips, knees) in females.
• Some also believe that an adequate intake of vitamins C and D can help to lessen the probability of developing OA.
• A small study from England suggested that a course of NSAIDs taken after a traumatic event seems to reduce the incidence of posttraumatic OA.

Related Medscape topic:
CME Vigorous Physical Activity May Improve Knee Joint Structures

Prognosis

• The prognosis is good for patients with osteoarthritis who have undergone joint replacement. The prosthesis may need revision 10-15 years after its installation, depending on the patient's activity level.

Patient Education

• Patient education is one of the primary therapeutic approaches to osteoarthritis (OA).²⁷ Several Arthritis Foundation studies have demonstrated that education in OA benefits the patient. Through education, patients can institute ways to reduce pain and increase joint function. Emphasize the need for physician follow-up visits.
• For excellent patient education resources, visit eMedicine's Arthritis Center. Also, see eMedicine's patient education article Osteoarthritis.

MISCELLANEOUS

Section 9 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical/Legal Pitfalls

• One potential source of medicolegal action against the physiatrist is the misdiagnosis of an underlying medical problem that causes joint pain as OA. The administration of NSAIDs can lead to GI bleeding, especially if risk factors for GI bleeding are present. Allergic reactions to medications are also possible. The prescription of open-chain kinetic exercises, particularly with respect to quadriceps strengthening, carries the potential for worsened pain and, thus, the potential for medicolegal action on the part of the patient against the physiatrist.

ACKNOWLEDGMENTS

Section 10 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Evish Kamrava, 4th year medical student, St. George's University School of Medicine, Class of 2009, assisted with the revision of this manuscript.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Media file 1:  This radiograph demonstrates osteoarthritis of the right hip, including the finding of sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip is a bilateral finding, but it may occur unilaterally in an individual who has a previous history of hip trauma that was confined to that one side.
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Media file 2:  This radiograph shows a knee without significant osteoarthritis (for comparison with radiographs demonstrating osteoarthritis).
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Media file 3:  This radiograph (lateral view) demonstrates a knee without significant osteoarthritis (for comparison with osteoarthritis radiographs).
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Media file 4:  This radiograph demonstrates osteoarthritis of bilateral knees. Radiographic findings of osteoarthritis are often graded using the Kellgren-Lawrence Grading System. These knees would be classified as Kellgren grade III.
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Media file 5:  Osteoarthritis of the knee, Kellgren stage III.
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Media file 6:  Osteoarthritis of the knee, Kellgren stage III.
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Media file 7:  Osteoarthritis of the bilateral knees, Kellgren stage II.
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Media file 8:  Osteoarthritis of the right knee, Kellgren stage II.
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Media file 9:  Osteoarthritis of the left knee, Kellgren stage II.
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Media file 10:  This radiograph demonstrates osteoarthritis of the cervical spine. Note the bridging osteophytes between the spinous processes, as well as the significant degree of degenerative disk disease.
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Media file 11:  This radiograph demonstrates osteoarthritis of the cervical spine. Note the bridging osteophytes seen between the spinous processes.
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Media file 12:  Osteoarthritis of the cervical spine, anteroposterior view.
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Media file 13:  Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history of previous trauma.
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Media file 14:  Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history of previous trauma.
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Media file 15:  Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history of previous trauma.
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REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

1. Poole AR. An introduction to the pathophysiology of osteoarthritis. Front Biosci. Oct 15 1999;4:D662-70. [Medline].
2. D'Ambrosia RD. Epidemiology of osteoarthritis. Orthopedics. Feb 2005;28(2 Suppl):s201-5. [Medline].
3. Felson DT. Epidemiology of hip and knee osteoarthritis. Epidemiol Rev. 1988;10:1-28. [Medline].
4. Felson DT, Anderson JJ, Naimark A. Obesity and knee osteoarthritis. The Framingham Study. Ann Intern Med. Jul 1 1988;109(1):18-24. [Medline].
5. Felson DT. Risk factors for osteoarthritis: understanding joint vulnerability. Clin Orthop Relat Res. Oct 2004;S16-21. [Medline].
6. Brandt KD. A pessimistic view of serologic markers for diagnosis and management of osteoarthritis. Biochemical, immunologic and clinicopathologic barriers. J Rheumatol Suppl. Aug 1989;18:39-42. [Medline].
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