AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

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

INTRODUCTION

Section 2 of 10  

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

Background

Osteoarthritis (OA) is the most common articular disease worldwide, affecting over 20 million individuals in the United States alone. Its high prevalence entails significant costs to society. Direct costs include physician visits, medications, and surgical intervention. Indirect costs include such items as time lost from work. Costs can be particularly significant for the elderly, who face potential loss of independence and who may need help with daily living activities. As the populations of developed nations age over the next few decades, the need for better understanding of OA and for improved therapeutic alternatives will continue to grow.

Pathophysiology

Traditionally, OA has been considered a disease of articular cartilage. The current concept holds that OA involves the entire joint organ, including the subchondral bone and synovium.

OA has always been classified as a noninflammatory arthritis; yet, there is increasing evidence for inflammation occurring with cytokine and metalloproteinase release into the joint. Therefore, the term degenerative joint disease is no longer appropriate when referring to OA.

The joints predominantly involved are weight bearing and include the knees, hips, cervical and lumbosacral spine, and feet. Other commonly affected joints include the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints of the hands.

Cartilage is grossly affected. Focal ulcerations eventually lead to cartilage loss and eburnation. Subchondral bone formation occurs as well, with development of bony osteophytes.

Frequency

United States

OA affects over 20 million individuals. Radiologic definition indicates that more than half of the population older than 65 years is affected.

International

OA is the most common articular disease. Estimates vary among different populations.

Mortality/Morbidity

• Disease progression characteristically is slow, occurring over several years or decades.
• Pain is usually the initial and principal source of morbidity in OA. The patient can become progressively more inactive leading to morbidities related to decreasing physical activity including potential weight gain.

Race

Different prevalences have been cited for different ethnic groups. African American women appear to have a greater prevalence of knee OA than other groups.

Sex

• Prevalence increases with age. Equivalent prevalence occurs in men and women aged 45-55 years. After age 55, prevalence becomes greater in women.
• DIP and PIP joint involvement resulting in Heberden's and Bouchard's nodes is more common in women.

Age

• OA can be defined epidemiologically (ie, using radiographic criteria) or clinically (eg, radiographs plus clinical symptoms). Radiographic criteria indicate that OA occurs in 30% of affected individuals aged 45-65 years and in more than 80% by their eighth decade of life, although most are asymptomatic.

CLINICAL

Section 3 of 10  

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

History

• Pain
• • This is the main reason patients seek medical attention.
  • Initially, symptomatic patients incur pain during activity, which can be relieved by rest and may respond to simple analgesics.
  • Morning stiffness in the joint usually lasts for less than half an hour.
  • Stiffness at times of rest (gelling) may develop.
  • Joints may become unstable with disease progression; therefore, the pain can become more prominent (even at times of rest) and may not respond to medications.

Physical

• Physical examination findings are mostly limited to the affected joints.
• • Malalignment with a bony enlargement (depending on the disease severity) may occur.
  • In most cases, erythema or warmth over the joint does not occur; however, an effusion may be present.
  • Limitation of joint motion or muscle atrophy around a more severely affected joint may occur.

• Sources of pain in OA
• • Joint effusion and stretching of the joint capsule

  • Increased vascular pressure in subchondral bone

  • Torn menisci

  • Inflammation of periarticular bursae

  • Periarticular muscle spasm

  • Psychological factors
  • Crepitus (a rough or crunchy sensation) may be palpated during motion of an involved joint.

Causes

• Risk factors
• • Age
  • Obesity
  • Female sex
  • Trauma
  • Infection
  • Repetitive occupational trauma

  • Genetic factors

  • History of inflammatory arthritis

  • Neuromuscular disorder

  • Metabolic disorder

• The etiopathogenesis of OA has been divided into the following 3 stages:
• • Stage 1: Proteolytic breakdown of the cartilage matrix occurs. Chondrocyte metabolism is affected, leading to an increased production of enzymes, which includes metalloproteinases (eg, collagenase, stromelysin) that destroy the cartilage matrix. Chondrocytes also produce protease inhibitors, including tissue inhibitors of metalloproteinases (TIMP) 1 and 2 but in amounts insufficient to counteract the proteolytic effect.
  • Stage 2: This stage involves the fibrillation and erosion of the cartilage surface, with a subsequent release of proteoglycan and collagen fragments into the synovial fluid.
  • Stage 3: The breakdown products of cartilage induce a chronic inflammatory response in the synovium. Synovial macrophage production of cytokines, such as interleukin 1 (IL-1), tumor necrosis factor-alpha, and metalloproteinases, occurs. These can diffuse back into the cartilage and directly destroy tissue or stimulate chondrocytes to produce more metalloproteinases. Other pro-inflammatory molecules (eg, nitric oxide [NO], an inorganic free radical) also may be a factor. Eventually, these events alter the joint architecture, and compensatory bone overgrowth occurs in an attempt to stabilize the joint. As the joint architecture is changed and further mechanical and inflammatory stress occurs on the articular surfaces, the disease progresses unchecked.

DIFFERENTIALS

Section 4 of 10  

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

Other Problems to be Considered

Diagnosis usually can be made on clinical grounds. The history and physical examination findings are sufficient. Radiographic findings confirm the initial impression, and laboratory values typically are within the normal range. The initial goal is to differentiate OA from other arthritides (eg, rheumatoid arthritis [RA]).

RA predominately affects the wrists and the metacarpophalangeal (MCP) and PIP joints. Rarely, if ever, does RA involve the DIP joints or lumbosacral spine. RA is associated with prominent morning stiffness lasting longer than 1 hour, and radiographic findings are bone erosion (eg, periarticular osteopenia, marginal erosions of bone) rather than formation. Laboratory findings that further differentiate RA include systemic inflammation, a positive rheumatoid factor, joint fluid with polymorphonuclear cell predominance, and a substantially elevated WBC count.

Clinical history and characteristic radiographic findings can differentiate spondyloarthropathy from sacroiliac and lumbosacral spine involvement.

Secondary OA must be considered in individuals with chondrocalcinosis, joint trauma, metabolic bone disorders, hypermobility syndromes, and neuropathic diseases.

Reiter syndrome is another problem that may be considered.

WORKUP

Section 5 of 10  

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

Lab Studies

• No specific laboratory abnormalities are associated with OA.
• • The acute-phase reactants and erythrocyte sedimentation rate are not elevated.
  • Synovial fluid analysis usually indicates a white cell count less than 2000 per mm³ with a mononuclear predominance.

Imaging Studies

• Radiography
• • Conduct imaging studies of the affected joint.
  • The presence of osteophytes (ie, spurs at the joint margins) is the most characteristic findings.
  • Other findings include asymmetric joint space narrowing, subchondral sclerosis, and subchondral cyst formation.
  • Roentgenographic findings are often poor predictors of the degree of symptomatology in a particular patient.

Procedures

• Arthrocentesis of the affected joint can help exclude inflammatory arthritis, infection, or crystal arthropathy.

Histologic Findings

Histologically, the earliest changes occur in the cartilage. Proteoglycan staining is diminished, and, eventually, irregularity of the articular surface with clefts and erosions occurs.

TREATMENT

Section 6 of 10  

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

Medical Care

• Nonpharmacologic interventions are the cornerstones of OA therapy and include patient education, temperature modalities, weight loss, exercise, physical therapy, occupational therapy, and joint unloading in certain joints (eg, knee, hip).
• Reduction of joint stress
• • Instruct the patient to avoid aggravating stress to the affected joint.

  • Implement correction procedures if the patient illustrates poor posture.

  • Encourage obese patients to lose weight, thus taking stress off the affected knees or hips.

  • Occupational adjustments may be necessary.

• Physical therapy
  • In OA of the knee, disuse atrophy of the quadriceps may occur. These muscles help protect the articular cartilage from further stress.

  • Instruct the patient to perform aerobic and muscle-strengthening exercises.

  • Hydrotherapy may be beneficial.
    

  • Some patients find relief with heat and capsaicin cream placed locally over the affected joint, and a minority of patients proclaim relief with ice.
• Pharmacologic therapy
• • The goals of treatment are pain alleviation and improvement of functional status. Presently, no proven practical medication-based disease/structure-modifying intervention exists.

  • Begin treatment with acetaminophen for mild or moderate pain without apparent inflammation.

  • If clinical response to acetaminophen is not satisfactory or if clinical presentation is inflammatory, consider nonsteroidal anti-inflammatory drug (NSAIDs). Use the lowest effective dose or intermittent dosing if symptoms are present intermittently and then try full doses if the patient's response is insufficient.

  • Options in patients at an elevated risk for GI toxicity due to NSAIDs include the addition of a proton-pump inhibitor or misoprostol to the treatment regimen or the use of a selective cyclooxygenase inhibitor instead of the nonselective NSAID.
  • In patients with highly resistant pain, consider the analgesic tramadol.

  • Muscle relaxants may benefit patients with evidence of muscle spasm.

  • Contemplate intraarticular injections of glucocorticoids to improve symptoms. It is recommended that no more than 4 glucocorticoid injections be administered to a single joint per year because of the concerns with long-term damage to cartilage. Do not use systemic glucocorticoids; they have no role in the management of OA. Intraarticular injections of hyaluronic acid (HA) are approved as symptomatic therapy of OA in the knee. Prescribe as a series of 3 or 5 injections (depending on the product). Each injection is administered 1 week apart.

  • Consider judicious use of narcotics (eg, acetaminophen with codeine) only in patients with severe OA.

Surgical Care

• Closed-needle joint lavage may benefit a small subgroup of patients.
• Arthroscopy may help patients with OA of the knee that has specific structural damage on imaging (eg, repairing meniscal tears, removing fragments of torn menisci that are producing symptoms). Overall, arthroscopy is not recommended for nonspecific "cleaning of the knee" in OA.
• Osteotomy
• • Consider this procedure for those patients with a malaligned hip or knee joint.

  • The procedure usually is recommended in younger patients with OA.

  • This surgery can lessen pain, although it can lead to more challenging surgery later if the patients requires arthroplasty.

• Arthroplasty
• • Perform this procedure if all other modalities are ineffective and osteotomy is not viable or if a patient cannot perform his or her daily activities despite maximal therapy.

  • This procedure alleviates pain and may improve function. Approximately 8-15 years of viability are expected from the joint replacement if there are no complications.

Consultations

• A physiatrist may help in formulating a nonpharmacologic management plan.
• A referral to an orthopedic surgeon may be necessary if a patient fails to respond to a medical management plan.
• A nutritionist may help the patient achieve some weight loss.

Diet

A diet to achieve some degree of weight loss may be beneficial.

Activity

OA may severely hinder the patient's ability to work or even to perform daily living activities, depending on the joints involved and the degree of involvement.

MEDICATION

Section 7 of 10  

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

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Pay careful attention to a particular pharmacologic regimen's adverse event profile.

Drug Category: Analgesic agents

Pain control is essential in the care of the patient with OA. The goals of treatment are pain alleviation and improvement of functional status. No proven disease/structure-modifying intervention presently exists.

Drug Category: Nonsteroidal anti-inflammatory drugs (NSAIDs)

Have analgesic, anti-inflammatory, and antipyretic activities. Used for the relief of OA pain when clinical response is unsatisfactory to acetaminophen. Mechanism of action is nonselective inhibition of cyclooxygenases 1 and 2, resulting in reduced synthesis of prostaglandins and thromboxanes. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

In more inflammatory presentations of OA, such as knee involvement with effusion, these agents may be used as first-line pharmacologic therapy.

Use lowest effective dose or intermittent therapy if symptoms are intermittent.

Patients at high risk for GI toxicity may consider adding misoprostol or a proton pump inhibitor to the regimen or substituting a COX-2–specific inhibitor for the NSAID.

Drug Category: COX-2 inhibitors

Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is less in nonaspirin users receiving COX-2 inhibitors than with traditional NSAIDs.

FOLLOW-UP

Section 8 of 10  

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

Deterrence/Prevention:

• If an overweight patient has early signs of OA or is at high risk, weight loss should be encouraged.
• Patients with OA of the knees should be recommended quadriceps strengthening exercises, except in those with pronounced valgus or varus deformity at the knees.

Prognosis:

• Prognosis depends on joints involved and severity. No proven disease/structure-modifying drugs for OA currently exist, and thus, the medication-based regimen is directed at symptom relief.

Patient Education:

• Educate the patient on the natural history and management options for OA. Explain the differences between OA and other more rapidly progressive arthritides such as RA.
• For excellent patient education resources, visit eMedicine's Arthritis Center. Also, see eMedicine's patient education article Osteoarthritis.

MISCELLANEOUS

Section 9 of 10  

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

Medical/Legal Pitfalls

• The risk of medications used to treat this disease include, but are not limited to, GI toxicities and potential cardiac toxicities of NSAIDs and potential complications of arthrocentesis. Discuss these risks with the patient.

• Complete a procedure note in the patient's chart for each arthrocentesis.

REFERENCES

Section 10 of 10

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

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• Altman R, Alarcon G, Appelrouth D. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand. Arthritis Rheum. Nov 1990;33(11):1601-10. [Medline].
• Altman R, Alarcon G, Appelrouth D. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip. Arthritis Rheum. May 1991;34(5):505-14. [Medline].
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• Altman RD, Lozada CJ. Clinical features of osteoarthritis. In: Hochberg, Silman, Smolen, Weinblatt, and Weismann, eds. Practical Rheumatology. 2004:503-10.
• Bernstein J, Quach T. A perspective on the study of Moseley et al: questioning the value of arthroscopic knee surgery for osteoarthritis. Cleve Clin J Med. May 2003;70(5):401, 405-6, 408-10. [Medline].
• Bradley JD, Brandt KD, Katz BP. Comparison of an antiinflammatory dose of ibuprofen, an analgesic dose of ibuprofen, and acetaminophen in the treatment of patients with osteoarthritis of the knee. N Engl J Med. Jul 11 1991;325(2):87-91. [Medline].
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• Buckwalter JA, Lohmander S. Operative treatment of osteoarthrosis. Current practice and future development. J Bone Joint Surg Am. Sep 1994;76(9):1405-18. [Medline].
• Chang RW, Falconer J, Stulberg SD. A randomized, controlled trial of arthroscopic surgery versus closed- needle joint lavage for patients with osteoarthritis of the knee. Arthritis Rheum. Mar 1993;36(3):289-96. [Medline].
• Felson DT. Epidemiology of hip and knee osteoarthritis. Epidemiol Rev. 1988;10:1-28. [Medline].
• Felson DT, Zhang Y, Anthony JM. Weight loss reduces the risk for symptomatic knee osteoarthritis in women. The Framingham Study. Ann Intern Med. Apr 1 1992;116(7):535-9. [Medline].
• Hochberg MC, Altman RD, Brandt KD. Guidelines for the medical management of osteoarthritis. Part I. Osteoarthritis of the hip.American College of Rheumatology. Arthritis Rheum. Nov 1995;38(11):1535-40. [Medline].
• Hogenmiller MS, Lozada CJ. An update on osteoarthritis therapeutics. Curr Opin Rheumatol. May 2006;18(3):256-60. [Medline].
• Lozada CJ. Management of osteoarthritis. In: Harris, Budd, Firestein, et al, eds. Kelley's Textbook of Rheumatology. 7^th ed. 2005:1528-40.
• McCarthy GM, McCarty DJ. Effect of topical capsaicin in the therapy of painful osteoarthritis of the hands. J Rheumatol. Apr 1992;19(4):604-7. [Medline].
• Pelletier JP, Martel-Pelletier J, Howell DS. Etiopathogenesis of Osteoarthritis. In: Arthritis and Allied Conditions. 13^th ed. 1997:1969-84.
• Puett DW, Griffin MR. Published trials of nonmedicinal and noninvasive therapies for hip and knee osteoarthritis. Ann Intern Med. Jul 15 1994;121(2):133-40. [Medline].
• Roberts J, Burch TA. Osteoarthritis prevalence in adults by age, sex, race, and geographic area. Vital Health Stat 1. Jun 1966;11(15):1-27. [Medline].

Article Last Updated: May 16, 2006