Osteoarthritis

Carlos J Lozada, MD, Director of Rheumatology Fellowship Program, Professor, Department of Medicine, Division of
Rheumatology and Immunology, University of Miami Miller School of Medicine
Eli Steigelfest, MD, Consulting Staff, Department of Rheumatology, The Consultant Group, PC
Updated: May 5, 2010

Introduction

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 of osteoarthritis include
clinician visits, 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 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 osteoarthritis and for improved therapeutic
alternatives will continue to grow.

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

Osteoarthritis has always been classified as a noninflammatory arthritis; however, increasing evidence has
shown that inflammation occurs as cytokines and metalloproteinases are released into the joint. Therefore, the
term degenerative joint disease is no longer appropriate when referring to osteoarthritis.

Osteoarthritis predominantly involves the weight-bearing joints, including 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 also occurs, with development of bony osteophytes.

Frequency
United States

Osteoarthritis affects over 20 million individuals in the United States. Based on the radiologic definition of
osteoarthritis, more than half of adults older than 65 years are affected.

International

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

Mortality/Morbidity

 The disease progression of osteoarthritis is characteristically slow, occurring over several years or
decades.
 Pain is usually the initial and principal source of morbidity in osteoarthritis. The patient can become
progressively less active, leading to morbidities related to decreasing physical activity (including
potential weight gain).
Race
The prevalence of osteoarthritis differs among different ethnic groups. Knee osteoarthritis appears to be more
common in African American women than in other groups.

Sex

 The likelihood of developing osteoarthritis increases with age. The disease is equally common among
men and women aged 45-55 years. After age 55 years, the disease becomes more common in
women.
 DIP and PIP joint involvement that results in Heberden and Bouchard nodes is more common in
women.

Age

 Osteoarthritis can be defined epidemiologically (ie, using radiographic criteria) or clinically (eg,
radiography findings plus clinical symptoms). Based on radiographic criteria, osteoarthritis 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

History

 Pain
o Pain is the main reason persons with osteoarthritis (OA) seek medical attention.
o Initially, symptomatic patients incur pain during activity, which can be relieved by rest and may
respond to simple analgesics.
o Morning joint stiffness usually lasts for less than 30 minutes.
o Stiffness during rest (gelling) may develop.
o 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

 Physical examination findings are mostly limited to the affected joints.

o Malalignment with a bony enlargement (depending on the disease severity) may occur.
o Most cases of osteoarthritis do not involve erythema or warmth over the affected joint(s);
however, an effusion may be present.
o Limitation of joint motion or muscle atrophy around a more severely affected joint may occur.
 Sources of pain in osteoarthritis include the following:
o Joint effusion and stretching of the joint capsule
o Increased vascular pressure in subchondral bone
o Torn menisci
o Inflammation of periarticular bursae
o Periarticular muscle spasm
o Psychological factors
o Crepitus (a rough or crunchy sensation) may be palpated during motion of an involved joint.
Causes

 Risk factors of osteoarthritis include the following:

o Increasing age
o Obesity
o Female sex
o Trauma
o Infection
o Repetitive occupational trauma
o Genetic factors
o History of inflammatory arthritis
o Neuromuscular disorder
o Metabolic disorder
 The etiopathogenesis of osteoarthritis has been divided into the following 3 stages:
o 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.
o 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.
o 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) may also 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.

Differential Diagnoses

Rhinosporidiosis

Other Problems to Be Considered

Osteoarthritis (OA) can usually be diagnosed on clinical grounds. The history and physical examination findings
are sufficient. Radiographic findings confirm the initial impression (see Imaging Studies), and laboratory values
are typically within the reference range. The initial goal is to differentiate osteoarthritis from other arthritides (eg,
rheumatoid arthritis).

Rheumatoid arthritis predominately affects the wrists and the metacarpophalangeal (MCP) and PIP joints.
Rheumatoid arthritis rarely, if ever, involves the DIP joints or lumbosacral spine. Rheumatoid arthritis is
associated with prominent prolonged (>1 h) morning stiffness. Radiographic findings of rheumatoid arthritis
include bone erosion (eg, periarticular osteopenia, marginal erosions of bone) rather than formation. Laboratory
findings that further differentiate rheumatoid arthritis include systemic inflammation, positive rheumatoid factor
results, joint fluid with polymorphonuclear cell predominance, and a substantially elevated WBC count.
Clinical history and characteristic radiographic findings can be used to differentiate spondyloarthropathy from
sacroiliac and lumbosacral spine involvement.

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

Reactive arthritis is another problem that may be considered.

Workup

Laboratory Studies

 No specific laboratory abnormalities are associated with osteoarthritis (OA).

o Levels of acute-phase reactants and erythrocyte sedimentation rate are within the reference
range.
o Synovial fluid analysis usually indicates a WBC count below 2000/µL with a mononuclear
predominance.

Imaging Studies

 Radiography
o Conduct imaging studies of the affected joint.
o The presence of osteophytes (ie, spurs at the joint margins) is the most characteristic findings.
o Other findings in osteoarthritis include asymmetric joint-space narrowing, subchondral
sclerosis, and subchondral cyst formation.
o 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, and/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

Medical Care
Nonpharmacologic interventions are the cornerstones of osteoarthritis (OA) therapy and include patient
education, temperature modalities, weight loss,[1 ]exercise, physical therapy, occupational therapy, and joint
unloading in certain joints (eg, knee, hip).

 Reduction of joint stress

o Instruct the patient to avoid aggravating stress to the affected joint.
o Implement correction procedures if the patient illustrates poor posture.
o Encourage obese patients to lose weight, thus relieving stress on the affected knees or hips.
o Occupational adjustments may be necessary.
  Physical therapy
o Osteoarthritis of the knee may result in disuse atrophy of the quadriceps. These muscles help
protect the articular cartilage from further stress.
o Instruct the patient to perform aerobic and muscle-strengthening exercises.
o Chaipinyo and Karoonsupcharoen (2009) found no significant difference between home-
based strength training and home-based balance training for knee pain caused by
osteoarthritis. However, more improvement was noted in the strength group in terms of knee-
related quality of life (improved 17 points out of 100 [95% CI, 5-28] more than the balance
group).[2 ]
o Hydrotherapy may be beneficial.
o Some patients with osteoarthritis benefit from heat and capsaicin cream placed locally over
the affected joint, and a minority of patients report relief with ice. [3 ]
 Pharmacologic therapy
o The goals of osteoarthritis treatment include pain alleviation and improvement of functional
status. Presently, no practical medication-based disease or structure-modifying intervention
has been proven.
o Begin treatment with acetaminophen for mild or moderate pain without apparent inflammation.
o If the clinical response to acetaminophen is not satisfactory or if the clinical presentation is
inflammatory, consider nonsteroidal anti-inflammatory drug (NSAIDs). Use the lowest effective
dose or intermittent dosing if symptoms are intermittent and then try full doses if the patient's
response is insufficient.
o 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.
o In patients with highly resistant pain, consider the analgesic tramadol.
o Muscle relaxants may benefit patients with evidence of muscle spasm.
o Contemplate intra-articular injections of glucocorticoids to improve symptoms. No more than 4
glucocorticoid injections should be administered to a single joint per year because of the risk
of long-term damage to cartilage. Systemic glucocorticoids have no role in the management of
osteoarthritis. Intra-articular injections of hyaluronic acid (HA) are approved as symptomatic
therapy of osteoarthritis in the knee. Prescribe as a series of 3 or 5 injections (depending on
the product). Each injection is administered one week apart.
o Judicious use of narcotics (eg, acetaminophen with codeine) is reserved for patients with
severe osteoarthritis.

Surgical Care

 Joint lavage: Closed-needle joint lavage may benefit a small subgroup of patients with osteoarthritis.
However, a 2010 meta-analysis of randomized controlled trials of joint lavage for knee osteoarthritis
suggests that, at 3 months, joint lavage alone does not significantly relieve pain or improve function. In
addition, the combination of joint lavage and intra-articular steroids injection is no more effective than
lavage alone. In their review of 6 trials including 855 patients, Avouac et al found that the pooled effect
size (ES) of joint lavage versus placebo was not significant for pain intensity (ES = 0.17 [-0.37, 0.71])
or physical function (ES = -0.15 [-0.34, 0.04]). Likewise, the pooled ES of joint lavage combined with
steroid injection versus joint lavage alone was not significant for pain intensity (ES = -0.82 [-2.47,
0.82]) or physical function (ES = 0.09 [-0.28, 0.45]). [4 ]
  Arthroscopy: Arthroscopy may help patients with osteoarthritis of the knee that in whom imaging
reveals specific structural damage (eg, for repairing meniscal tears, removing fragments of torn
menisci that are producing symptoms). Overall, arthroscopy is not recommended for nonspecific
"cleaning of the knee" in osteoarthritis.
 Osteotomy
o Consider this procedure in patients with a malaligned hip or knee joint.
o The procedure is usually recommended in younger patients with osteoarthritis.
o Osteotomy can lessen the pain, although it can lead to more challenging surgery later if the
patient requires arthroplasty.
 Arthroplasty
o 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.
o This procedure alleviates pain and may improve function. Approximately 8-15 years of viability
are expected from the joint replacement in the absence of complications.

Consultations

 A physiatrist may help in formulating a nonpharmacologic management plan.

 A referral to an orthopedic surgeon may be necessary if the osteoarthritis fails to respond to a medical
management plan.
 A nutritionist may help the patient lose weight.

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

Activity
Osteoarthritis 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

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

Analgesic agents
Pain control is essential in the management of osteoarthritis (OA). The goals of treatment include pain
alleviation and improvement of functional status. Currently, disease/structure-modifying intervention has been
proven

Acetaminophen (Tylenol, Panadol, Aspirin-Free Anacin)

Initial trial warranted in patients with mild-to-moderate symptoms from osteoarthritis who fail to get sufficient
relief with nonpharmacologic measures. DOC for patients with documented hypersensitivity to aspirin or
NSAIDs, history of upper GI disease, or on anticoagulants.
Dosing

Adult

1000 mg PO tid/qid; not to exceed 4 g/d

Pediatric

Disease state not seen in pediatrics

Interactions

Rifampin may reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and
isoniazid may increase hepatotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity can occur with various dose levels in persons with chronic alcoholism; severe or recurrent pain
or high or continued fever may indicate a serious illness; contained in many OTC products, and combined use
with these products may result in cumulative doses exceeding recommended maximum dose/d

Nonsteroidal anti-inflammatory drugs (NSAIDs)

These agents have analgesic, anti-inflammatory, and antipyretic activities. They are used for to relieve
osteoarthritis pain when the clinical response is unsatisfactory to acetaminophen. The mechanism of action is
nonselective inhibition of cyclooxygenases 1 and 2, resulting in reduced synthesis of prostaglandins and
thromboxanes. Other mechanisms may also exist, such as inhibition of 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, these agents may
be used as first-line pharmacologic therapy.

Use the 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.

Ibuprofen (Ibuprin, Advil, Motrin)

Relieves pain and inflammation. Widely available. Relatively inexpensive as a generic drug.

Dosing

Adult
400 mg PO tid prn; not to exceed 2400 mg/d

Pediatric

Disease state not seen in pediatrics

Interactions

May decrease effects of loop diuretics; coadministration of anticoagulants may increase PT (monitor and watch
for signs of bleeding); may increase serum lithium levels and risk of methotrexate toxicity; probenecid may
increase toxicity of NSAIDs

Contraindications

Documented hypersensitivity to ibuprofen, other NSAIDs, or aspirin; avoid in peptic ulcer disease, recent GI
bleeding or perforation, renal insufficiency, and high risk of bleeding

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, decreased renal and hepatic function, anticoagulation
abnormalities, or during anticoagulant therapy; adjust dose in renal insufficiency
Black Box Warning
NSAIDs may increase risk of serious cardiovascular thrombotic events, MI, and stroke, which can be fatal;
NSAIDs also increase risk of serious adverse GI effects, including stomach or intestinal bleeding, ulceration,
and perforation, which can be fatal; elderly patients are at greater risk for serious GI events

Meloxicam (Mobic)

To some extent, more selective for COX-2 receptors, compared to traditional NSAIDs. Decreases activity of
cyclooxygenase, which in turn inhibits prostaglandin synthesis. These effects decrease formation of
inflammatory mediators.

Dosing

Adult

7.5 mg PO qd prn; may increase to 15 mg PO qd prn

Pediatric

Not established

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may
increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking
anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity;
phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; active GI bleeding

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits
outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may
occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal
perfusion; reversible leukopenia may occur, (discontinue if there is persistent leukopenia, granulocytopenia, or
thrombocytopenia)
Black Box Warning
NSAIDs may increase risk of serious cardiovascular thrombotic events, MI, and stroke, which can be fatal;
NSAIDs also increase risk of serious adverse GI effects, including stomach or intestinal bleeding, ulceration,
and perforation, which can be fatal; elderly patients are at greater risk for serious GI events

Esomeprazole and naproxen (Vimovo)

Naproxen component is indicated for relief of signs and symptoms of osteoarthritis, rheumatoid arthritis, and
ankylosing spondylitis. Naproxen is an NSAID that inhibits inflammatory reactions and pain by decreasing
activity of cyclo-oxygenase, which is responsible for prostaglandin synthesis.
Esomeprazole component is indicated to decrease risk of gastric ulcers in patients at risk of developing NSAID-
associated gastric ulcers. Esomeprazole is the S-isomer of omeprazole, a proton pump inhibitor. Inhibits gastric
acid secretion by inhibiting H+/K+-ATPase enzyme system at secretory surface of gastric parietal cells.

Dosing

Adult

1 tab PO bid at least 30 min ac

Delayed-release tab; swallow whole and do not chew, crush, dissolve, or split
Available in 2 dosage strengths: Esomeprazole 20 mg and naproxen 375 mg per tab or esomeprazole 20 mg
and naproxen 500 mg per tab

Pediatric

<18 years: Not established

Interactions
Concomitant use of NSAIDs may reduce antihypertensive effect of ACE inhibitors, diuretics, and beta-blockers;
NSAIDs increase lithium plasma levels; concomitant use with methotrexate may increase methotrexate toxicity;
concomitant use with warfarin may result in increased risk of bleeding complications (monitor INR and
prothrombin time); esomeprazole inhibits gastric acid secretion and may interfere with absorption of drugs for
which gastric pH is an important determinant of bioavailability (eg, ketoconazole, iron salts, digoxin, atazanavir,
nelfinavir); esomeprazole inhibits CYP2C19 and therefore may alter serum levels/activity of CYP2C19
substrates; esomeprazole is extensively metabolized by CYP2C19 and CYP3A4

Contraindications

Documented hypersensitivity; NSAIDs are contraindicated for perioperative pain in the setting of coronary
artery bypass graft surgery (increased risk of MI and stroke); NSAIDs are contraindicated during late pregnancy
(risk of premature closure of ductus arteriosus)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits
outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Black Box Warning

NSAIDs may increase risk of serious cardiovascular thrombotic events, MI, and stroke, which can be fatal;
NSAIDs also increase risk of serious adverse GI effects, including stomach or intestinal bleeding, ulceration,
and perforation, which can be fatal; elderly patients are at greater risk for serious GI events
Precautions
May cause anaphylactoid reaction; not recommended with severe hepatic impairment or moderate-to-severe
renal impairment; common adverse effects (>5%) include erosive gastritis, dyspepsia, gastritis, diarrhea,
gastric ulcer, upper abdominal pain, and nausea

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.

Celecoxib (Celebrex)

COX-2–specific inhibitor. At therapeutic concentrations, COX-2 (inducible by cytokines at sites of inflammation

such as the joints) is inhibited and COX-1 isoenzyme (present in platelets and GI tract) is spared; therefore, in
nonaspirin users, incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and
obstructions, is decreased when compared to nonselective NSAIDs. COX-2 is expressed in the kidney;
however, the renal safety profile is not significantly superior to that of NSAIDs.

Dosing

Adult
100 mg PO bid or 200 mg PO qd

Pediatric

Disease state not seen in pediatrics

Interactions

Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition
of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma
concentrations

Contraindications

Documented hypersensitivity to celecoxib, sulfonamides, NSAIDs or aspirin

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits
outweigh risk to fetus

Precautions

Avoid in late pregnancy to avoid closure of ductus arteriosus; may cause fluid retention and peripheral edema;
caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention, presence of
existing controlled infections, severe heart failure and hyponatremia because may deteriorate circulatory
hemodynamics; NSAIDs may mask usual signs of infection; evaluate symptoms suggesting liver dysfunction or
in abnormal liver lab results; adjust dose in renal insufficiency
NSAID labeling carries a warning about increased risk of hypertension, stroke, and cardiovascular events,
including myocardial infarction

Follow-up

Deterrence/Prevention

 Overweight patients who have early signs of osteoarthritis (OA) or who are at high risk should be
encouraged to lose weight.
 Recommend quadriceps-strengthening exercises in patients with osteoarthritis of the knees, except in
those with pronounced valgus or varus deformity at the knees.

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

Patient Education

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

Miscellaneous

Medicolegal Pitfalls

 The risk of medications used to treat osteoarthritis (OA) 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.

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Keywords
osteoarthritis, osteoarthrosis, OA, knee osteoarthritis, hip osteoarthritis, spinal osteoarthritis, foot osteoarthritis,
secondary osteoarthritis, secondary OA, knee OA, hip OA, spinal OA, foot OA, osteophytes, joint pain, back
pain, noninflammatory arthritis, degenerative joint disease, articular disease, articular cartilage disease, bony
osteophytes

Contributor Information and Disclosures

Author

Carlos J Lozada, MD, Director of Rheumatology Fellowship Program, Professor, Department of Medicine,
Division of Rheumatology and Immunology, University of Miami Miller School of Medicine
Carlos J Lozada, MD is a member of the following medical societies: American College of Physicians and
American College of Rheumatology
Disclosure: Pfizer Honoraria Speaking and teaching

Coauthor(s)

Eli Steigelfest, MD, Consulting Staff, Department of Rheumatology, The Consultant Group, PC
Disclosure: Nothing to disclose.

Medical Editor

John Varga, MD, Professor, Department of Internal Medicine, Division of Rheumatology, Northwestern
University
John Varga, MD is a member of the following medical societies: American College of Physicians, American
College of Rheumatology, Central Society for Clinical Research, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Managing Editor

Elliot Goldberg, MD, Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine,
Temple University School of Medicine
Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of
Physicians, and American College of Rheumatology
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of
Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American
College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD, Professor of Medicine, Temple University School of Medicine; Chairman Emeritus,
Department of Internal Medicine, Western Pennsylvania Hospital
Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College
of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa
Disclosure: ACP PEER Honoraria Independent contractor; Stock ownership in multiple Pharmaceutical
companies Ownership interest Other

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