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
y y
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).

The disease is equally common among men and women aged 45-55 years. the disease becomes more common in women. y . although most are asymptomatic. Clinical History y Pain o o o o o Pain is the main reason persons with osteoarthritis (OA) seek medical attention.Race The prevalence of osteoarthritis differs among different ethnic groups. using radiographic criteria) or clinically (eg. 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. Sex y The likelihood of developing osteoarthritis increases with age. Joints may become unstable as the osteoarthritis progresses. o Most cases of osteoarthritis do not involve erythema or warmth over the affected joint(s). o Limitation of joint motion or muscle atrophy around a more severely affected joint may occur. the pain may become more prominent (even during rest) and may not respond to medications. however. DIP and PIP joint involvement that results in Heberden and Bouchard nodes is more common in women. Morning joint stiffness usually lasts for less than 30 minutes. Knee osteoarthritis appears to be more common in African American women than in other groups. osteoarthritis occurs in 30% of affected individuals aged 45-65 years and in more than 80% by their eighth decade of life. symptomatic patients incur pain during activity. Stiffness during rest (gelling) may develop. Based on radiographic criteria. y Age y Osteoarthritis can be defined epidemiologically (ie. radiography findings plus clinical symptoms). therefore. which can be relieved by rest and may respond to simple analgesics. After age 55 years. Physical y Physical examination findings are mostly limited to the affected joints. an effusion may be present. Initially. o Malalignment with a bony enlargement (depending on the disease severity) may occur.

Radiographic findings of rheumatoid arthritis include bone erosion (eg. an inorganic free radical) may also be a factor. Laboratory findings that further differentiate rheumatoid arthritis include systemic inflammation. Chondrocytes also produce protease inhibitors. y Differential Diagnoses Rhinosporidiosis Other Problems to Be Considered Osteoarthritis (OA) can usually be diagnosed on clinical grounds. leading to an increased production of enzymes. Chondrocyte metabolism is affected. These can diffuse back into the cartilage and directly destroy tissue or stimulate chondrocytes to produce more metalloproteinases. these events alter the joint architecture. and metalloproteinases. marginal erosions of bone) rather than formation. Synovial macrophage production of cytokines. which includes metalloproteinases (eg. if ever. Rheumatoid arthritis rarely. Radiographic findings confirm the initial impression (see Imaging Studies). joint fluid with polymorphonuclear cell predominance. and laboratory values are typically within the reference range. o Stage 2: This stage involves the fibrillation and erosion of the cartilage surface. rheumatoid arthritis). positive rheumatoid factor results. Rheumatoid arthritis is associated with prominent prolonged (>1 h) morning stiffness. such as interleukin 1 (IL-1). periarticular osteopenia. The history and physical examination findings are sufficient. tumor necrosis factor-alpha. Eventually. and a substantially elevated WBC count. including tissue inhibitors of metalloproteinases (TIMP) 1 and 2 but in amounts insufficient to counteract the proteolytic effect. Rheumatoid arthritis predominately affects the wrists and the metacarpophalangeal (MCP) and PIP joints. involves the DIP joints or lumbosacral spine. occurs.Causes y 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. the disease progresses unchecked. with a subsequent release of proteoglycan and collagen fragments into the synovial fluid. As the joint architecture is changed and further mechanical and inflammatory stress occurs on the articular surfaces. collagenase. . Other pro-inflammatory molecules (eg. stromelysin) that destroy the cartilage matrix. and compensatory bone overgrowth occurs in an attempt to stabilize the joint. nitric oxide [NO]. o Stage 3: The breakdown products of cartilage induce a chronic inflammatory response in the synovium. The initial goal is to differentiate osteoarthritis from other arthritides (eg.

Proteoglycan staining is diminished. occupational therapy. subchondral sclerosis. infection. physical therapy. Procedures Arthrocentesis of the affected joint can help exclude inflammatory arthritis. and neuropathic diseases.Clinical history and characteristic radiographic findings can be used to differentiate spondyloarthropathy from sacroiliac and lumbosacral spine involvement. Reactive arthritis is another problem that may be considered. metabolic bone disorders. o Occupational adjustments may be necessary. and subchondral cyst formation. o Encourage obese patients to lose weight. temperature modalities. Workup Laboratory Studies y No specific laboratory abnormalities are associated with osteoarthritis (OA). thus relieving stress on the affected knees or hips. eventually. o Other findings in osteoarthritis include asymmetric joint-space narrowing. o The presence of osteophytes (ie. . Histologic Findings Histologically. Treatment Medical Care Nonpharmacologic interventions are the cornerstones of osteoarthritis (OA) therapy and include patient education. the earliest changes occur in the cartilage. and joint unloading in certain joints (eg. joint trauma. o Synovial fluid analysis usually indicates a WBC count below 2000/µL with a mononuclear predominance. hypermobility syndromes. y Reduction of joint stress o Instruct the patient to avoid aggravating stress to the affected joint. Imaging Studies y Radiography o Conduct imaging studies of the affected joint. o Roentgenographic findings are often poor predictors of the degree of symptomatology in a particular patient. weight loss. o Levels of acute-phase reactants and erythrocyte sedimentation rate are within the reference range. Secondary osteoarthritis must be considered in individuals with chondrocalcinosis. knee. irregularity of the articular surface with clefts and erosions occurs. spurs at the joint margins) is the most characteristic findings. and. o Implement correction procedures if the patient illustrates poor posture. and/or crystal arthropathy. hip).[1 ]exercise.

0.82 [-2. o Muscle relaxants may benefit patients with evidence of muscle spasm. Use the lowest effective dose or intermittent dosing if symptoms are intermittent and then try full doses if the patient's response is insufficient.[4 ] .45]). 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. no practical medication-based disease or structure-modifying intervention has been proven. These muscles help protect the articular cartilage from further stress. the pooled ES of joint lavage combined with steroid injection versus joint lavage alone was not significant for pain intensity (ES = -0.17 [-0. 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. In their review of 6 trials including 855 patients.15 [-0. Presently.[2 ] o Hydrotherapy may be beneficial. at 3 months. consider the analgesic tramadol.82]) or physical function (ES = 0.47.34.09 [-0. Surgical Care y Joint lavage: Closed-needle joint lavage may benefit a small subgroup of patients with osteoarthritis. Likewise. However. However. Avouac et al found that the pooled effect size (ES) of joint lavage versus placebo was not significant for pain intensity (ES = 0. o In patients with highly resistant pain.y y Physical therapy o Osteoarthritis of the knee may result in disuse atrophy of the quadriceps. o Begin treatment with acetaminophen for mild or moderate pain without apparent inflammation. consider nonsteroidal anti-inflammatory drug (NSAIDs). o Some patients with osteoarthritis benefit from heat and capsaicin cream placed locally over the affected joint. Each injection is administered one week apart. o Judicious use of narcotics (eg. the combination of joint lavage and intra-articular steroids injection is no more effective than lavage alone.37. and a minority of patients report relief with ice. acetaminophen with codeine) is reserved for patients with severe osteoarthritis. Prescribe as a series of 3 or 5 injections (depending on the product).04]). 5-28] more than the balance group). more improvement was noted in the strength group in terms of kneerelated quality of life (improved 17 points out of 100 [95% CI. a 2010 meta-analysis of randomized controlled trials of joint lavage for knee osteoarthritis suggests that. Intra-articular injections of hyaluronic acid (HA) are approved as symptomatic therapy of osteoarthritis in the knee.28. 0. o Chaipinyo and Karoonsupcharoen (2009) found no significant difference between homebased strength training and home-based balance training for knee pain caused by osteoarthritis.[3 ] Pharmacologic therapy o The goals of osteoarthritis treatment include pain alleviation and improvement of functional status. o Instruct the patient to perform aerobic and muscle-strengthening exercises. joint lavage alone does not significantly relieve pain or improve function. o Contemplate intra-articular injections of glucocorticoids to improve symptoms. In addition. 0.71]) or physical function (ES = -0. 0. Systemic glucocorticoids have no role in the management of osteoarthritis. o If the clinical response to acetaminophen is not satisfactory or if the clinical presentation is inflammatory.

arthroscopy is not recommended for nonspecific "cleaning of the knee" in osteoarthritis. o This procedure alleviates pain and may improve function. Osteotomy o Consider this procedure in patients with a malaligned hip or knee joint. A referral to an orthopedic surgeon may be necessary if the osteoarthritis fails to respond to a medical management plan. . Consultations y y y A physiatrist may help in formulating a nonpharmacologic management plan. Diet A diet to achieve some degree of weight loss may be beneficial. o The procedure is usually recommended in younger patients with osteoarthritis. Analgesic agents Pain control is essential in the management of osteoarthritis (OA). history of upper GI disease. removing fragments of torn menisci that are producing symptoms). disease/structure-modifying intervention has been proven Acetaminophen (Tylenol. 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. although it can lead to more challenging surgery later if the patient requires arthroplasty. Panadol. Pay careful attention to a particular pharmacologic regimen's adverse-event profile. Approximately 8-15 years of viability are expected from the joint replacement in the absence of complications. Aspirin-Free Anacin) Initial trial warranted in patients with mild-to-moderate symptoms from osteoarthritis who fail to get sufficient relief with nonpharmacologic measures. depending on the joints involved and the degree of involvement. Medication The goals of pharmacotherapy are to reduce morbidity and to prevent complications. The goals of treatment include pain alleviation and improvement of functional status. or on anticoagulants. A nutritionist may help the patient lose weight. Overall. Currently. for repairing meniscal tears. o Osteotomy can lessen the pain. DOC for patients with documented hypersensitivity to aspirin or NSAIDs.y y y Arthroscopy: Arthroscopy may help patients with osteoarthritis of the knee that in whom imaging reveals specific structural damage (eg. Activity Osteoarthritis may severely hinder the patient's ability to work or even to perform daily living activities.

these agents may be used as first-line pharmacologic therapy. They are used for to relieve osteoarthritis pain when the clinical response is unsatisfactory to acetaminophen. In more inflammatory presentations of osteoarthritis. coadministration with barbiturates. lipoxygenase activity. carbamazepine. and various cell-membrane functions. 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. Advil. Other mechanisms may also exist. lysosomal enzyme release. severe or recurrent pain or high or continued fever may indicate a serious illness.Widely available. anti-inflammatory. such as inhibition of leukotriene synthesis.Relatively inexpensive as a generic drug. resulting in reduced synthesis of prostaglandins and thromboxanes. 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. neutrophil aggregation. Use the lowest effective dose or intermittent therapy if symptoms are intermittent. and isoniazid may increase hepatotoxicity Contraindications Documented hypersensitivity Precautions Pregnancy B . such as knee involvement with effusion. Ibuprofen (Ibuprin. The mechanism of action is nonselective inhibition of cyclooxygenases 1 and 2.Dosing Adult 1000 mg PO tid/qid.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. Motrin) Relieves pain and inflammation. not to exceed 4 g/d Pediatric Disease state not seen in pediatrics Interactions Rifampin may reduce analgesic effects. hydantoins. contained in many OTC products. and antipyretic activities. Dosing Adult .

Fetal risk not confirmed in studies in humans but has been shown in some studies in animals D .5 mg PO qd prn. may increase serum lithium levels and risk of methotrexate toxicity. anticoagulation abnormalities. Decreases activity of cyclooxygenase. or during anticoagulant therapy. use only if benefits outweigh risk to fetus Precautions Caution in congestive heart failure. coadministration of anticoagulants may increase PT (monitor and watch for signs of bleeding). which in turn inhibits prostaglandin synthesis. not to exceed 2400 mg/d Pediatric Disease state not seen in pediatrics Interactions May decrease effects of loop diuretics. compared to traditional NSAIDs. MI. probenecid may increase concentrations and. recent GI bleeding or perforation. may increase to 15 mg PO qd prn Pediatric Not established Interactions Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects. and . captopril. ulceration. which can be fatal. and perforation. adjust dose in renal insufficiency Black Box Warning NSAIDs may increase risk of serious cardiovascular thrombotic events. elderly patients are at greater risk for serious GI events Meloxicam (Mobic) To some extent. avoid in peptic ulcer disease.Fetal risk shown in humans. including stomach or intestinal bleeding. renal insufficiency. NSAIDs also increase risk of serious adverse GI effects. more selective for COX-2 receptors. other NSAIDs. which can be fatal. These effects decrease formation of inflammatory mediators. toxicity of NSAIDs. Dosing Adult 7. may decrease effect of hydralazine. and stroke. probenecid may increase toxicity of NSAIDs Contraindications Documented hypersensitivity to ibuprofen. or aspirin. and high risk of bleeding Precautions Pregnancy B . hypertension.400 mg PO tid prn. possibly. decreased renal and hepatic function.

crush. may decrease diuretic effects of furosemide and thiazides. and renal papillary necrosis may occur. (discontinue if there is persistent leukopenia. dissolve.Fetal risk shown in humans. which can be fatal. 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 . Esomeprazole is the S-isomer of omeprazole.Fetal risk revealed in studies in animals but not established or not studied in humans. which is responsible for prostaglandin synthesis. interstitial nephritis. use only if benefits outweigh risk to fetus Precautions Acute renal insufficiency. phenytoin levels may be increased when administered concurrently Contraindications Documented hypersensitivity. and ankylosing spondylitis. a proton pump inhibitor. NSAIDs also increase risk of serious adverse GI effects. Inhibits gastric acid secretion by inhibiting H+/K+-ATPase enzyme system at secretory surface of gastric parietal cells. may increase risk of methotrexate toxicity. which can be fatal. including stomach or intestinal bleeding. hyponatremia. swallow whole and do not chew. rheumatoid arthritis. MI. and stroke. Naproxen is an NSAID that inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase. reversible leukopenia may occur. or thrombocytopenia) Black Box Warning NSAIDs may increase risk of serious cardiovascular thrombotic events. Dosing Adult 1 tab PO bid at least 30 min ac Delayed-release tab. ulceration. and perforation. granulocytopenia. hyperkalemia.beta-blockers. increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion. Esomeprazole component is indicated to decrease risk of gastric ulcers in patients at risk of developing NSAIDassociated gastric ulcers. 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. may use if benefits outweigh risk to fetus D . may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding). active GI bleeding Precautions Pregnancy C .

may use if benefits outweigh risk to fetus D . not recommended with severe hepatic impairment or moderate-to-severe renal impairment. diuretics. esomeprazole is extensively metabolized by CYP2C19 and CYP3A4 Contraindications Documented hypersensitivity. concomitant use with warfarin may result in increased risk of bleeding complications (monitor INR and prothrombin time). dyspepsia. COX-2 is expressed in the kidney.Fetal risk revealed in studies in animals but not established or not studied in humans. upper abdominal pain. digoxin. use only if benefits outweigh risk to fetus Precautions Black Box Warning NSAIDs may increase risk of serious cardiovascular thrombotic events. ketoconazole. such as endoscopic peptic ulcers.Fetal risk shown in humans. MI. diarrhea. in nonaspirin users. however. ulceration. and obstructions. including stomach or intestinal bleeding. the renal safety profile is not significantly superior to that of NSAIDs. Dosing Adult . esomeprazole inhibits CYP2C19 and therefore may alter serum levels/activity of CYP2C19 substrates. Celecoxib (Celebrex) COX-2±specific inhibitor. incidence of GI toxicity. gastric ulcer. nelfinavir). therefore. At therapeutic concentrations. NSAIDs are contraindicated for perioperative pain in the setting of coronary artery bypass graft surgery (increased risk of MI and stroke). NSAIDs also increase risk of serious adverse GI effects. NSAIDs increase lithium plasma levels. which can be fatal. bleeding ulcers. concomitant use with methotrexate may increase methotrexate toxicity. and nausea COX-2 inhibitors Although increased cost can be a negative factor. and beta-blockers. common adverse effects (>5%) include erosive gastritis.Concomitant use of NSAIDs may reduce antihypertensive effect of ACE inhibitors. and perforation. iron salts. esomeprazole inhibits gastric acid secretion and may interfere with absorption of drugs for which gastric pH is an important determinant of bioavailability (eg. gastritis. and stroke. which can be fatal. elderly patients are at greater risk for serious GI events Precautions May cause anaphylactoid reaction. the incidence of costly and potentially fatal GI bleeds is less in nonaspirin users receiving COX-2 inhibitors than with traditional NSAIDs. perforations. atazanavir. is decreased when compared to nonselective NSAIDs. NSAIDs are contraindicated during late pregnancy (risk of premature closure of ductus arteriosus) Precautions Pregnancy C . 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.

Explain the differences between osteoarthritis and other more rapidly progressive arthritides such as rheumatoid arthritis. presence of existing controlled infections. the medication-based regimen is directed at symptom relief. 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. caution in compromised cardiac function. Patient Education y Educate the patient on the natural history of and management options for osteoarthritis. and cardiovascular events. may cause fluid retention and peripheral edema. including myocardial infarction Follow-up Deterrence/Prevention y y Overweight patients who have early signs of osteoarthritis (OA) or who are at high risk should be encouraged to lose weight. except in those with pronounced valgus or varus deformity at the knees. Recommend quadriceps-strengthening exercises in patients with osteoarthritis of the knees. coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations Contraindications Documented hypersensitivity to celecoxib.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. . thus. Prognosis The prognosis of osteoarthritis depends on joints involved and severity. severe heart failure and hyponatremia because may deteriorate circulatory hemodynamics. may use if benefits outweigh risk to fetus Precautions Avoid in late pregnancy to avoid closure of ductus arteriosus.Fetal risk revealed in studies in animals but not established or not studied in humans. hypertension. conditions predisposing to fluid retention. NSAIDs or aspirin Precautions Pregnancy C . No proven disease/structure-modifying drugs for osteoarthritis currently exist. NSAIDs may mask usual signs of infection. stroke. sulfonamides.

et al. Rheumatology (Oxford). [Medline].29(8):1039-49. y References 1. Aust J Physiother. Alarcon G. 9. Practical Rheumatology. Vicaut E. . [Medline]. Clinical features of osteoarthritis. but are not limited to.34(5):505-14. [Medline]. Feb 2010. [Best Evidence] Avouac J. Apr 1992. 6. The Framingham Study. 8. Semin Arthritis Rheum. Also. Altman R. 2009. Karoonsupcharoen O. Zhang Y. Dean D. J Rheumatol. Silman. Arthritis Rheum.18(4 Suppl 2):1-3. 4. 7. see eMedicine's patient education article Osteoarthritis. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip. Appelrouth D. Weight loss reduces the risk for symptomatic knee osteoarthritis in women. Asch E. Altman RD. and Weismann. Arthritis Rheum. Introduction and overview. Classification of osteoarthritis of the knee. Lozada CJ. Anthony JM.49(2):334-40. Ann Intern Med. 3.33(11):1601-10. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand.116(7):535-9. Complete a procedure note in the patient's chart for each arthrocentesis. et al. Aug 1986. Effect of topical capsaicin in the therapy of painful osteoarthritis of the hands. 2. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association. Efficacy of joint lavage in knee osteoarthritis: meta-analysis of randomized controlled studies. [Best Evidence] Chaipinyo K. Altman RD. [Medline]. Arthritis Rheum. Discuss these risks with the patient. In: Hochberg. May 1991. eds. visit eMedicine's Arthritis Center. May 1989. Nov 1990. Miscellaneous Medicolegal Pitfalls y The risk of medications used to treat osteoarthritis (OA) include. Development of criteria for the classification and reporting of osteoarthritis. Weinblatt. 2004:503-10.y For excellent patient education resources. No difference between home-based strength training and home-based balance training on pain in patients with knee osteoarthritis: a randomised trial. Felson DT. [Medline]. [Medline]. McCarthy GM. et al. Smolen. Altman R. Alarcon G. 5. McCarty DJ. [Medline]. Bardin T.55(1):25-30. Apr 1 1992.19(4):604-7. GI toxicities and potential cardiac toxicities of NSAIDs and potential complications of arthrocentesis. Pain in osteoarthritis. et al. Appelrouth D. Bloch D. [Medline]. Altman R. Richette P.

405-6. Buckwalter JA. 14. [Medline]. May 2003. Pelletier JP. 18. controlled trial of arthroscopic surgery versus closed. Abramson S. Kirkley A. Osteoarthritis Cartilage. [Medline]. 13th ed. Part I. Operative treatment of osteoarthrosis. N Engl J Med. 11. eds. 17. et al. [Guideline] Zhang W. Lohmander S. Firestein. Epidemiology of hip and knee osteoarthritis. Guidelines for the medical management of osteoarthritis. 20. Roberts J. A perspective on the study of Moseley et al: questioning the value of arthroscopic knee surgery for osteoarthritis. and acetaminophen in the treatment of patients with osteoarthritis of the knee. Puett DW. [Medline]. Jul 11 1991.325(2):87-91. [Medline]. Keywords . 19. Hogenmiller MS. Osteoarthritis of the hip. Ann Intern Med. Lozada CJ. Arthritis Rheum. An update on osteoarthritis therapeutics. Giffin JR.70(5):401. et al. [Guideline] Hochberg MC. Clin Orthop Relat Res. 408-10. May 2006. Bradley JD. Brand RA.16(2):137-62.(147):181-4. Birmingham TB. Sep 1994. Kelley's Textbook of Rheumatology. [Medline]. Osteoarthritis prevalence in adults by age.10:1-28. Feb 2008. Jul 15 1994. 16.10. 12. [Medline]. 21.36(3):289-96. Lozada CJ. Nuki G. Current practice and future development. Moskowitz RW.American College of Rheumatology. Curr Opin Rheumatol. N Engl J Med. J Bone Joint Surg Am. 2005:1528-40. MarApr 1980. Altman RD. Crowninshield RD. 7th ed. [Medline]. 15. 1988. Epidemiol Rev. Katz BP. [Medline]. A randomized trial of arthroscopic surgery for osteoarthritis of the knee. [Medline]. expert consensus guidelines. et al. Litchfield RB. Stulberg SD. race. Arden N. Brandt KD. Bernstein J.1-27. [Medline]. Nov 1995. Management of osteoarthritis. Quach T.76(9):1405-18. Wong CJ. 1997:1969-84.359(11):1097-107. Cleve Clin J Med.121(2):133-40.38(11):1535-40. In: Harris. an analgesic dose of ibuprofen. Burch TA. A randomized. Etiopathogenesis of Osteoarthritis. Falconer J. Willits KR. Chang RW. Published trials of nonmedicinal and noninvasive therapies for hip and knee osteoarthritis. In: Arthritis and Allied Conditions. Part II: OARSI evidence-based. The effect of cane use on hip contact force. Comparison of an antiinflammatory dose of ibuprofen. Jun 1966. [Medline].needle joint lavage for patients with osteoarthritis of the knee. 13. 23. 22. Martel-Pelletier J. and geographic area. [Medline]. et al. Howell DS. Mar 1993. et al. Brandt KD. OARSI recommendations for the management of hip and knee osteoarthritis. Felson DT. sex. Griffin MR. Sep 11 2008. Vital Health Stat 11. Budd.18(3):256-60. Arthritis Rheum. Altman RD.

MD. knee OA. osteophytes. Department of Internal Medicine. and Society of General Internal Medicine Disclosure: Nothing to disclose. PC Disclosure: Nothing to disclose. Chairman Emeritus. Professor. Pharmacy Editor Francisco Talavera. MD. Division of Rheumatology and Immunology. articular disease. MD. The Consultant Group. FACP. eMedicine Disclosure: eMedicine Salary Employment Managing Editor Elliot Goldberg. hip osteoarthritis. OA. Professor. and Society for Investigative Dermatology Disclosure: Nothing to disclose. Northwestern University John Varga. Department of Internal Medicine. FACP is a member of the following medical societies: Alpha Omega Alpha. PharmD. Western Pennsylvania Hospital . foot osteoarthritis. bony osteophytes Contributor Information and Disclosures Author Carlos J Lozada. Senior Pharmacy Editor. Professor. MD. American College of Physicians-American Society of Internal Medicine. spinal OA. University of Miami Miller School of Medicine Alex J Mechaber. Central Society for Clinical Research. Associate Professor of Medicine. PhD. Director of Rheumatology Fellowship Program. Temple University School of Medicine. Associate Dean for Undergraduate Medical Education. Consulting Staff. Chief Editor Herbert S Diamond. Temple University School of Medicine Elliot Goldberg. joint pain. hip OA.osteoarthritis. spinal osteoarthritis. knee osteoarthritis. American College of Physicians. and American College of Rheumatology Disclosure: Nothing to disclose. degenerative joint disease. foot OA. secondary OA. CME Editor Alex J Mechaber. Department of Medicine. secondary osteoarthritis. articular cartilage disease. Department of Medicine. American College of Rheumatology. MD is a member of the following medical societies: Alpha Omega Alpha. osteoarthrosis. Department of Rheumatology. 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. Dean of the Western Pennsylvania Clinical Campus. MD is a member of the following medical societies: American College of Physicians. Medical Editor John Varga. MD. back pain. MD. Professor of Medicine. University of Miami Miller School of Medicine Carlos J Lozada. noninflammatory arthritis. Division of Rheumatology.

American College of Rheumatology.medscape. American College of Physicians.2011 by Medscape. American Medical Association. Stock ownership in multiple Pharmaceutical companies Ownership interest Other Further Reading © 1994. All Rights Reserved (http://www. and Phi Beta Kappa Disclosure: ACP PEER Honoraria Independent contractor.com/public/copyright) .Herbert S Diamond. MD is a member of the following medical societies: Alpha Omega Alpha.

Sign up to vote on this title
UsefulNot useful