Osteoarthritis
Osteoarthritis
Kevin deWeber
Basics
Description
A predominantly noninflammatory, slowly progressing, degenerative condition of articular cartilage, sometimes known as “degenerative joint disease”
Epidemiology
Prevalence
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Radiographic osteoarthritis (OA) seen in about 40 million Americans, although only 10–30% of them have significant pain or disability.
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Prevalence of symptomatic OA significantly increases with age and varies with affected joint (1):
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Knee: 6% of adults >30, and 10–15% >60
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Hip: 1–4% of adults
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Hand: 10–15% of the elderly
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Risk Factors
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Systemic risk factors (1) contribute to development of OA by creating an environment where the joint is vulnerable:
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Age (10-fold increase from 30–65 yrs of age)
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Gender:
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Men <50 have higher incidence than women (may be related to risk of joint injury)
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Women >50 have higher incidence than men (possible protective role of estrogen is gone after menopause)
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Genetics
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Nutritional factors:
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Lower risk of OA in persons with middle and highest tertiles of vitamin C intake or highest levels of vitamin D (Framingham data)
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Ethnicity:
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Chinese have lower rates of hip and hand OA.
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African Americans have higher rates of hip and knee OA.
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Joint biomechanical risk factors (1) cause direct trauma to articular cartilage:
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Joint injury (fractures, dislocations, ligament and meniscal ruptures, articular surface damage)
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Obesity (knee, hip, even hand OA)
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Occupations involving high physical demands: Repetitive use of joints, heavy lifting, frequent squatting
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Sports with significant risk of acute joint injury
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Abnormal joint biomechanics (dysplasia, malalignment, instability, abnormal innervation)
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Excessive running (>60 miles a wk) has relative risk of 2–12 times for hip OA (Systematic Review 2003)
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Genetics
OA has a genetic component, especially in women. Primary, generalized OA is polygenic and multifactorial; environmental factors play a significant role in gene expression.
General Prevention
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Avoidance of joint trauma
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Weight management:
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50% reduction in OA risk with 11-lb weight loss in women (1)[C]
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Adequate vitamin C and D intake (1)[C]
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Avoid extremes of joint activity (joint immobilization or gross overuse)
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Estrogen replacement after menopause may be protective (1)[C].
Etiology
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OA is caused by an imbalance between breakdown and repair of joint tissue, usually due to multiple risk factors:
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Cartilage matrix (collagen, water, proteoglycans) slowly degrades
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Chondrocytes are unable to maintain adequate repair.
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Mechanical forces contribute to progressive cartilage loss.
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Early stages: Cartilage fibrillation (fine fraying)
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Middle and late stages: Formation of extra subchondral bone and cysts and osteophytes (usually at joint margins)
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Predominantly noninflammatory, but occasional mild inflammatory clinical flares
Commonly Associated Conditions
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Degenerative meniscal tears in knee OA
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Labral tears in hip OA
Diagnosis
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Primary classification (idiopathic): Usually generalized
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Secondary classification: Causes include previous trauma/internal derangement, metabolic disorder, and deposition diseases
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Most commonly affected joints include the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints of the hands; metacarpophalangeal joints of the thumb; and the hallux, hips, knees, cervical, and lumbar spine
History
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Insidious onset over months to years is typical.
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Most common symptoms are pain (especially after excessive activity), crepitus or grinding, and joint swelling
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There is typically short-lived (<30 min) stiffness after immobilization (ie, upon awakening), improving with mobilization.
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Some patients experience muscular weakness in the surrounding soft tissue.
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There may be a personal history of antecedent joint trauma or a family history of OA.
Physical Exam
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Joint line tenderness is common in hands and knees.
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Joints may have crepitus, decreased range of motion (ROM), effusion, and atrophy of surrounding muscles
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In hands, may see nodules in the DIP and PIP joints, termed Heberden and Bouchard nodes, respectively
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In the hips, decreased and painful internal rotation are early signs.
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Severely affected joints may appear misshapen or deformed due to osteophytes or malalignment.
Diagnostic Tests & Interpretation
OA is diagnosed primarily through history and physical examination and confirmed by plain films.
Lab
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Laboratory assessment only used to rule out other disorders, if clinically suspected:
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CBC, chemistry profile, and urinalysis are normal.
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Markers of inflammation (erythrocyte sedimentation rate, C-reactive protein) usually are normal, but may be slightly elevated during inflammatory flare-ups.
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Rheumatoid factor and antinuclear antibody titers are negative.
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Imaging
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Plain films are the modality of choice (2)[D]:
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Weight-bearing films are most sensitive in early knee and hip OA.
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X-ray characteristics include osteophytes, joint space narrowing, subchondral sclerosis, and cyst formation.
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Radiographic severity does not correlate with symptom severity.
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CT and MRI do not play a large role in diagnosis of 0A. May be used if other conditions suspected.
Diagnostic Procedures/Surgery
Arthrocentesis and joint fluid examination are not routinely necessary unless the diagnosis is in question, there is a possibility of septic arthritis/crystal deposition disease, or for treatment of tense effusion.
Differential Diagnosis
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Rheumatoid arthritis
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Collagen vascular diseases
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Crystal deposition disease
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Gout
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Calcium pyrophosphate deposition disease
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Meniscal or labral tears
Treatment
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Optimal management requires a combination of nonpharmacological and pharmacological modalities (3)[D].
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A multidisciplinary approach may help patients make the most of available therapies:
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Providers, physical therapists, personal exercise trainers, health care educators, nutritionists
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Surgical therapy is best reserved for patients with severe pain that affects quality of life or activities of daily living who have failed multiple conservative measures (3)[C].
P.425
Medication
No disease-modifying agents are yet available.
First Line
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Acetaminophen (up to 4 g/day) is modestly effective and should be encouraged as the first-line medication due to its relative safety (3)[A].
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Oral glucosamine sulfate (not hydrochloride) 1,500 mg/day is modestly effective in reducing pain in some patients (3)[A]:
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Use for several years can slow progression of joint space narrowing; consider use even if no symptomatic benefit (3)[A].
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Oral NSAIDs effective, but have higher risks; reserved for short-term therapy (3)[A].
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COX-2 inhibitors are not more effective; less GI toxicity, but not without risks.
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Discourage chronic use of NSAIDs; if necessary, add gastroprotection with a proton pump inhibitor or misoprostol.
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Viscosupplementation with intra-articular injection of hyaluronate derivatives is modestly effective in pain reduction (3)[A]:
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3–5 weekly injections
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2–5-wk delay in effects
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1–6-mo duration of effects
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Second Line
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Tramadol 50–100 mg t.i.d. is effective but has sedating and constipating properties similar to narcotics (3)[A].
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Topical NSAIDs are effective; effect takes 1–2 wks (3)[A].
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Topical capsaicin is effective; high incidence of local irritation (3)[A].
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Weak opioids or narcotics can be considered for short-term refractory pain; those requiring long-term use may benefit from maximization of nonpharmacologic therapies and/or surgery (3)[A].
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Intra-articular injections with corticosteroids are effective for 2–4 wks (3)[A]:
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Reserve for patients not responding to oral medications or inflammatory flare-ups.
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Limit to 2–3 injections per year per joint.
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Observe for significant incidence of systemic side effects.
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Additional Treatment
General Measures
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Patient education is effective (3)[A]:
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Set reasonable expectations on outcome (pain reduction, increased function, not cure)
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Modification of activities to minimize pain and risk of joint trauma
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Importance of nonpharmacologic therapies
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Weight reduction is paramount (3)[A].
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Aerobic conditioning with nonpainful activities (walking, deep-water running and other aquatic exercise, cycling) (3)[A]
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ROM and muscle strength exercises are effective (3) for hip [D] and knee [A] OA.
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Physical therapy referral may be effective (3)[D].
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Walking aids for knee and hip OA may be effective (cane, crutch in contralateral hand; walkers for bilateral OA) (3)[D].
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Knee brace for patients with varus or valgus instability improves stability and reduces fall risk (3)[A].
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Footwear with lateral wedge insoles for medial knee compartment OA (3)[A]
Complementary and Alternative Medicine
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Thermal therapies (heat, cold) may be effective (3)[A].
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Transcutaneous electrical nerve stimulation can provide short-term relief (3)[A].
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Acupuncture may be effective in knee OA (3)[A].
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Pulsed electromagnetic field therapy may be effective in improving function 4 [A].
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Balneotherapy (spa, mineral baths) may be effective 5 [A].
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Static magnets: No evidence for support; effectiveness cannot be ruled out 6 [A].
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Intra-articular autologous platelet-rich plasma injection: Success in 1 series; under study
Surgery/Other Procedures
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Indicated in patients with recalcitrant pain and interference with activities of daily living despite maximizing conservative management (3)[C]
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Arthroscopic lavage and debridement NOT effective (3)[A]; only indicated for concomitant non-OA conditions
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Medial or compartment knee OA:
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Wedge osteotomomy may be effective (7)[B].
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Unicompartmental arthroplasty (replacement) effective (7)[B]
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Interposition arthroplasty (joint spacer insertion); no data on safety/efficacy
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Total knee arthroplasty (TKA): Very effective (3)[C]:
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Hardware durable 10–15 yrs
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Try to delay TKA until after 55 by maximizing other treatments.
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Rate of hardware failure <10 yrs is 3 time in <55 vs >70 yrs of age
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Patellofemoral joint (PFJ) OA in isolation (rare):
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Elevation of tibial tubercle may be effective
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PFJ arthroplasty sometimes used
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Total hip arthroplasty or joint resurfacing is effective in hip OA (3)[B].
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Glenohumeral OA: Total shoulder replacement more effective/durable than humeral head replacement (8)[B], but both are effective.
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Cartilage replacement techniques gaining in popularity and evidence:
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Autologous cartilage implantation: Arthroscopy harvests patient's cartilage, chondrocytes are replicated in culture, and 2nd arthroscopy fills cartilage defect with cells.
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Osteoarticular cartilage transplant: Cartilage from patient's nonweight-bearing surface in knee joint is placed into defect.
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Cartilage allografts (cadaver cartilage) to fill defects
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Ongoing Care
Follow-Up Recommendations
As needed based on symptoms and function
Diet
Ensure adequate vitamin C and D intake.
Patient Education
Good education has proven benefit for successful management:
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In office by professionals
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Public education materials (eg, www.myosteoarthritiscentral.com)
Prognosis
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OA is a progressive arthropathy with highly variable course
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Oral glucosamine shown to slow rate of radiographic progression over >3 yrs
References
1. Garstang SV, Stitik TP. Osteoarthritis: epidemiology, risk factors, and pathophysiology. Am J Phys Med Rehabil. 2006;85:S2–S11.
2. American College of Radiology Expert Panel on Musculoskeletal Imaging, 2008. http://74.125.93.132/search?q=cache:Up16N8YvlbEJ:www.acr.org/SecondaryMainMenuCategories/quality/safety/app/criteria/pdf/ExpertPanelonMusculoskeletalImaging/nontraumaticKneePainDoc15.aspx+american+college+of+radiology+panel+on+musculoskeletal+imaging+osteoarthritis&cd=1&hl=en&ct=clnk&gl=us.
3. Zhang W, Moskowitz RW, Nuki G, et al. OARSI recommendations for the management of hip and knee osteoarthritis, Part II: OARSI evidence-based, expert consensus guidelines. Osteoarthritis Cartilage. 2008;16:137–162.
4. Vavken P, Arrich F, Schuhfried O, et al. Effectiveness of pulsed electromagnetic field therapy in the management of osteoarthritis of the knee: A meta-analysis of randomized controlled trials. J Rehabil Med. 2009;41:406–411.
5. Harzy T, Ghani N, Akasbi N, et al. Short- and long-term therapeutic effects of thermal mineral waters in knee osteoarthritis: a systematic review of randomized controlled trials. Clin Rheumatol. 2009;28:501–507.
6. Pittler MH, Brown EM, Ernst E. Static magnets for reducing pain: systematic review and meta-analysis of randomized trials. CMAJ. 2007;177:736–742.
7. Richmond JC. Surgery for osteoarthritis of the knee. Med Clin North Am. 2009;93:213–222.
8. Radnay CS, Setter KJ, Chambers L, et al. Total shoulder replacement compared with humeral head replacement for the treatment of primary glenohumeral osteoarthritis: A systematic review. J Shoulder Elbow Surg. 2007.
Codes
ICD9
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715.91 Osteoarthrosis, unspecified whether generalized or localized, involving shoulder region
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715.92 Osteoarthrosis, unspecified whether generalized or localized, involving upper arm
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715.93 Osteoarthrosis, unspecified whether generalized or localized, involving forearm