DefinitionEtiologyEpidemiologyPathophysiologyClinical Presentation
WorkupGoalsMed ChoicesClinical TrialsPipeline AgentsResourcesRefs

A chronic joint disease involving progressive loss of joint cartilage, bone remodeling, hypertrophy and osteophyte formation.

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Biomechanical, biochemical, inflammatory, and immunologic factors are implicated in the pathogenesis.

Idiopathic OA

  • Commonly seen with no underlying condition, often localized to distal interphalangeal (DIP) joints and proximal interphalangeal (PIP) joints of hands, first metatarsophalangeal (MTP) joints, hip or knee; or may be generalized involving 3 or more joints

Secondary OA

Conditions which may cause or enhance the risk of developing OA include:

  • Developmental disorders of joints
  • Calcium pyrophosphate dihydrate deposition disease (CPPD)
  • Rheumatoid arthritis, gouty arthritis, paget's disease
  • Diabetes mellitus, acromegaly, hypothyroidism, neuropathic (Charcot) arthropathy, hemochromatosis
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Approximately 10% of Canadians have OA

  • Leading cause of work disability in those who are <65 years of age in North America
  • Symptoms often arise >40 years of age
  • Shows female preponderance between 40-70 years
  • After the age >70 years, M and F equally affected
  • 80% of people will have radiographic evidence of OA after the age of 65 years
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  • Entire joint involved, including cartilage, subchondral bone and synovium
  • Begins with tissue damage usually from mechanical injury (e.g. torn meniscus)
  • Tissue damage leads to attempted repair through chondrocyte activation, which initially increases production of proteoglycans and collagen
  • Efforts at repair also stimulate the release of enzymes that degrade cartilage as well as other inflammatory mediators, including prostaglandins
  • Failure of repair processes combined with inflammation lead to cartilage degradation. Eventually chondrocytes undergo apoptosis
  • Cartilage destruction exposes bone which then becomes eburnated and sclerotic

1-OA-Pathophysiology-Pathological Findings

Pathological Findings:


  • Patchy cartilage damage and bone hypertrophy
  • Subchondral bone microfractures, sclerosis with osteophyte formation


  • Edema of the extracellular matrix and cartilage micro cracks
  • Diminished proteoglycan staining
  • Fissuring and pitting of the subchondral bone
  • Articular surface irregularity due to clefts and erosions
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Clinical Presentation:

Main symptom associated with OA is pain, which is typically exacerbated by activity and relieved by rest.

  • Gradual onset of pain
  • Morning stiffness always <20-30 minutes
  • Crepitations may be noted with movement of joint
  • Joint involvement progresses slowly and irreversibly

Differences in symptomatology with or without inflammation

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Investigation and Workup:
  • Diagnosis is based on:
    • Classical symptoms
    • Physical examination
    • Labs
    • Imaging
  • The involvement of joints that are not usually affected by idiopathic disease (e.g. the shoulder, elbow, wrist, and ankle) suggests other etiologies
  • Severe acute onset of pain is unlikely, joint aspiration is recommended to exclude other causes (gout, pseudogout, infection)


  • Morning stiffness
  • Joint trauma
  • Work or hobby - induced trauma through repetitive stressful joint movements e.g. dancers
  • Smoking
  • Presence of diabetes, acromegaly, gout, other forms of inflammatory arthritis
  • Family history

Physical examination:

Common findings that may be present:

  • Joint tenderness with or without inflammation
  • Joint effusion
  • Joint crepitus
  • Bone/Joint enlargement ± osteophytes may be palpable
  • Joint malalignment and decrease in range of motion

Laboratory studies

There is no blood test to diagnose osteoarthritis. The following tests may be ordered when history and physical findings indicate OR when considering inflammatory vs. non-inflammatory presentations or when monitoring disease status and/or medications:

  • Hematology profile: Required either for a chronic or inflammatory condition, such as baseline to monitor NSAIDs
  • Creatinine: If considering treatment with NSAIDs
  • ESR
  • C-reactive protein: If suspecting septic arthritis
  • ANA: When considering connective tissue disease
  • RF factor: Rule out rheumatoid arthritis
  • Synovial fluid analysis:
    • Typically inflammatory markers will be normal in OA
    • Joint fluid will have a Leukocyte count <2000/ml
    • (WBC= conventional units are 2000x109/L)

Imaging studies:

  • Usually recommended for persistent unexplained pain
  • Always specify the X-rays are for OA
  • X-ray of affected joints typically shows:
    • Narrowed joint space (may be asymmetric or focal)
    • Osteophyte formation
    • Subchondral bony sclerosis
    • Subchondral cyst formation
    • Erosions may occur on the surface of distal and proximal interphalangeal joints when OA is associated with inflammation (erosive osteoarthritis)


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Treatment Goals:
  • Reduce joint pain and limit functional disability
  • Maintain and improve joint function and mobility
  • Maintain normal articular and periarticular structures
  • Prevention of further joint or cartilage damage
  • Identify and treat any associated condition
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Therapeutic Choices:

A) Non-pharmacologic interventions:

Play a central role in OA therapy and includes weight loss, rest, physical therapy, and exercise along with other modalities.

1. Weight loss:

  • Small reductions in weight may be beneficial

2. Rest:

  • Recommended for short periods
  • Pacing of activities is important

3. Physical therapy and assistive devices:

  • Reducing load on the affected joints by assistive devices (orthotics, cane, braces)
  • Braces and splints: Beneficiall for symptomatic relief

4. Exercise:

Deficiencies in gait, strength, flexibility, aerobic power, and exercise capacity can be safely reversed with a variety of exercise regimens.

  • Symptomatic relief: Motion and strengthening exercises can reduce pain and increase mobility
  • Joint protection: Joint protection can be achieved by exercising in warm water

5. Group exercise programs:

The Arthritis Society of Canada ( provides many programs, including group exercise, aqua-fit and Arthritis Self-Management Programs (ASMP).

6. Patient compliance: Can be maximized through several techniques, including

  • Simplifying regimens & setting attainable goals
  • Emphasizing and educating the importance and benefits of exercise

7. Heat and cold:

  • Moist heat and superficial cold both, can raise the pain threshold, and decrease muscle spasm

8. Patient education and psychosocial support:

Assess, evaluate and educate the effects of OA which include:

  • Physical limitations
  • Feelings of frustration and dependency
  • Depression
  • Decreased motivation to comply with diet exercise and medication

9. Other:

  • Acupuncture, massage, herbs, relaxation techniques, counter irritants and mud pack therapies have been tried with varying degrees of response

B) Pharmacologic therapy:

Therapy depends on disease severity as well as presence or absence of inflammation.

Inflammatory and non-inflammatory OA

Both inflammatory and non-inflammatory OA can be polyarticular, oligoarticular, or monoarticular. A generalized approach to treatment is as follows:

1. Mild disease:

  • OA ± inflammation is initially managed using a non-pharmacological approach
  • If symptoms persist, addition of simple analgesics on a PRN basis is advised (acetaminophen for non-inflammatory OA and NSAIDs for inflammatory OA)

2. Moderate Disease:

  • Scheduled/regular dosing of NSAIDs and/or acetaminophen
  • Intraarticular injections of corticosteroids may be helpful (rapid recovery lasting for 1-3 months)
  • Viscosupplementation for knee joint - requires 1-3 injections although expensive, show 60-75% response, and effect lasts up to 6-9 months

3. End stage disease:

  • For both inflammatory and non-inflammatory OA, a surgical approach such as total joint replacement may be indicated. If surgery is not an option then opioid analgesics may be considered if other medications are ineffective or contra-indicated
  • Consider opioid analgesics if surgery is not an option and other medications are ineffective

Analgesics for mild to moderate disease:

  • Acetaminophen up to 1000 mg PO QID for the short-term use. Chronic dose usually restricted to 2.6-3.2 g/day
  • Topical NSAIDs provide short-term benefit in Knee OA
  • If acetaminophen or topical NSAIDs are ineffective, then the addition or substitution by an oral NSAID/COX-2 inhibitor should be considered. Use the lowest effective dose for the shortest possible period of time. Prolonged use is not usually recommended
  • Oral corticosteroids have no role. However, intra-articular depot corticosteroids help in relieving pain and increasing joint flexibility


For mild-moderate disease:

  • Use of duloxetine in knee OA is now approved in Canada
  • Recommended dose: 60 mg/day

Ref: Chappell AS, Ossanna MJ, etal. Pain. 2009; 46:253-60.



NSAIDs - Analgesic

  • Salicylates
  • Acetic acid derivatives
  • Enolic acid (oxicam) derivatives
  • Napthylkanone derivatives
  • Propionic acid derivatives (profens)
  • COX-2 inhibitors


  • Prostaglandins are common locally produced chemicals mediating pain, fever, and inflammation
  • These drugs reversibly inhibit cyclooxygenase-1 and 2 (COX-1 and 2) enzymes
  • This results in decreased formation of prostaglandin precursors
  • Acetylsalicylic acid in addition to above mechanisms, irreversibly interferes with the production of thromboxane A2 within the platelet, thus inhibiting platelet aggregation




  • 325-650 mg PO every 4-6 hours; Max. 4 g/day


  • 500-1000 mg/day PO in 2 divided doses; Max. daily dose 1.5 g

Renal impairment:

  • Decrease the dose by 50% if ClCr <50mL/minute


Acetic acid derivatives


  • Immediate-release: 150 mg PO daily in 3-4 divided doses; Max. 150 mg/day
  • Slow-release: 150-200 mg PO daily in 2-4 divided doses
  • Canadian labeling: 150 mg/day PO in 3 divided doses (75-150 mg/day of slow release tablet)
  • Rectal suppository: 50-100 mg/day, as single dose then maximum 100 mg/day or combined dose (rectal + oral) is 150 mg/day


  • 50 mg/200 mcg and 75 mg/200 mcg tablets; Max. 150 mg diclofenac/day
  • Note: Misoprostol 800 mcg is the maximum daily dose. Not recommended in advanced renal disease


  • Immediate-release: 400-500 mg PO BID; or 300 mg 2-3 times/day; Max. 1000 mg/day
  • Extended release: 400-1000 mg once daily


  • Immediate-release: 25 mg PO BID or TID; Max. 200 mg/day
  • Extended-release: 75 mg PO daily; may increase 75 mg PO BID if needed; Max. 150 mg/day
  • Rectal: 25 mg 2-3 times daily


  • 150 mg PO BID; Max.400 mg/day


Enolic acid (oxicam) derivatives


  • 7.5 mg PO daily; may increase for additional benefit to 15 mg/day; Max. 15 mg/day


  • 10-20 mg PO in 1-2 divided doses; Max. 20 mg/day


  • 10-20 mg PO daily for 7-14 days
  • 20 mg IM / IV daily for 1-2 days


Napthylkanone derivatives


  • 1 g PO daily; may increase upto 2 g PO in 2 divided doses

Renal impairment:

  • ClCr 30-49 mL/minute: 750 mg/day may increase upto 1500 mg/day


Propionic acid derivatives (profens)


  • 300-600 mg PO TID or QID; Max. 3.2 g/day


  • 200-300 mg/day in 2, 3, or 4 divided doses. Do not administer more than 100 mg per single dose; Max 300 mg/day


  • 200-800 mg PO 3-4 times a day; Max dose 3.2 g/day; usual dose 800 mg PO BID


  • Regular release: 50 mg PO QID or 75 mg PO TID; Max. 300 mg/day
  • Extended release: 200 mg PO daily

Renal impairment:

  • Mild: Maximumn dose is 150 mg/day
  • Severe (ClCr <25mL/min): Maximum dose is 100 mg/day


  • Regular release: 500-1000 mg/day in 2 divided doses; may increase to 1.5 g/day


  • 600-1200 mg PO daily; Max. 1800 mg/day. Titrate it to lowest possible dose


COX-2 Inhibitors


  • 200 mg PO daily as a single dose or in 2 divided doses; Max. 200 mg/day


Analgesic, Non-NSAID

  • Acetaminophen


  • Analgesic action: Inhibits the synthesis of prostaglandins in the central nervous system
  • Antipyretic action: Inhibits the hypothalamic heat-regulating center



  • 325-650 mg PO or 1000 mg PO TID or QID; not to exceed 1 g/dose; Max. 4 g/day

Analgesic, Opioid

  • Morphine
  • Oxycodone
  • Tramadol
  • Codeine
  • Tapentadol
  • Buprenorphine transdermal patch


  • Bind to opioid receptors in the CNS
  • Inhibit reuptake of serotonin and/or norepinephrine in the CNS (tramadol, tapentadol)
  • Inhibit ascending pain pathways, and alter the perception of and response to pain



  • Start 10 mg PO every 4-6 hours in opiate naïve patients; patients with previous exposure may need higher doses


  • Immediate release: 5-10 mg PO every 4-6 hours
  • Controlled release: 10-20 mg PO BID or higher as needed


  • Conventional release: 25 mg PO four times daily; may increase total daily dosage by 50 mg every 3 days as tolerated, up to 200 mg daily (50 mg four times daily)
    • After titration, 50-100 mg can be given every 4-6 hours, up to Max. of 400 mg daily
  • Extended release: 100 mg PO daily; may increase dose in 100 mg increments every 5 day as needed; Max. 300 mg/day


Controlled release:

  • Start 50 mg PO BID may titrate to effective dose

Immediate release:

  • Day 1: 50-100 mg PO every 4-6 hours as needed; may administer the second dose after an hour of the first dose; Max. dose on day 1: 700 mg
  • Day 2 and onwards: 50-100 mg PO every 4-6 hours as needed; Max. 600 mg/day


  • Regular release: Start at 30 mg PO every 4-6 hours; maintain at 15-120 mg PO every 4-6 hours as needed; may start with higher initial dose in patients with prior opiate exposure
  • Controlled release: 50-300 mg PO BID; may administer higher dose in opioid-tolerant patients

Buprenorphine (Transdermal):

  • Opioid-naive patients: Initially apply 5 mcg/hour applied once every 7 days; maintain at 5-20 mcg/hour patch once every 7 days; Max. 20 mcg/hour
  • Opioid-experienced patients (oral morphine equivalent <30 mg/day): Initially apply 5 mcg/hour once every 7 days; Max. 20 mcg/hour
  • Opioid-experienced patients (oral morphine equivalent 30-80 mg/day): Initially apply 10 mcg/hour once every 7 days; Max. 20 mcg/hour

Note: Prior to starting therapy, taper dose for up to 7 days to ≤30 mg/day of oral morphine

Analgesic, Topical Agents

  • Transient Receptor Potential Vanilloid 1 (TRPV1) Agonist
    • Capsaicin
  • Nonsteroidal Anti-inflammatory Agents
    • Diclofenac sodium


Transient Receptor Potential Vanilloid 1 (TRPV1) Agonist

  • Exact mechanism of action unknown
  • Selectively binds nerve membrane TRPV1 receptor
  • Stimulates and desensitizes cutaneous nociceptive neurons
  • Also depletes Substance P, which helps in reducing pain impulse transmission from periphery to the CNS

Nonsteroidal Anti-inflammatory Agents

  • Prostaglandins mediate the production of pain, fever, and inflammation
  • These drugs inhibit cyclooxygenase-1 and 2 (COX-1 and 2) enzymes
  • This results in decreased formation of prostaglandin precursors



  • Apply 3-4 times/day to the affected area

Diclofenac sodium:

Topical gel:

  • Lower limb: Apply 4 g of 1% gel to the affected area 4 times/day; Max. 16 g per joint /day
  • Upper limb: Apply 2 g of 1% gel to the affected area 4 times/day; Max. 8 g per joint/day

Note: Maximum total body dose should not exceed 32 g per day

Topical solution - Knee:

  • Canadian labeling: Apply 40 drops four times/day or 50 drops three times/day to the affected knee for up to 3 months
  • U.S. labeling: Apply 40 drops four times/day to the affected knee


  • Betamethasone
  • Methylprednisolone acetate (most commonly used)
  • Triamcinolone acetonide
  • Triamcinolone hexacetonide


  • Decreases inflammation and the normal immune response through multiple mechanisms, also suppresses adrenal function at high dose, also has mineralocorticoid activity


Betamethasone: (Intra-articular)

  • Hip: 1-2 ml
  • Knee, ankle, shoulder: 1 ml
  • Elbow, wrist: 0.5-1 ml
  • Metacarpophalangeal, sternoclavicular: 0.25-0.5 ml

Methylprednisolone: (Intra-articular)

  • Hip: 80-160 mg
  • Ankle, shoulder: 40 mg
  • Knee: 40-80 mg
  • Elbow, wrist: 20-40 mg
  • Small joint like MCP, PIP, DIP, SC: 10 mg

Triamcinolone acetonide: (Intra-articular)

  • Large joints: 5-40 mg
  • Small joints: 2.5-10 mg

Triamcinolone hexacetonide: (Intra-articular)

  • Large joints: 10-20 mg
  • Small joints: 2-6 mg

Antirheumatic Agent, Viscosupplements

  • Sodium hyaluronate
  • Hylan GF 20
  • Stabilized hyaluronic acid


  • Works as a lubricant and also act as a viscoelastic support maintaining a separation between tissues
  • Helps in maintaining synovial fluid viscosity
  • Supports the articular cartilage in shock absorption


Sodium hyaluronate: (Orthovisc, Euflexxa, Neovisc, Hyalgan, Suplasyn)

  • Intra-articular: Inject 2 ml every week for 3 weeks

Sodium hyaluronate: (Monovisc)

  • Intra-articular: Inject 4 ml once

Hylan GF 20: (Synvisc)

  • Intra-articular: Inject 2 ml every week for 3 weeks

Hylan GF20: (Synvisc One)

  • Intraarticular: Inject 6 ml once

Stabilized hyaluronic acid: (Durolane)

  • Intraarticular: Inject 3 ml once


Serotonin/Norepinephrine Reuptake Inhibitor

  • Duloxetine


Exact mechanism of action is unknown.

  • A potent serotonin and norepinephrine reuptake inhibitor
  • Weakly inhibits dopamine reuptake
  • Has a centrally acting analgesic effect; demonstrating pain relief in peripheral neuropathy and fibromyalgia
  • Due to its central effect; has now been approved for knee OA

Ref: Chappell AS, Ossanna MJ, etal. Pain. 2009; 46:253-60.



  • 60 mg PO once daily; recommended for knee osteoarthritis


Combination, Analgesic

  • Acetaminophen and Codeine
  • Acetaminophen and Oxycodone
  • Acetaminophen and Tramadol



  • Analgesic action: Likely inhibits the synthesis of prostaglandins in the central nervous system
  • Antipyretic action: Inhibits the hypothalamic heat-regulating center


  • Bind to opioid receptors in the CNS
  • Inhibits reuptake of serotonin and norepinephrine in the CNS (tramadol only)
  • Also inhibit ascending pain pathways, and alter the perception of and response to pain


Acetaminophen and Codeine (#1, #2, #3 and # 4):

  • 1-2 tablet PO every 4-6 hours as required; Max. 4 g/24 hours based on acetaminophen component (Max. 12 tablet for # 1/2/3 and 6 tablets for # 4)

Acetaminophen and Oxycodone:

  • Based on oxycodone content 2.5-5 mg PO every 4-6 hours; Max. 4 g/24 hours based on acetaminophen component

Acetaminophen and Tramadol:

  • 1-2 tablets PO every 4-6 hours as needed; Max. 8 tablets/day


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Clinical Trials:
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Pipeline Agents:

Currently unavailable

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Pharmacist Resources:

Tips for patient care


  • Advise to use appropriate adaptive devices to perform of activities the daily living
  • To wear appropriate footwear and any assistive device, if required
  • Teach self management & provide resources
  • Emphasize the importance of appropriate exercise, joint protection and strengthening of muscles supporting the joint
  • Encourage participation in activities of daily living but avoid overwork and fatigue
  • Encourage weight loss to decrease stress on weight-bearing joints


  • There is no known cure for OA
  • Consider concurrent risk factors and disease states with the prescribed therapy
  • Evaluate risks and benefits of pharmacological therapy
  • Advisable to use only one NSAID at a time (with the exception of low-dose ASA for vascular protection where indicated)
  • Misoprostol (~600 mcg/day), high dose H2 blockers or proton pump inhibitors are recommended in patients who require NSAIDs but are also at increased risk for upper gastrointestinal adverse events.
  • NSAIDs impact renal function particularly in combination with ACE inhibitors and diuretics
  • If possible avoid NSAIDs and opioid analgesics for long term daily treatment
  • NSAIDs can promote hypertension
  • Evaluate cost and affordability and insurance coverage for patients

Unlabelled/Alternate Uses include, but are not limited to:

  • Acetylsalicylic acid
    • Pre-eclampsia
    • Antiphospholipid syndrome
  • Ibuprofen
    • Acute migraine
    • Cystic fibrosis


  • Advise use of cane with appropriate height
  • Correction of posture and body mechanics should be taught by demonstrating techniques
  • Teach therapeutic exercise (e.g. range of motion, strengthening and aerobic activity)
  • Inform patient who are taking NSAIDs that GI bleeds can occur with or without warning symptoms
  • Emphasize importance of staying active and having a regular exercise routine
  • Occupational therapy should be available for people with OA


  • Discontinue NSAIDs (except ASA) and celecoxib in patients presenting with unstable angina or non-ST segment elevation myocardial infarction
    • If required, an opioid analgesic (e.g. morphine) may be used as an alternative for pain control in this setting
  • COX-2 inhibitors also carry a risk for peptic ulcer disease
  • Increased risk of cardiovascular events may occur with some NSAIDs
  • Educate about the side effects of long term NSAID s use which include:
    • GI bleeding
    • Cardiovascular events
    • Renal and hepatic toxicity


  • Non-stressful exercise, such as swimming/water aerobics are good to preserve mobility
  • Quadriceps-strengthening exercises helps in relieving knee pain and disability
  • Usually takes about two to four weeks to evaluate the efficacy of a NSAIDs
  • Periodic monitoring of CBC, renal function tests, stool for occult blood is important in patients on long term NSAIDs therapy
  • Nonacetylated salicylates and Nabumetone have less antiplatelet activity
  • Drink plenty of water with NSAID ingestion as these agents are a common cause of pill esophagitis
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Core Resources:

  • Compendium of Pharmaceuticals and Specialties (CPS). Canadian Pharmacist association. Toronto: Webcom Inc. 2012
  • Day RA, Paul P, Williams B, et al (eds). Brunner & Suddarth's Textbook of Canadian Medical-Surgical Nursing. 2nd ed. Philadelphia: Lippincott Williams and Wilkins; 2010
  • Foster C, Mistry NF, Peddi PF, Sharma S, eds. The Washington Manual of Medical Therapeutics. 33rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010
  • Gray J, ed. Therapeutic Choices. Canadian Pharmacists Association. 6th ed. Toronto: Webcom Inc. 2011
  • Katzung BG, Masters SB, Trevor AJ, eds. Basic and Clinical Pharmacology. 11th ed. New York: McGraw-Hill; 2009
  • Longo D, Fauci A, Kasper D, et al (eds). Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2011
  • McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis & Treatment. 49th ed. New York: McGraw-Hill; 2010
  • Moskowitz RW, Altman RD, Hochberg MC et al. (2007). Osteoarthritis: Diagnosis and medical/surgical management.(4th ed) Philadelphia:Lippincot Williams and Wilkins
  • Pagana KD, Pagana TJ eds. Mosby's Diagnostic and Laboratory Test Reference. 9th ed. St. Louis: Elsevier-Mosby; 2009
  • Skidmore-Roth L. ed. Mosby's drug guide for nurses. 9th ed. St. Louis: Elsevier-Mosby; 2011
  • Skidmore-Roth L, ed. Mosby's nursing drug reference. 24th ed. St. Louis: Elsevier-Mosby; 2011
  • Online resource/weblinks:
    • The Merck Manuals
    • RheumInfo
    • The Arthritis Society, Canada


Online Pharmacological Resources:

  • e-therapeutics
  • Lexicomp
  • Rxlist
  • Epocrates Online
  • Canadian Guideline for Safe and Effective Use of Opioids for Chronic Non-Cancer Pain


Journals/Clinical Trials:

  • Altman, R, Asch, E, Bloch, D et al. Development of criteria for the classification and reporting of osteoarthritis, classification of osteoarthritis of the knee.ArthritisRheum 1986; 29:1039
  • Chan FKL, Lanas A, Scheiman J et al. Celecoxib versus Omeprazole and Diclofenac in Patients with Osteoarthritis and Rheumatoid Arthritis (CONDOR).The Lancet, 2010;376:173-179
  • Chappell AS, Ossanna MJ, et al. Duloxetine, a centrally acting analgesic, in the treatment of patients with osteoarthritis knee pain: a 13-week, randomized, placebo-controlled trial. Pain. 2009; 46:253-60
  • Clegg DO, Reda DJ, Harris CL, et al. Glucosamine, Chondroitin Sulfate, and the Two in Combination for Painful Knee Osteoarthritis (GAIT). N Engl J Med. 2006;354:795-808
  • Kopec JA, Rahman MM, Berthelot JM Descriptive Epidemiology of Osteoarthritis in British Columbia, Canada 2006; J Rheumatol 2007;34:386-93
  • Kraus VB. Pathogenesis and treatment of osteoarthritis. Med Clin North Am. 1997; 81:85-112
  • Masuhara, K, Nakai, T, Yamaguchi, K, et al. Significant increases in serum and plasma concentrations of matrix metalloproteinase's 3 and 9 in patients with rapidly destructive osteoarthritis of the hip. Arthritis Rheum 2002; 46:2625
  • Oliveria SA, Felson DT, Reed JI, et al. Incidence of symptomatic hand, hip, and knee osteoarthritis among patients in a health maintenance organization Arthritis Rheum.1995; 38:1134-1141
  • Peat, G, Thomas, E, Duncan, R, et al. Estimating the probability of radiographic osteoarthritis in the older patient with knee pain. Arthritis Rheum 2007; 57:794
  • Rosenberg, ZS, Shankman, S, Steiner, GC, et al. Rapid destructive osteoarthritis: clinical, radiographic, and pathologic features. Radiology 1992; 182:213
  • Silverstein FE, Faich G, Goldstein JL, Simon LS, Pincus T et al. Gastrointestinal Toxicity with Celecoxib vs Nonsteroidal Anti-inflammatory Drugs for Osteoarthritis and< Rheumatoid Arthritis (CLASS Study). JAMA. 2000; 284:1247-55
  • Wong R, Davis AM, Badley et al. Prevalence of Arthritis and Rheumatic Diseases around the World. A Growing Burden and Implications for Health Care Needs. Arthritis Community Research and Evaluation Unit- Models of Care. 2010


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Philip A. Baer, MDCM, FRCPC, Internal medicine (Rheumatology), Chair, OMA Section on Rheumatology, VP, Ontario Rheumatology Association
.......................................... PHARMACY REVIEWER:
Cathy Sochasky, B.Sc.(Pharm), FCSHP, Drug Information Pharmacist, Health Sciences Centre, Winnipeg, MB Canada

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