Osteoarthritis (OA)



Thanks to Dr. Philip A. Baer, MDCM, FRCPC, Internal medicine (Rheumatology), Chair, OMA Section on Rheumatology, VP, Ontario Rheumatology Association, ON Canada, and Sadie Sattan, RN, BScN, MN, School of Nursing, Faculty of Health Sciences, McMaster University/Mohawk College, Hamilton, ON Canada for their expertise with the initial review of this topic.


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


Biomechanical, biochemical, inflammatory, and immunologic factors are all 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

Factors contributing to development of disease:

  • Excessive use or stress on a joint
  • Genetic predisposition
  • Other factors include:
      • Congenital structural defect
    • Metabolic disturbance
    • Repeated intraarticular hemorrhage
    • Neuropathic arthropathies


  • 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 of age
  • 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


  • 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 initiation of repair through chondrocyte activation, and 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

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
Clinical Manifestations:

Main symptom is pain, which typically increases with activity and relieved by rest

  • Gradual onset
  • Morning stiffness always <20-30 minutes
  • Crepitations may be noted with movement of joint
  • Joint involvement progresses slowly and irreversibly, and is related to the specific joint involved
  • In advanced disease, sleep may be disrupted because of nocturnal pain
  • Increasing pain is accompanied by progressive loss of function
  • Body coordination and posture may be affected as a result of pain and loss of mobility
  • Advanced disease is complicated by gross deformity and subluxation (partial dislocation) caused by deterioration of cartilage, collapse of subchondral bone and extensive bony overgrowth
  • The joints that are commonly involved include:
    • Distal and first interphalangeal joint(s) of the fingers, hips, knees and lower lumbar and cervical vertebrae
  • Nodules – Herberden’s nodules are common, especially in women with primary osteoarthritis (OA). These nodes are reactive bony overgrowths located at the distal interphalangeal joints. Bouchard’s nodes are less common in OA and involve the proximal interphalangeal joints. Both Herbeden’s and Bouchard’s nodes may present with redness, swelling, tenderness and aching. They often begin in one finger and spread to others
  • Hips – OA of the hips may be tremendously disabling. Loss of range of motion (ROM) is significant with increased limitation of extension and internal rotation
  • Knees – Softening of the posterior surface of the patella is most commonly observed in young people. Degeneration of weight-bearing surfaces is usually observed in older women and is associated with limitation of motion, crepitus and flexion deformity
  • Vertebral column – OA in spine may cause localized stiffness and pain. Herniation of the degenerating intervertebral discs may lead to muscle spasm or radicular pain

Differences in symptomatology with or without inflammation

Workup and Diagnosis

Patient usually present with complain of deep pain of the joints.

Inquire about:

  • Location of pain, quality, intensity and relation to activity
  • History of joint trauma
  • Presence of diabetes, acromegaly, gout or other forms of inflammatory arthritis
  • Family history of arthritis
  • Morning stiffness always <20-30 minutes
  • Crepitations may be noted with movement of joint
  • Work or hobby-induced trauma through repetitive stressful joint movements e.g. dancers
  • Smoking

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 the 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:

  • 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 2000×109/L)

Imaging Studies:

  • Usually recommended for persistent unexplained pain
  • Always specify the X-rays are for OA
  • X-ray of affected joints typically shows:
    • 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)
RN/Medical Management:

Goal is to relieve pain, stabilize and optimize joint functions, by combining both pharmacological and non-pharmacological modalities

Patients with OA will need to:

  • Balance between rest and activity
  • Use joint protection measures to improve activity tolerance
  • Modify the home and work environment to include work-saving and joint-protecting assistive device
  • Perform ROM, muscle-strengthening and aerobic exercise regularly

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:

  • The combination of diet and exercise is effective in reducing weight and disease progression hence improve joint pain and function

2. Rest:

  • Recommended when acute pain and inflammation are present (~12 to 24 hrs)
  • Prolonged rest may lead to muscle atrophy and restricted joint movements hence pacing of activities is important
  • Pacing of activities is important

3. Physical therapy and assistive devices:

  • May help to improve outcome and decrease pain by:
    • Improving flexibility
    • Strengthening muscles
    • Reducing load on the affected joints by assistive devices (orthotics, cane, braces)
  • Unloading the joints: Use of cushioned, supportive shoes can decrease the joint load on impact
  • Manual therapy Stretching and joint manipulation may be beneficial for hip OA
  • Braces and splints: Useful for symptomatic improvement
  • Patellofemoral syndrome: Occurs due to patellar misalignment. Symptomatic benefits can be achieved with knee bracing and taping as well as quadriceps strengthening

4. Exercise:

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

  • Exercise programs: High intensity aerobic exercise program benefit those with mild disease
  • Symptomatic relief: Motion and strengthening exercises can reduce pain and increase mobility in patients with OA
  • Joint protection: Can be achieved by exercising in warm water
  • Disability prevention: Exercise does not need to be intense in order to improve mobility and disability. The benefits that can be achieved are:
    • Improvement in pain and mobility
    • Reversal of muscular atrophy
    • Increase bone mineral density, which decreases the risk of osteoporotic fractures
  • Aerobic versus resistance (strengthening) exercise: Both have moderate effects on pain and range of motion

5. Group exercise programs:

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

6. Patient compliance:

  • Simplifying regimens and setting attainable goals
  • Emphasize and educate 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 lasts for 1-3 months)
  • Viscosupplementation for knee joint-requires 1-3 injections although expensive, show 60-75% response, and effect lasts upto 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

For mild to moderate disease consider the following analgesic options:

  • Acetaminophen up to 1000 mg PO QID for the short-term. 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:

  • Duloxetine can be use in knee OA
  • Recommended dose: 60 mg/day

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


  • Topical NSAID use may reduce the side effects of oral NSAIDs


  • Intra-articular depot corticosteroids help relieve pain and increase joint flexibility. The amount of agent generally used depends on the size of the joint. Methylprednisolone 10 mg in small joints while 40 mg in large joints like hip Joint
  • Hyaluronate and hylan G-F 20, agents known as viscosupplements, administered over time through intra-articular injections into the knee, known to have some benefits
  • Triamcinolone acetonide extended-release intra-articular injection is a nonopioid that provides knee pain relief over 12 weeks

C) Surgical intervention:

Only recommended when pain becomes intolerable and mobility is compromised leading to poor quality of life. Options include

  • Osteotomy
  • Debridement and joint fusion
  • Arthroscopy and arthroplasty

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 the 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 <50 mL/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 up to 2 g PO in 2 divided doses

Renal impairment:

  • ClCr 30-49 mL/minute: 750 mg/day may increase up to 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: Maximum 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 a 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 days 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)

  • 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


  • 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:

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

Triamcinolone hexacetonide:

  • 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 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


  • 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, et al. 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 tablets 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
Diagnosis and Goals:


  • Acute or chronic pain related to joints
  • Pain related to physical activity and lack of knowledge of pain self-management techniques
  • Sleep disturbance due to pain
  • Reduced physical activity (impaired mobility) affecting daily routine due to pain
  • Impaired physical mobility related to weakness, stiffness and/or pain on ambulation
  • Self-care deficits (bathing, grooming, cleaning) related to pain and limited joint movement
  • Altered nutrition: Less than usual body requirements since intake related to energy output
  • Self-esteem disturbance related to changing social and work roles


  • Reduce pain and improve function of the joints
  • Optimize physical activity and prevent further articular damage
  • Patient education
Nursing Intervention:

Relieving pain

  • Advice patient to take prescribed NSAIDs or OTC analgesics as directed to relieve inflammation and pain. May alternate with opiod analgesic, if prescribed
  • Avoid excessive use stabilize involved joints by:
    • Use of splints, braces, collars and corsets for support
    • Taking time out for rest periods
  • Avoid activities that may cause pain
  • Heat may be applied for muscle spasm and stiffness, but not for prolong periods as this may induce inflammation and flare ups
  • Poor posture may lead to chronic pain and muscle tension; teach correct posture and body mechanics
  • To avoid stress on hip and knee joints consider using crutches or braces
  • Teach use of cane in hand on side opposite to the involved hip/knee
  • For foot disorders, corrective shoes and metatarsal supports should be advised
  • Encourage weight loss – provide nutritional counseling for weight reduction
  • Assist the patient and family in overcoming feelings of helplessness and encourage active participation in managing chronic symptoms
  • The correct combination of joint protection, exercise (ROM – isometric and isotonic), heat and cold therapy and medication can restore self-esteem and improve physical functioning

Increasing physical mobility:

  • Physical activity and joint mobility should be maintained without causing stress or pain to the affected joint
  • Teach isometric and graded exercises to improve muscle strength around the involved joint
  • Advise to move joints by doing ROM exercises after periods of inactivity (e.g. automobile ride)

Promote self-care:

  • Performing activities in morning, after stiffness has been alleviated; and before pain starts
  • Adopt lifestyle modifications such as wearing loose clothes without buttons, placing bench in tub or shower for bathing, sitting at table or counter in kitchen to prepare meals
  • Help with obtaining assistive devices, such as padded handles for utensils and grooming aids, to promote independence
  • Refer to occupational therapist (OT) for additional assistance if required

Patient education and health maintenance:

  • Suggest swimming or water aerobics or walking
  • Encourage adequate diet and sleep to enhance general health.
  • Refer for additional information and support to the Arthritis Foundation (www.arthritis.org) and The Arthritis Society, Canada (www.arthritis.ca)
  • Safety measures includes, removing scatter rugs, providing rails at stairs and bathtub, using night-lights, and wearing well-fitted shoes
  • Assistive devices such as canes, walkers, elevated toilet seats, and grab bars reduce joint load and promote safety
  • Sexual counseling helps the patient and loved one to enjoy physical closeness by learning to adapt positions, alter timing, and increase awareness of the partner’s needs
  • Teaching should include information about the nature and treatment of the disease, pain management, correct posture, body mechanics, correct use of assistive devices such as cane or walker, principles of joint protection and energy conservation, and a therapeutic exercise program
  • Home care goals should be individualized to meet the patient’s needs. Family and social support should be included in goal setting and education
Nursing Alerts:
  • Elderly patients are at greater risk for GI bleeding and renal failure associated with NSAID use
  • Encourage administration with meals, and monitor stool for occult blood. Some NSAIDs are also associated with development of hypertension
  • Monitor BP in patients taking NSAIDs and if required inform the treating physician


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
  • Gomoll A, Spitzer A, Richmond JC, et al. Repeat administration of triamcinolone acetonide extended-release affords consistent, clinically relevant improvements in pain: results from a phase 3B, single-arm, open-label study. Osteoarthritis and Cartilage, Volume 27, S505 – S506. doi: https://doi.org/10.1016/j.joca.2019.02.570
  • Gray J, ed. Therapeutic Choices. Canadian Pharmacists Association. 6th ed. Toronto: Webcom Inc. 2011
  • Harris H, Crawford A. Recognizing and managing osteoarthritis. Nursing. 2015;45(1):36-43. doi:10.1097/01.NURSE.0000458918.87973.15
  • Katzung BG, Masters SB, Trevor AJ, eds. Basic and Clinical Pharmacology. 11th ed. New York: McGraw-Hill; 2009
  • Kodadek M. Managing osteoarthritis. Nursing for Women’s Health. 2015;19(1):71-76. doi: 10.1111/1751-486x.12178
  • 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
  • Ryan S. Managing lifestyle factors in adults with osteoarthritis. Nurs Stand. 2015;29(46):43-50. doi:10.7748/ns.29.46.43.e994
  • 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
  • Evaniew AL, Evaniew N. Knee osteoarthritis: Therapeutic alternatives in primary care. World J Orthop. 2017;8(2):187-191. Published 2017 Feb 18. doi:10.5312/wjo.v8.i2.187
  • 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