This document provides information on osteoarthritis (OA), including its pathophysiology, risk factors, clinical presentation, diagnosis, and treatment approaches. It discusses how OA most commonly affects weight-bearing joints in older adults. The goals of treatment are outlined as relieving pain, maintaining mobility, and preserving joint integrity. First-line treatment involves non-pharmacological approaches like education, exercise, and weight loss, along with acetaminophen and topical or oral NSAIDs. For patients who do not respond to initial treatment, options include tramadol, duloxetine, intra-articular corticosteroids, and opioids. Treatment is tailored based on the specific joints affected, with topical therapies emphasized for hand

1. 1
Osteoarthritis

2. Learning objectives
• At the end of this session, the students are expected
to:
– Explain the pathophysiologic mechanisms
involved in the development of osteoarthritis
(OA).
– Identify risk factors associated with OA
– Understand the clinical presentation of OA
– Determine the goals of therapy for individual
patients with OA.
– Formulate a rational treatment modalities for
patients with OA.
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3. Osteoarthritis
• is the most common form of arthritis.
• Weight-bearing joints (e.g., hips and knees) are
most susceptible
• non-weight-bearing joints, especially the hands,
may also be involved.
• Because of its high prevalence & involvement
of joints critical for daily functioning, the
disease causes tremendous morbidity &
financial burden
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4. Osteoarthritis
• the leading cause of chronic mobility disability
and the most common reason for total-hip and
total-knee replacement
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5. Classification
• Primary (idiopathic) osteoarthritis
– The predominant form
– occurs in the absence of a known precipitating event.
– Localized (involving one or two sites)
– Generalized (involving three or more sites)
– Erosive (an erosive pattern of bone destruction)
• Secondary osteoarthritis
– results from congenital or developmental disorders or
inflammatory, metabolic, or endocrine diseases
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6. Epidemiology
• High-income countries, which generally have
older populations, have a higher prevalence
than low-income countries
• The prevalence is greater in women by 1.5-2-
fold & tend to have more generalized disease
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7. Risk factors
• Older age
– The risk of osteoarthritis increases with age.
• Sex
– Women are more likely to develop osteoarthritis, though it isn't clear why.
• Obesity
– Carrying extra body weight contributes to osteoarthritis in several ways, and the
more you weigh, the greater your risk.
– Increased weight puts added stress on weight-bearing joints, such as your hips &
knees.
– In addition, fat tissue produces proteins that may cause harmful inflammation in
and around your joints.
• Joint injuries
• Genetics
– Some people inherit a tendency to develop osteoarthritis.
• Bone deformities
– Some people are born with malformed joints or defective cartilage, which can
increase the risk of osteoarthritis
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8. Pathophysiology
• characterized by damage to diarthrodial joints and
joint structures
• The pathophysiology is multifactorial & typified by
progressive destruction of joint cartilage, erratic new
bone formation, thickening of subchondral bone &
the joint capsule
• The earliest stages are characterized by increasing
water content & softening of cartilage in weight-
bearing joints
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9. Pathophysiology
• As the disease progresses, proteoglycan content of
cartilage declines & cartilage becomes hypo-
cellular
• catabolic proteinases such as protease enzymes
are proliferated which has important role in the
initiation and progression of the disease
• Progressive loss of joint cartilage, subchondral
damage, narrowing of joint spaces, and changes in
the underlying bone and soft tissues may
culminate in deformed, painful joints
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10. Clinical features
• Patients usually are >50 years old.
• Presentation may range from asymptomatic to severe
joint
• pain and stiffness with functional limitations.
• Joint involvement has an asymmetric local distribution
without systemic manifestations.
• In contrast to some other arthritic conditions (eg,
rheumatoid arthritis, gout), inflammation usually is
absent or mild & localized when present
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11. Clinical features
• The most common symptoms are joint pain,
reduced range of motion & brief joint stiffness
after periods of inactivity.
• The cardinal symptoms are use-related joint
pain, typically described as deep and aching in
character& stiffness.
• In advanced cases, pain may be present during
rest.
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12. Clinical features
• Joint stiffness abates with motion & recurs with
rest.
• Joint stiffness generally lasts <30 minutes after
periods of inactivity
• One or more joints may be involved, usually in an
asymmetric pattern.
• Joint examination may reveal local tenderness,
bony proliferation, soft tissue swelling
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13. Diagnosis
• No laboratory tests are specific for diagnosing OA.
• The ESR, hematologic and chemistry panels are usually
unremarkable
• Radiographic changes
– are often absent in early OA.
– As the disease progresses, joint-space narrowing,
subchondral bone sclerosis, and osteophytes may be
detected.
– Gross joint deformity and joint effusions may occur
in late severe OA.
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14. Management
• Goals of therapy
–relieving pain
–maintaining or restoring mobility
–minimizing functional impairment and associated
adverse outcomes (e.g., falls)
– preserving joint integrity
–improving quality of life
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15. Management
• Non-pharmacologic Therapy
–The cornerstone of treatment
–education, exercise, weight loss & cognitive
behavioral intervention are integral
components
• Pharmacologic Therapy
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16. Non-pharmacologic Therapy
• Educational programs include systematic educational
activities designed to improve health behaviors and
health status, thereby slowing OA progression
• Lifestyle modification such as low-impact exercise is
advisable for most patients, especially those with knee
or hip OA.
• weight reduction through a combination of dietary
modification and increased physical activity in
overweight & obese patients.
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17. Non-pharmacologic Therapy
• Application of heat or cold to involved joints improves
range of motion, reduces pain & decreases muscle
spasms
• Surgical intervention
– generally is reserved for patients who fail to respond
to medical therapy and have progressive limitations
in activities of daily living
– In joint replacement surgery (arthroplasty), the
damaged joint surfaces are replaced with metal or
plastic prosthetic devices.
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18. Pharmacologic Therapy
• Acetaminophen
• NSAIDs
• Opioids
• Duloxetine
• Corticosteroids
• Glucosamine and chondroitin
• Topical agents
• Simple analgesics such as acetaminophen &
NSAIDs) are first-line agents
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19. Treatment: Knee and Hip
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❖Acetaminophen Vs. NSAIDs :
❖may be modestly less effective, but it has a lower risk of serious
GI and CVAE and hence is preferred first-line
Up to 4 g/day, should be tried initially (2-3wks) in all
patients if no hepatic problem
• If acetaminophen fails, nonspecific or COX-2 selective
NSAIDs, depending on patient risk factors, as a first-line
option.
• COX-2 selective carry less risk for both minor and serious GI
adverse events
Except Diclofenac!!!

20. Treatment: Knee and Hip
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❖Oral NSAIDS
• Provide superior pain relief in comparison to
acetaminophen, but no NSAID has proven superior to
another.
• The reduced GI risk with COX-2 selectivity persists past 3
to 6 months?
• PPIs and misoprostol significantly reduce the
occurrence of GI adverse events
• Nonselective and COX-2–selectives: pose higher risks for
GI, renal, and ACVE

21. Treatment: Knee and Hip
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CVD and GI/RENAL risk

22. Treatment: Knee and Hip
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❖GI and CVDE risk consideration

23. Treatment: Knee and Hip
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❖Topical NSAIDS-knee
• First-line if the patient fails on acetaminophen
• Preferred over oral NSAIDs for those >75yrs
• Associated with more frequent local (application site)
adverse events compared to oral NSAIDs

24. Treatment: Knee and Hip
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❖Intra-Articular Corticosteroids
❖The most commonly used
1. Triamcinolone acetonide
2. Methylprednisolone acetate.
• The branched esters of triamcinolone and methylprednisolone
are preferred
• Because of the reduced solubility that allows the agents
to remain in the joint space longer

25. Treatment: Knee and Hip
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❖Intra-Articular Corticosteroids
• Alternative first-line when acetaminophen or NSAIDs filed/
suboptimal
• Can also be administered with concomitant oral analgesics
as needed for additional pain control
• Safe and well tolerated
• But should not be administered more frequently than once
every 3 months due to risks of systemic adverse effects

26. Treatment: Knee and Hip
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❖Intra-Articular Corticosteroids
• Lidocaine or bupivacaine are commonly combined to
provide rapid pain relief
• Limited to three or four injections per year
• The patient should minimize activity and stress on the joint
for several days.
• Initial pain relief may be seen within 24 to 72 hours after
injection, with peak pain relief about 7 to 10 days after
injection and lasting up to 4 to 8 weeks

27. Treatment: Knee and Hip
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❖Intra-Articular Corticosteroids
• Systemic AE
• Hyperglycaemia, edema, elevated blood pressure, flushing,
dyspepsia, and hypercortisolism
• Limit corticosteroids dose as doses > 40 mg for
triamcinolone or methylprednisolone have not been
shown to provide any additional benefit.

28. Treatment: Knee and Hip
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❖Tramadol
• Alternative first-line treatment in those who:
1. Failed treatment with scheduled full-dose
acetaminophen and topical NSAIDs
2. Are not appropriate candidates for oral NSAIDs
3. Unable to receive intra-articular corticosteroids.
4. Safely be added to partially effective acetaminophen
or oral NSAID therapy

29. Treatment: Knee and Hip
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❖Second line agents
❖Opioid analgesics
Indications
1. Inadequate response to both nonpharmacologic and first-
line pharmacologic therapies
2. Who are at high surgical risk, precluding joint arthroplasty
• Serious adverse events include falls, respiratory
depression, and addiction

30. Treatment: Knee and Hip
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❖Second line agents
❖Duloxetine
• Adjunctive treatment in patients with a partial response to
first-line analgesics
• A preferred second-line medication in patients with both
neuropathic and musculoskeletal OA pain
• Had demonstrated efficacy primarily as add-on therapy
when there has been less than optimal response to
acetaminophen or oral NSAIDs
• Reduction in pain occurs at about 4 weeks after initiation

31. Treatment: Knee and Hip
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❖Second line agents
❖Duloxetine
❖Dose-related adverse events
• Commonly GI with nausea, vomiting, and constipation being the most
common.
❖The recommended dose is 60 mg po/daily.
❖However, some patients may benefit from higher doses; up to
a maximum dose of 120 mg daily

32. Treatment: Hand OA
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33. Treatment: Hand OA
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❖First line agents
❖NSAIDs
1. Topical NSAIDS
Oral NSAIDs
• Alternatives first line agents in those who
1. Cannot tolerate local skin reactions
2. Received inadequate relief from topical NSAIDs First-
line

34. Treatment: Hand OA
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❖First line agents
❖Capsaicin
• Depletes substance P from afferent nociceptive nerve fibers.
• Substance P has been implicated in the transmission
of pain in arthritis
• Used regularly, and it may take up to 2 weeks to take effect

35. Treatment: Hand OA
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❖First line agents
2. Topical Capsaicin
• Nonprescription product available as a cream, gel, solution,
lotion, or patch in concentrations ranging from 0.025% to
0.15%
• Apply 3-4times/day to the affected joint
• Adverse effects
• Primarily skin irritation and burning
• Alternative for patients not able to take oral NSAIDs.

36. Treatment: Hand OA
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❖First line agents
3. Tramadol
• For patients who do not respond to topical therapy
• Not candidates for oral NSAID treatment because of high
GI, cardiovascular, or renal risks.
• May also be used in combination with partially effective
acetaminophen, topical therapy, or oral NSAIDs
• Monotherapy????

37. Treatment: OA summary
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38. Treatment: OA summary
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❖First line agents
❖NSAIDs
• Topical NSAIDS:

39. Outcome evaluation
• At baseline, assess range of motion of affected
joints & identify activities of daily living that are
impaired.
• In patients treated with acetaminophen or oral
NSAIDs, assess pain control after 2-3 weeks.
–It may take longer for the full ant-inflammatory
effect of NSAIDs to occur.
• Use radiography to assess severity of joint
destruction
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40. Outcome evaluation
• In patients taking oral NSAIDs, monitor for
increases in blood pressure, weight gain, edema and
skin rash
• Evaluate serum creatinine, complete blood count,
and serum transaminases at baseline and at every 6
to 12 months in patients treated with oral NSAIDs
or acetaminophen.
• Perform stool guaiac in patients taking oral
NSAIDs when clinically indicated.
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