The document defines osteoarthritis as a progressive loss of cartilage in the joints due to aging, injury, or other factors. It causes pain, stiffness, and loss of movement. Symptoms worsen with activity and weather changes. Treatment focuses on reducing pain, maintaining a healthy weight, and exercising. Medications may help early on but surgery is an option for severe cases unresponsive to other treatments. Lifestyle changes can help prevent further joint damage.

1. Osteoarthritis
By
Blossom Sam
2nd yr BSc Physician Assistant
Global college of AHS
Chennai
03/08/13 1

2. Definition
 Also known as
degenerative joint
disease or “wear and tear
arthritis”.
 Progressive loss of
cartilage with remodeling
of subchondral bone and
progressive deformity of
the joint.
 Cartilage destruction may
be a result of a variety of
etiologies
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3. Epidemiology
 The prevalence increases with age( mostly above 60
years)
 Under 45 yrs it is equally common in men and women
 Over 55 yrs its more common in women than men
 It is not an inevitable part of aging, some people are
more susceptible than others
 A combination of different factors are involved.
 Both mechanical and biologic destructive processes play
a role in OA.
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4. Causes
 Aging
 Heredity
 Obesity
 Joint injuries
 Joint over use
 Playing sports
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5.  Medical conditions that can lead to OA include:
1. Bleeding disorders that cause bleeding in the joint, such
as hemophilia
2. Disorders that block the blood supply near a joint and
lead to avascular necrosis
3. Other types of arthritis, such as chronic gout,
pseudogout, or rheumatoid arthritis
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6. Classification
Primary Secondary
 Idiopathic  Post-traumataic
 Localized or generalized  Congenital or
 Local: knee, hip, spine, developmental
hands  Localized or generalized
 Generalized: large joints  Calcium deposition
and spine disease
 Small peripheral joints  Other:
and spine  Inflammatory
 Mixed and spine  Avascular necrosis
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7. Inflammatory OA
 OA is generally a non-inflammtory arthritis.
 Increasing evidence for inflammatory type: caused by
cytokines, metalloproteinase release.
 This erosive inflammatory type may have flares but later
acts like typical OA.
 Primarily in women
 May be suspected from evidence of active synovitis,
chondrocalcinosis on x-rays, morning stiffness greater
than 30 mins, history of swelling and night pain.
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8. Signs and symptoms
 Pain and stiffness of the joint
 A physical exam can show:
1. Joint movement may cause a cracking (grating) sound,
called crepitation
2. Joint swelling (bones around the joints may feel larger
than normal)
3. Limited range of motion
4. Tenderness when the joint is pressed
5. Normal movement is often painful
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9. Overview of the process
 Articular cartilage gets
disrupted
 Damage progresses
deeper to subchondral
bone
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10.  Fragments of cartilage
released into joint
 Matrix degenerates
 Eventually there is
complete loss of cartilage
 Bone is exposed
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12. Investigation
No single test can diagnose osteoarthritis.
• Medical history
• Physical exam
• X rays
• Other tests such as blood tests or exams of the fluid in
the joints.
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13.  left: Normal x-ray
 Right: worn away cartilage reflected by decreased joint
space
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15. X-ray features
 Radiographic changes visible relatively late in the
disease
 Subchondral sclerosis
 Joint space narrowing especially where there is stress
 Subchondral cysts
 Osteophytes
 Bone mineralization should be normal
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16.  Joint space narrowing
where there is more
stress
 Subchondral bone has
thickened
 bony overgrowth
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17. Clinical features and diagnosis
 Pain
Sources
 Joint effusion and stretching of the joint capsule
 Torn menisci
 Inflammation of periarticular bursae
 Periarticular muscle spasm
 Psychological factors
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18. Characteristics
 Deep, aching localized to the joint
 Slow in onset
 Worsened with activity in initial stages
 Occurs at rest with advanced disease
 May be referred
eg. hip pain referred to the thigh, groin, knee.
 Pain may be aggravated with weather changes
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19. Examination
 Joint line tenderness
 Bony enlargement of joint
 +/- effusion
 Crepitus
 Decreased range of
motion
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20. Involved joints
 DIP, PIP
 1st carpometacarpal
 cervical/lumbar facet
joints
 1st metatarsophalangeal
 Hips
 Knees
Uncommon
 Wrist, elbows, shoulders,
ankles
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21.  1st metatarso-phalangeal most commonly affected in OA
of the foot.
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22. Typical findings
 Heberden’s nodes
 Bouchard’s nodes
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23. Rt: varus deformity of the knee
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24. Treatment
 Osteoarthritis treatment plans can involve:
• Improve joint function
• Keep a healthy body weight
• Control pain
• Achieve a healthy lifestyle.
• Exercise
• Medicines
• Complementary and alternative therapies
• Rest and joint care
• Surgery.
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25. Medications
 Non-pharmacokinetic
 No proven medication-based disease modifying
intervention exists.
 Analgesics (acetominophen)
 NSAIDS
Help pain symptoms but controversial for long term use
in non-inflammatory OA because of risks vs benefits
 Narcotics
 Intra-articular steroids
 Chondroprotective agents
 Anti-depressants
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26. Side effects
 Rash/hypersensitivity
 GI bleeding
 CNS dysfunction in elderly
 Impairment of renal/hepatic/platelet function.
 By interfering with vasodilator renal PG and causing
renal ischemia.
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27. Surgical:
Arthroscopy
 arthroscopy is not recommended for nonspecific
"cleaning of the knee“.
 Used to fix specific structural damage on imaging
(repairing meniscal tears, removing fragments of torn
menisci that are producing symptoms).
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28. Joint replacement
 If all other rx ineffective,
and pain is severe
 Loss of joint function
 Joints last 8-15 years
without complications
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29. Prognosis
 Every person with OA is different. Pain and stiffness
may prevent one person from performing simple daily
activities, while others are able to maintain an active
lifestyle that includes sports and other activities. The
patient’s movement may become very limited over time.
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30. Prevention
 Try not to overuse a painful joint at work or during
activities.
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32. QUESTIONS
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