Osteoarthritis Flashcards

1
Q

Osteoarthritis

A

“AKA Osteoarthrosis since no inflammation occurs”
-A common chronic, disabling degenerative joint disease characterised by:
•Progressive softening and disintegration of articular cartilage. The erosion of the cartilage leads to secondary changes in the underlying bone:
•Reactive growth of cartilage
•Cartilaginous outgrowths from the margins of the joint become ossified
•New (reactive) bone growth at the joint margins (osteophytes)
•Capsular fibrosis

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2
Q

OA affects:

A
  • Mainly the weight bearing joints:
    • SC •AC •Hips •Knee •Wrist
  • Distal interphalangeal joints of fingers
  • Joint involvement is asymmetrical
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3
Q

Current OA Definition:

A

A common, age-related, heterogeneous group of disorders characterised pathologically by focal areas of loss of articular cartilage in synovial joints, associated with varying degrees of osteophyte formation, subchondral bone change, and synovitis

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4
Q

OA Pattern 1:

A
  • Begins with an “inflammatory” phase
  • Affects many joints
  • Is the most common pattern
  • Often occurs in middle-aged or older women
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5
Q

OA Pattern 2:

A
  • OA affects a single joint
  • This pattern often occurs in young adults
  • Usually related to an injury or congenital joint abnormality
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6
Q

OA Pattern 3:

A
  • OA affects a few large weight-bearing joints of the leg

* Often occurs in middle-aged people

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7
Q

OA Epidemiology:

A
•20% of elderly males and females have severe OA
•OA is common in some professions eg. coal miners: elbow, golfers 1st met, footballers: knees
•2% have pre-existing bone disposition
•Most do not have predisposing factors
Most common arthritis
•♀>♂
•usually occurs after 45 yrs of age
•Present in 10% of adults
•Present in 50% of adults>60yrs
•20% of adults>70yrs have severe OA
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8
Q

OA/ Articular degeneration Cause:

A

-The exact cause of articular degeneration is unknown
-Articular cartilage in OA has been found to have several abnormalities:
•Change’s to ground substance composition
•Collagen composition is altered
•↑ed activity of matrix-degrading enzymes
•↑ed water content of matrix

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9
Q

OA/ Articular degeneration Current* Cause:

A
  • A recent observation is that the viscosity of the synovial fluid is reduced
  • This results in increased pressure on articulating surfaces, and thus increased wear & tear on cartilage
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10
Q

Factors ] implicated in the development of OA:

A
  • genetic predisposition
  • metabolic influences on cartilage
  • hormonal influences on cartilage
  • pre-existing joint disposition
  • patterns/magnitude of joint usage
  • damage to cartilage
  • weight bearing stresses
  • failure to repair repeated minor trauma
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11
Q

OA Structural Changes

A
  • Primary changes (articular cartilage)
  • Secondary changes (subchondral bone)

Two pathological processes are thought to coexist:
•Initial biochemical changes in the synovial joint articular cartilage resulting in catabolism& accelerated wear of cartilage
•Subsequent reparative processes including low grade inflammation, neovascularisation and fibrosis Walsh DA, (2004) Angiogenesis in osteoarthritis and spondylosis:

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12
Q

Early Changes in OA:

A
  1. Biochemical changes
  2. Altered cartilage wears away more quickly, chondrocytes compensate
  3. Cartilage loss exceeds cartilage replacement. Abnormalities, gradually appear n the articular cartilage of (especially) weight bearing joints.
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13
Q

Early Changes in OA.

1 Biochemical changes:

A

1.Biochemical changes appear in the articular cartilage:
•Increased water content of cartilage matrix
•Proteoglycans: decreased molecular size, Increased rate of synthesis

**These changes are associated with a decrease elasticity and compliance of articular cartilage

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14
Q

Early Changes in OA.

2 Altered Cartilage:

A
  1. Altered cartilage wears way more quickly. Chondrocytes compensate by:
    •Increased metabolic activity
    •Increased cellular turnover results in the release of proteolytic enzymes which cause further damage
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15
Q

Early Changes in OA.

3 Cartilage Loss:

A

3 Cartilage Loss exceeds cartilage replacement. Abnormalities gradually appear in the articular cartilage of (especially) weight bearing joints eg:
•Slight surface irregularity
•Irregular fragmentation (fibrillation) of cartilage - the thinning of cartilage
*similar changes seen in 2nd and 3rd decade of life as part of natural wear and tear.

  • Discrete area of full thickness cartilage loss
  • Continued thinning and degeneration of the articular cartilage
  • Exposed subchondral bone appears as shiny foci on the articular surface “eburnation” (MODERATE CHANGE)
  • Areas of reactive cartilage growth
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16
Q

Early Changes in OA.

Neovascularisation

A

The altered balance between angiogenic & antiangiogenic factors is disturbed, allowing new blood vessels to grow into normally avascular structures such as:
•Articular cartilage
•Intervertebral disc

17
Q

Cartilage degradative products in synovial fluid of OA:

A

Various cartilage degradative products have been isolated in the synovial fluid of osteoarthritic joints:

 * Cartilage fragments
 * Soluble proteoglycan
 * Type II collagen
18
Q

OA Pathogenesis Degradative products stimulate:

A

These cartilage degradative products stimulate local macrophages to release:
•Inflammatory mediators resulting in low grade inflammation
•Growth factors

19
Q

OA Pathogenesis: Role of Monocyte/Mφ’s

A

•Monocyte-derived peptides may also induce increased chondrocyte proliferative activity and matrix degradation

20
Q

OA Pathogenesis: Synovitis

A
  • Angiogenic factors stimulate vascular growth in the osteoarthritic synovium. The synovium becomes hyperaemic & hypertrophied.
  • Linked to poorer clinical outcome
21
Q

Synovitis + Chrondrocytes (Reactive cartilage growth)

A

The inflamed synovium and activated chondrocytes produce excessive:
•cytokines
•inflammatory mediators
•Growth factors Which inhibit cartilage matrix synthesis & promote its degradation

22
Q

OA Pathogenesis: Angiogenesis

A
  • Inflammation can stimulate angiogenesis, and angiogenesis can facilitate inflammation
  • Angiogenesis can also promote chondrocyte hypertrophy and endochondral ossification, contributing to radiographic changes in the joint
23
Q

Angiogenesis definition:

A

•is the formation of new blood vessels. This process involves the migration, growth, and differentiation of endothelial cells, which line the inside wall of blood vessels

24
Q

OA Pathogenesis: Angiogenesis and Neovascularisation

A

Angiogenesis is key in:
•New bone formation in osteophytes
•New bone formation in at the osteochondral junction
•Disease progression

•Additionally, innervation of new blood vessels may contribute importantly to chronic pain

25
Q

OA CF

A
  • Painful joints (worsens with exercise, repetitive use or prolonged inactivity; restricts movement)
  • Stiffness of joints (restricting movement)
  • Swelling of the affected joint
  • Deformity of joint (usually swelling due to osteophytes)
  • Muscle weakness (surrounding affected joints)
  • Crepitus
  • Loss of function
26
Q

Bouchards Nodes

A

Pips

27
Q

Heberdens Nodes

A

Dips

28
Q

Observational OA Changes

A

As the cartilage surfaces erode, the knee collapses causing deformities such as bow-leggedness (varus) or knock knees (valgus), which contribute to pain and functional losses.

29
Q

Osteophytes may cause:

A
  • ↓ed ROM (rare)
  • Ankylosis (rare)
  • Nerve root impingement
  • Heberdens or Bouchards nodes
30
Q

OA Clinical Course Key Features

A
  • Usually presents in middle age, with a slow progression
  • Intermittent course: alternating periods of varying length, characterized by low level/absent ssx, periods of exacerbation
  • Only a few joints are symptomatic at a particular time
  • Joint instability may occur
  • Pain reduces over time, but stiffness and loss of function remain
31
Q

OA Radiographic

A

Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

32
Q

OA X-ray Features: VERTEBRAL JOINTS

A
  1. Facet narrowing & eburnation
  2. Foraminal stenosis
  3. Stenosis of spinal canal
  4. Osteophyte formation
33
Q

Formal Diagnosis of Knee OA

A

Knee pain plus at least three of the following:
•Age greater than 50 years
•Morning stiffness lasting less than 30 min.
•Crepitus
•Bony tenderness of the knee
•Bony enlargement of the knee
•No detectable warmth of the joint to the touch

Laboratory tests and x-rays are often used in addition to these criteria to dx knee OA

34
Q

Formal Diagnosis of hand OA

A

Hand pain plus at least three of the following:
•Bony enlargement of >2 of 10 selected joints
•Bony enlargements of >2 DIP joints
•Fewer than three swollen metacarpophalangeal (MCP) joints
•Deformity of at least one of the ten selected joints Hand OA can often be diagnosed on the basis of these criteria alone; laboratory tests & x-rays may be unnecessary

35
Q

Formal Diagnosis of hip OA

A

Hip pain plus at least two of the following:
•A normal ESR
•The presence of osteophytes on x-rays
•The presence of joint space narrowing on x-rays, indicating a loss of cartilage The dx of hip OA will usually require laboratory tests and x-rays

36
Q

Hypertrophic Osteoarthropathy

Classification

A

Primary: Hypertrophic Osteoarthropathy: Classification
Not associated with other systemic disease

Secondary: Is associated with:

  • lung cancer (usually adenocarcinoma)
  • other tumors (eg, nasopharyngeal cancer)
  • nonmalignant pulmonary disorders
  • right-to-left cardiac shunts
37
Q

Hypertorphic Osteoathropathy

A
  • The pathogenesis is thought to be related to circulatory bypass of the lung
  • One hypothesis is that megakaryocytes escape normal fragmentation in the lung and reach distal extremities, where they release growth factors normally inactivated in the lungs
  • Recently, vascular endothelial growth factor has been implicated in the pathogenesis