Pathology of OA Flashcards

1
Q

Name the 6 progressive characteristics of OA?

A
  1. Progressive degradation of articular cartilage
  2. Synovitis (begins as intermittent bouts –> becomes chronic)
  3. Soft tissue length changes (capsular fibrosis)
    o Ligaments
    o Tendons
    o Fibrocartilaginous joint capsule
  4. Formation of new bone at the joint surface and edges (subchondral sclerosis and osteophyte formation)
  5. Cyst formation in the subchondral bone
  6. Collapse of the joint surfaces
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2
Q

What is the clinical presentation of OA?

A
Increased pain 
Joint swelling
Progressive loss of ROM
Muscle inhibition/insufficiency/atrophy
Joint deformity and body enlargement
Functional limitations
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3
Q

What is primary OA?

A

No known cause

Contribution of genetic factors, chondrocyte dysfunction and initiating factors from the bone/synovium

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4
Q

What makes up the cellular components of cartilage?

A

Immature chondroblasts

Mature chondrocytes

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5
Q

What makes up the extracellular matrix of cartilage?

A

water (60%)
Proteoglycans
Collagen

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6
Q

What is the role of chondrocytes?

A

synthesis and maintain the ECM - normal turnover occurs

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7
Q

What is the role of proteoglycans?

A

brush like structure acts as a molecular sponge - to bind water

Protien core with side chains of chondroitin sulphate and keratin sulphate

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8
Q

What is the role and organisation of collagen in cartilage?

A

Hold the ECM and cells in place

 Superficial horizontal collagen fibres
 Intermediate collagen arcade
 Deep vertical collagen fibres

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9
Q

What are the 4 functions fo the hyaline cartilage?

A
  • Low friction self-lubricating surface for joint movement
  • Distribution of load – acts as a shock absorber
  • Protects the subchondral bone
  • Durable, strong and resilient – resistant to wear
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10
Q

How is nutrition supplied to cartilage?

A

Avasular - nutrition via the sweep and squeeze mechanism and the underlying subchondral bone

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11
Q

What is are the two phases of early OA?

A

Cartilage matrix dysfunction and cartilage fibrilation

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12
Q

What occurs during cartilage matrix dysfunction?

A

o Degrading enzymes - produced by chondrocytes and synovial cells
o Cause the break down in structure of proteoglycans –> water is released
o Decreased water content –> softening of the cartilage –> decreased tissue stiffness –> Cartilage becomes less resilient to normal stresses
o Breakdown of collagen fibres –> loosens the collagen arcade –> weakens the cartilage framework
o Cartilage begins to split up

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13
Q

What occurs during the fibrillation phase?

A

o Drying out of the cartilage causes it to be more fragile – breaking off of small parts of collagen
o Tiny particles of cartilage which have broken off cause synovial irritation
o Leads to inflammatory response by synovial membrane –> Increase in synovial cell activity
• Increased amounts of mucin & increased volume and viscosity of the fluid
o Intermittent bouts of this ‘inflammatory synovitis’ causes joint effusion

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14
Q

Why might a patient feel grating or crepitus?

A

Due to fibrillation - as disease progresses there is a change from fine grating to coarse grating

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15
Q

What are the 7 stages of late OA?

A
  1. recurrent and chronic synovitis
  2. progressive and uneven loss of cartilage thickness
  3. fissuring in deep vertical collagen fibres
  4. Increased sclerosis of subchondral bone
  5. Marginal osteophytes
  6. Subchondral cysts
  7. Flattening and collapse of joint surfaces
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16
Q

What occurs as a result of chronic synovitis?

A

Joint capsule fibrosis due to consistent stretch from the swelling

17
Q

What is the result of progressive uneven loss of cartilage?

A
  • Reduced ROM
  • Contraction or lengthening of surrounding soft tissues – resulting in weakness
    • Knee held in loose pack position - Lengthening of quads, Shortening of hamstrings
  • Increased sclerosis of subchondral bone due to increased stress
18
Q

What occurs to cause fissuring of cartilage?

A

increased loss of water means more collagen fibres are displaced - fissures deep vertical collagen fibres - may extend into the bone causing subchondral microfractures

19
Q

What is sclerosis and why does it occur?

A

Increased bone density – since there is no cartilage to distribute load, there is increased load on the underling bone – it compensates by increasing in density

20
Q

What are subchondral cysts?

A

Progression of fissures allows synovial fluid to leak into the bone

21
Q

What is the result of osteophytes?

A

usually form on joint edges - limit the end of ROM

22
Q

What is the presentation of a patient with medial compartment OA knee?

A

Varus deformity

23
Q

What is the presentation of OA hip?

A

FFD

24
Q

Why does degeneration occur during OA?

A

Imbalance in sythesis and degradation of the matrix - due to biomechanics or biochemical changes in the joint

Changes in the loading of the chondrocytes or chondrocyte dysfunction

25
Q

What limits cartilage repair in OA?

A

Sparse arrangements of chondrocytes
Chondrocyte dysfunction
Avascular nature