Developmental Orthopaedic Disease Flashcards

1
Q

What is endochondral ossification?

A

Starting with a new cartilage template that is going to grow and develop - in utero

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2
Q

What is formed continuously during growth?

A

New cartilage

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3
Q

In which two locations in the bone is endochondral ossification occurring i.e. growth regions?

A
  • Metaphyseal growth plate (Epiphyseal side)

- Articular-epiphyseal cartilage complex

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4
Q

Describe the growth and development of cuboidal bones

A

Have secondary centres of ossification within them and they don’t have a growth plate so they grow by the Articular-epiphyseal cartilage complex mechanism of growth

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5
Q

Describe the histological anatomy of a growth plate

A
  • Resting cartilage
  • Zone of proliferation
  • Zone of hypertrophy
  • Zone of calcification of matrix
  • Matrix reabsorption and ossification
  • Secondary spongiosa
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6
Q

What is required in bone for mineralisation to take place?

A

Blood supply

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7
Q

How could the physeal growth plate malfunction?

A
  • Abnormal deposition of matrix
  • Abnormal mineralisation
  • Poor conversion to bone
  • Retention of cartilage
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8
Q

What are the results of physeal growth plate malfunction?

A
  • Slow growth

- Uneven growth

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9
Q

How could the articular-epiphyseal cartilage complex malfunction?

A
  • Abnormal deposition of matrix
  • Abnormal mineralisation
  • Retention of cartilage
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10
Q

What are the results of epiphyseal cartilage complex malfunction?

A
  • Slow growth
  • Uneven growth
  • Cartilage flaps
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11
Q

Which 3 factors are effected by endochondral ossification abnormalities?

A
  • Rate of growth
  • Direction of growth
  • Health of articular cartilage
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12
Q

Define chondrodysplasia

A

Abnormal endochondral ossification

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13
Q

Define osteochondrosis

A

Cartilage abnormalities

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14
Q

Define osteochondritis

A

Inflammation associated with disease

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15
Q

Define osteochondrosis/ osteochondritis dissecans

A

Cartilaginous or osteochondral flap/defects within the joint

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16
Q

At which stages can abnormalities leading to osteochondritis dissecans occur?

A
  • Disruption of blood supply
  • Abnormal chondrocyte maturation
  • Defective matrix production
  • Persistence of hypertrophic chondrocytes
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17
Q

What are chondrocytes?

A

The only cells found in healthy cartilage.

They produce and maintain the cartilaginous matrix, which consists mainly of collagen and proteoglycans.

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18
Q

What are the 2 consequences of abnormalities leading to osteochondritis dissecans?

A
  • Thickened, retained hypertrophic cartilage

- Disruption of the subchondral bone plate (AECC)

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19
Q

How does a disruption of the blood supply lead to osteochondritis dissecans?

A
  • Affects mineralisation of the subchondral bone
  • Alters biochemical and biomechanical properties of cartilage and subchondral bone
  • Affects ability to adapt to and withstand force (esp. shear)
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20
Q

Describe the pathophysiological steps in osteochondritis dissecans

A

Shear forces and weight-bearing ->
Separation at osteochondral junction ->
Cartilage flaps and fragmentation ->
Exposed subchondral bone

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21
Q

What clinical signs would be expected with osteochondritis dissecans?

A
  • Effusion = filling of the synovial structure with fluid in response to hyperaemia and increased leakiness of the capillaries (main sign)
  • Leads to pain and lameness
  • Osteoarthritis secondary to low grade inflammation caused by an OCD lesion
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22
Q

How does the cartilage appear in osteochondritis dissecans

A

Irregular, raised articular cartilage

23
Q

What are the 4 aetiological causes of osteochondritis dissecans?

A
  • Rapid growth
  • Genetic predisposition
  • Nutrition
  • Trauma
24
Q

What are some causes of rapid growth?

A
  • Genetic potential for growth: Breed, Family lines
    Hormonal influence: Testosterone
  • Nutritional influence: Excess energy and protein, Ca:P imbalances, Cu:Zn imbalances
25
Q

Which radiographic abnormalities will be seen with osteochondritis dissecans?

A
  • Irregular subchondral bone

- Osseous densities: mineralised cartilage, osteochondral fragments

26
Q

Which bone abnormalities most commonly affected horses?

A
  • Osteochondrosis: OCD and Subchondral bone cysts
  • Physitis
  • Angular limb deformities
  • Flexural deformities
27
Q

Which bone abnormalities most commonly affected dogs?

A
  • Osteochondrosis
  • Hypertrophic osteodystrophy
  • Legg Calve Perthes
  • Hip Dysplasia
28
Q

Which bone abnormalities most commonly affected bovine?

A
  • Osteochondrosis

- Flexural deformities

29
Q

Describe the Aetiology of sub-chondral cyst like lesions

A
Abnormal endochondral ossification:
- Retention of cartilage core
- Collapse of cartilage 
Trauma- articular cartilage and SC bone:
- Pressure from synovial fluid
30
Q

What is physitis?

A

Enlargement of the physis

  • Inflammation
  • Disrupted endochondral ossification
31
Q

What are the clinical signs of physitis?

A

Lameness

Stiff gait

32
Q

Which age/spp are prone to hypertrophic osteodystophy?

A

Large breed dogs between 2-8 months of age

33
Q

What is the cause of hypertrophic osteodystrophy?

A

Idiopathic

  • Infection - Viral (CDV) or bacterial
  • Over supplementation with vitamins and minerals
  • Vascular abnormality
34
Q

Describe the pathogenesis of hypertrophic osteodystrophy

A
  • Necrosis of the capillary loops of the cartilage of the metaphyseal physis (blood supply failure)
  • Cuff of metaplastic cartilage and bone
35
Q

What are the clinical signs of hypertrophic osteodystrophy

A
  • Lameness, fever, lethargy, painful bone
  • Primarily long bones – distal aspect
  • Bilateral and symmetric
36
Q

What are some radiographic abnormalities seen in hypertrophic osteodystophy?

A
  • Abnormal bone on diaphyseal side of physis
  • Decreased radiodensity parallel to physis
  • Irregular widening of the physis
  • Sub and extra-periosteal new bone
37
Q

Which age/spp are affected by panosteitis?

A

5-18 months old, Large breeds of dog

38
Q

Describe the pathogenesis of panosteitis

A

Fibrosis of bone tissue

  • Increased osteoblastic and fibroblastic activity
  • Disorganised trabecular formation in subchondral bone
  • Affects the whole bone
39
Q

What is the cause of panosteitis?

A

Idiopathic

40
Q

What are the clinical signs of panosteitis?

A

Acute lameness, shifting (multiple limbs) lethargy, pain

41
Q

What are the radiographic abnormalities seen with panosteitis?

A
  • Increased opacity of medullary cavity
  • Indistinct trabecular pattern
  • Increased endosteal opacity
  • Normal radiolucent bone marrow is much whiter in colour
42
Q

Which spp/age is affected by Legg-Calve-Perthes disease?

A

4-11 months, toy breeds

43
Q

Describe the pathogenesis of Legg-Calve-Perthes disease

A
  • Avascular necrosis of the femoral head
  • Bone remains mechanically stable initially
  • When SCB loses mechanical strength – collapse of articular surface
44
Q

What are the clinical signs of Legg-Calve-Perthes disease

A
  • Acute onset lameness

- Fracture/collapse of the femoral head

45
Q

What radiographic abnormalities are seen with Legg-Calve-Perthes disease

A
  • Osteolysis of femoral head – SCB resorption
  • Collapsed and thickened femoral neck
  • Fracture
46
Q

What is hip dysplasia?

A
  • Genetic predisposition to laxity of the hip joint

- Abnormal anatomy of femoral head and acetabulum

47
Q

Which 3 processes make up canine elbow dysplasia?

A
  • Osteochondritis dissecans
  • Ununited anconeal process
  • Fragmented coronoid process
48
Q

What are the two types of angular limb deformities?

A

Valgus – lateral deviation distally

Varus – medial deviation distally

49
Q

Where are the potential locations for angular limb deformities?

A
  • Metaphyseal growth plate
  • Epiphysis
  • Cuboidal bones
  • Metaphysis
50
Q

Describe angular bone deformities in canines

A
  • Asynchronous growth of a pair of bones
  • Radius and ulna > tibia and fibula
  • Differential growth between bones, after damage to one
51
Q

How does differential bone growth occur in canine angular limb deformities?

A
  • Trauma to growth plate – damage to BVs, replacement of normal tissue with fibrous tissue so the growth plate becomes unfunctional
  • Asynchronous growth: shorter (affected) bone acts to create bowing of longer bone - bend and rotate
52
Q

Describe the pathogenesis of flexural deformities in equine and bovine species

A
  • Disproportionate growth
  • Muscle-tendon unit vs bony skeleton
  • Bone functionally longer
53
Q

What are the two types of flexural deformities in equine and bovine species?

A

Congenital - Newborn foals

Acquired - Rapidly growing foals and yearlings, acute or chronic