Developmental Orthopaedic Disease Flashcards

1
Q

What can cause developmental orthopaedic disease?

A

*Genetics
*Trauma
*Abnormal biomechanics
*Nutrition - mineral deficiency, excessive energy source

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2
Q

What can developmental orthopaedic disease lead to?

A

*Lameness issues
*Welfare concerns
*Reduced production
*Ethical questions around breeding

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3
Q

What are some equine developmental orthopaedic disease?

A

*Osteochondrosis
*Physitis
*Angular limb deformities
*Flexural deformities

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4
Q

What are some canine developmental orthopaedic disease?

A

*Osteochondrosis
*Angular limb deformities
*Hip / elbow dysplasia
*Legg calve perthes disease
*Hypertrophic osteodystrophy

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5
Q

What are developmental orthopaedic diseases of production animals?

A

*Osteochondrosis
*Angular limb deformities
*Flexural deformities

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6
Q

What can disturbance in one or more component of endochondral ossification lead to?

A

*Alter rates of growth
*Affect direction of growth leading to abnormal angulation (e.g. valgus/varus)
*Lead to dysfunction of cartilage (Abnormal cartilage development

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7
Q

What are possible factors of developmental orthopaedic disease?

A

*Rapid growth - large, fast-growing breeds
*Nutrition - high energy / protein intake
*Mineral imbalance - excessive calcium / phosphorus, Low copper diets
*Trauma / abnormal exercise loads
*Genetic predisposition

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8
Q

What is the pathogenesis of osteochondrosis?

A
  1. Premature interruption to vascular supply
  2. Abnormal chondrocyte maturation
  3. Defective matrix production
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9
Q

What does disruption to vascular supply to cartilage cause?

A

*Leads to islands of retained / necrotic cartilage - similar to OC-lesions

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10
Q

What does abnormal cartilage maturation cause?

A

*Chondrocytes from osteochondritic lesions show signs of up-regulation then loss of viability
*Abnormally elevated signalling pathways affect maturation+ ossification in cartilage and subchondral bone

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11
Q

How does defective extracellular matrix production occur?

A
  • Increased ECM production around activated chondrocytes involved in early repair process in OC-lesions
  • Alterations in collagen expression from chondrocytes in OC-lesions may lead to abnormal biomechanical properties
  • Increased expression of proteases (cathepsins) in OC-lesions
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12
Q

What does osteochondrosis involve?

A

1.A vascular incident leading to cartilage island retention
2. A reparative phase which exhausts the chondrocytes and then failure to undergo hypertrophy and apoptosis as part of normal endochondral ossification
3. The reparative response results in abnormal extracellular matrix production and enzyme release which affects the biochemical and hence biomechanical properties of cartilage
4. Cartilage is then prone to separation/fragmentation (e.g. OCD) or infolding to form a cyst (e.g. OCLL)

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13
Q

What presentation of osteochondrosis is seen with shear forces across the cartilage?

A

Fragmentation / flaps are found

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14
Q

What presentation of osteochondrosis is seen with compressive forces?

A

Cysts are found = OCLL

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15
Q

How is osteochondrosis diagnosed?

A

*Signalment - young fast growing animals
*CLinical signs
*Diagnostic imaging

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16
Q

What are the clinical signs of osteochondrosis?

A

–Lameness, joint swelling,
focal joint pain
–Poor performance
–Poor production/failure to
thrive

17
Q

What would be seen on diagnostic imaging with osteochondrosis?

A

– Radiography
* Irregular subchondral bone surface/defects
* Osteochondral fragmentation (OCD)
* Radiolucent cystic lesions (OCLL)
– (Ultrasound)
* Cartilage/subchondral bone quality

18
Q

How is osteochondrosis managed?

A
  • Conservative management
    – Some young animals may improve/resolve
    – Dietary alteration
  • Reduce energy intake, correct mineral imbalances
    – Rest/reduce exercise-induced trauma
    – Intra-articular medication
  • e.g. corticosteroids to reduce synovitis
  • Surgical management
19
Q

What is physitis?

A

Swelling around growth plates in young animals

20
Q

What can physitis be secondary to?

A

*Trauma
*Over-exercise
*Over-loading limb

21
Q

What are the clinical signs of physitis?

A

*Focal heat, swelling and pain over physeal region
*May have concurrent angular / flexural limb deformity
*Stilted gait, lying down, lameness

22
Q

How is physitis diagnosed?

A

Radiography

23
Q

How is physitis managed?

A

*Rest
*NSAIDs
*Reduce energy intake
- usually self-limiting

24
Q

What is valgus / varus?

A

Valgus = lateral deviation distally
Varus = medial deviation distally

25
Q

What is the aetiology of angular limb deformities? (Valgus/Varus)

A

*Congenital - born with ALD
*Acquired - acquires ALD from
-period of rapid growth
-trauma to growth plate
-contralateral limb issue

26
Q

What are the causes of ALD in horses?

A

*Cuboidal bone hypoplasia
*Periarticular laxity
*Asymmetrical physeal growth

27
Q

What does cuboidal bone hypoplasia occur in? What should be done + why?

A

*Premature / dysmature foals
*High risk of crushing injury = protect limb (splint) until ossification

28
Q

What does periarticular laxity occur in? How is it treated?

A

*Young foals
*Resolves with age, controlled exercise + glue on extensions

29
Q

What are the common presentations of asymmetrical physeal growth? How is it treated?

A

*Carpal Valgus (FL)
*Fetlock varus (HL)
*Conservative tx = trimming / glue-on shoes
*Surgical tx = Periosteal strip / transphyseal bridge

30
Q

What are congenital flexural limb deformities common in? What are the causes + how is it treated?

A

*Common in new-born calves
-Intra-uterine positioning
-large foetus
-feed toxins
-hereditary
*TX = physical therapy + Bandaging

31
Q

What is the pathogenesis of acquired flexural deformities?

A

– Disproportionate growth between muscle-tendon unit vs bony skeleton
– Bone functionally longer (not “contracted tendons”)
– Described in relation to joint affected: i.e. DIPJ, fetlock or carpus

32
Q

How is acquired flexural deformities managed?

A

– Trimming/toe extensions
– Pain relief/exercise
– Surgery

33
Q

What are other forms of developmental orthopaedic disease?

A
  • Dysplasia
    – e.g. hip/elbow in dogs
    – e.g. shoulder dysplasia in Shetlands
  • Legg Calve Perthes disease
  • Hypertrophic osteodystrophy
  • Cervical vertebral malformation