Equine Tendon Healing Flashcards

1
Q

I have wings and I have a tail, across the sky is where I sail. Yet I have no eyes, ears or mouth, and I bob randomly from north to south. What am I?

A

A kite

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2
Q

Label tendons of distal equine limb?

A
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3
Q

What is the structural hiearchy of tendon and ligament?

A
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4
Q

Describe the normal ultrasonographic appearance of the metacarpal SDFT and DDFT?

A
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5
Q

Describe the normal ultrasonographic appearance of the palmar pastern?

A
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6
Q

What is the function of the SDFT?

A
  • Function
    • To support the MCP joint
    • Elastic energy store for energy
    • efficient locomotion
    • (to flex the digit –max muscle contraction only 2mm)
  • Loaded early in the stride
  • Subject to very high
    • Stress (1 tonne peak load; 1cm 2 CSA
    • Strain –16% at gallop ( in vitro rupture 12-20%)
    • Strain rate –200%/sec
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7
Q

Discuss superficial digital flexor tendonitis?

A
  • Among the most common musculoskeletal injuries suffered by Thoroughbred racehorses
  • Each training season 10-15% National Hunt and Flat racehorses affected
  • Also common in event horses and showjumpers
  • Frequently career ending (particularly racehorses)
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8
Q

How can SDFT tendonitis be diagnosed?

A

Diagnosis

Observe

  • Characteristic palmar bow

Palpate

  • weight-bearing
  • limb lifted

Assess

  • BOTH LIMBS
  • Heat
  • Pain on palpation
  • Suppleness of tendons
  • Size of tendon
  • Peritendonous oedema
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9
Q

What is the role of diagnostic ultrasonography?

A

Role:

  • Diagnosis
    • Both limbs
    • Echogenicity
    • core lesion
    • CSA
    • Fibre alignment
  • Assessment of severity
    • ~7 days after injury
    • Prognosis
    • initial severity
    • fibre alignment pattern when returns to full work
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10
Q

What can be seen here?

A

typical core lesion (hypo/anechoic regiion in centre of tendon)

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11
Q

What is the consequence of tendon injury?

A
  • Tendon heals (fibroses) after injury but does not regenerate
  • Healed tendon is stiffer as a structure compared to normal tendon
    • Re-injury common
      • 56% for NH horses (Dyson, 2004)
    • Less efficient energy-store
      • poorer performance
  • Aim of treatment should be regeneration
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12
Q

How does tendon adadption work?

A
  • Load induces matrix deformation
  • Tenocytes are able to detect this and through mechanotransduction a cellular response in seen
  • This enables remodelling of the tendon matrix according to imposed loads
  • The result is tendon adaptation
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13
Q

What are Matrix Metalloproteinases?

A
  • Tightly regulated group of proteinase enzymes able to degrade tendon matrix
  • Specific MMPs are able to degrade different components of the matrix
  • Activity regulated by
    • tissue inhibitors of metalloproteinases (TIMPs)
    • whether the molecules are in their active form (zymogens)
    • their location within the matrix
  • Crucial for normal matrix turn-over and repair
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14
Q

How does the immature tendon adapt?

A

Immature tendon adapts to strains levels and exercise as a juvenile

  • Tendon optimised as a ‘ spring ’
    • Increased matrix -> stiffer -> less efficient energy store
    • Decreased matrix -> more elastic -> less efficient energy store
  • Tendon at skeletal maturity sufficient to withstand normal athletic endeavour
    • Sufficient for escaping from predators
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15
Q

Why do tendons fail?

A
  • Degeneration precedes injury
  • Tendon operating close to its functional limit –low tolerance
  • Degeneration in matrix / structural properties dramatically increase risk of tendinopathy
  • Tendon ageing!
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16
Q

What is tendon degeneration?

A
  • Accumulation of microdamage which occurs in the central region of the SDFT
  • Gross mechanical properties of tendon unaffected
  • If not repaired by tenocytes >> accumulation results in clinical injury
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17
Q

Outline the stages of tendon damage?

A

Stage I

  • Tendon matrix degradation
  • Cumulative -‘ageing’

Stage II

  • Fibrillar slippage n breakage of cross-links

Stage III

  • Fibril rupture

Stage IV

  • Complete rupture
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18
Q

Draw a schematic why tendons fail?

A
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19
Q

What are the mechanisms of tendon inflammation and degeneration/cumulative fatigue damage?

A
  • Exercise
  • High number of loading cycles
  • Faster gaits
  • Physical disruption
20
Q

How do abnormal loading events occur?

A
  • Muscle fatigue >> inco-ordination and abnormal loading
  • Fast twitch DDF muscle fatigues earlier >> reduced metacarpophalangeal stabilisation>> abnormal SDFT loading
  • Increased risk of tendon injury at end of race
21
Q

After skeletal maturity tendon loses its ability to adapt –why??

A
  • Aged tenocytes have reduced anabolism
  • Aged tendon has reduced numbers of tenocytes and intercellular communication
    • reduced co-ordinated response to load
22
Q

How does exercise effect the tendon?

A
  • Exercise
  • Energy loss through hysteresis
  • Results in rise in tendon core temperature up to 45ºC
  • Although tenocytes appear relatively “heat resistant”, high Tº >> increased cytokine production
  • Altered physicochemical environment
23
Q

What happens at a cellular level during tendon inflammation?

A
  • The loss of ultimate tensile strength induced by cyclical loading is dependent on the presence of live cells
  • Tissue culture media from cyclically loaded explants have elevated levels of both active and proMMP-2
  • Inhibition of MMP activity prevents loss of UTS
24
Q

Discuss crimp?

A
  • Tendons should have crimp
  • IN FIRST PHASE OF LOADING CRIMPING STRETCHES OUT
  • In older horse they loose that crimp which moves the stress at which they rupture to the left
25
Q

Look at a change in crimp with age?

A
26
Q

Discuss COMP?

A

Cartilage oligomeric matrix protein (COMP)

  • Large pentameric glycoprotein
  • In all ‘ loaded ’ tissues –tendon, ligament, cartilage, meniscus, intervertebral disc
  • COMP accelerates collagen fibril formation
  • Organisational molecule
  • Correlates with mechanical strength at skeletal maturity –high COMP = high strength
27
Q

Discuss COMP variation with age and tendon type and site?

A
28
Q

What is the proposed mechanism for ST ageing?

A
29
Q

In tendon injury what can be seen in the acute inflammatory phase (days)?

A

Clinical signs

  • Lameness
  • Pain on palpation
  • Heat
  • Swelling

Pathology

  • Haemorrhage
  • Inflammation
    • neutrophils
    • macrophages and monocytes
    • increased blood flow
    • oedema
    • proteolytic enzymes
30
Q

In tendon injury what can be seen in the subacute reparative phase (weeks)?

A

Clinical signs

  • Reduction or absence of lameness
  • Resolution of signs of inflammation
  • Tendon still palpably enlarged and soft
  • Signs of re-injury if exercised too early

Pathology

  • Angiogenesis
  • Fibroplasia
    • ++ fibroblasts
    • collagen III
    • small collagen fibrils formed
31
Q

In tendon injury what can be seen in the chronic remodelling phase (months)?

A

Clinical signs

  • Tendon size decreases
  • Tendon less pliable
  • Reduced fetlock extension
  • (Contractures)

Pathology

  • Collagen transformation from III to I
  • Cross-linking
  • Thicker collagen fibrils
32
Q

How should the acute inflammatory phase of tendon injury be treated?

A

Acute phase; anti-inflammatory

Physical therapy

  • application of cold
  • compression bandage
  • MCP joint support
  • rest

Medical treatments

  • NSAID’s
  • Corticosteroids (early)
33
Q

How should the subacute phase of tendon injury be treated?

A

Subacute phase - fibroplasia

Mobilisation

  • early
  • progressive

Regular ultrasonographic monitoring

  • CSA’s
34
Q

How does chronic phase remodelling look like?

A
35
Q

What are some treatments for tendonitis?

A
  • Stem cells (best evidence rate behind it for reducing reinjury but reinjury rates are still high)
  • Bone marrow aspirate concentrate
36
Q

What is the role of stem cells in treating tendonitis?

A

REGENERATION versus REPAIR

Treatment should be aimed at:

  • Making more functional scar tissue
  • Reforming tendon matrix

Intralesional treatment needs to be within month of injury as past this the tendon is just full of fibrous tissue

37
Q

Discuss stem cell therapy?

A
  • Supporting experimental data in vitro and vivo
  • Mechanism of beneficial effect uncertain – synthesis of matrix or orchestration of healing??
  • Cell survival appears to be transient
  • Recent clinical case series supportive of beneficial effects
38
Q

How can prevention or reinjury of the tendon be achieved?

A

Surgery Desmotomy of the ALSDFT

  • ? higher incidence of suspensory desmitis

Prognosis

  • Potential for reduced rate of re-injury
39
Q

How can a support boot be used to prevent reinjury?

A
40
Q

Prevention is better than cure. What methods are there for prevention of tendonitis?

A
  • Maximise the quality of the tendon prior to skeletal maturity
  • Reduce degeneration after skeletal maturity
  • Reduce risk factors for tendonitis
  • (Early detection)
41
Q

Discuss the window of opportunity for maximising tendon prior to skeletal maturity?

A

Can’t improve on pasture exercise in the young animal

42
Q

Look at the effect of early tendon conditioning?

A
43
Q

Summarise recommendations for ‘ tendon training’?

A
  • Pasture exercise vital for tendon development
  • ?Low numbers of high load cycles
  • ?Extra exercise beneficial but tendon also easily injured
  • Different tissues most sensitive to exercise at different ages
  • ?tendon/ligament (?and cartilage) most responsive prior to yearling stage
  • ?bone most responsive at yearling stage
  • In adult, training has no effect on tendon but induces degeneration
    • adult training only for cardiovascular (?and respiratory) systems, bone and muscle
44
Q

How can you reduce tendon degeneration in the adult?

A

Prevent cumulative matrix damage

  • reduce number of damaging loading cycles

Take home message

  • avoid ‘tendon’ training in the adult
45
Q

What are the risk factors related to tendon injury?

A

Related to high impact on tendon

  • Speed
    • ground surface
  • Inco-ordination
    • fatigue
  • Jumping
  • Weight
  • Shoeing
46
Q

What may be used for early detection of tendonitis?

A

Molecular Markers

  • Potentially a more sensitive screening tool for detecting subclinical injury
  • Lots of markers looked at but none yet sufficiently accurate
  • Ongoing area of research