Lecture 7 - Meniscus, Tendons and Ligaments Flashcards

1
Q

What are menisci?

A

Fibrocartilaginous structures existing in a number of joints (e.g. knee)

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2
Q

Menisci in the knee: Morphology + where do they exist?

A

Two crescent-shaped wedges of fibrocartilage
–> wedge shaped in cross-section

Between femoral condyles and tibial plateau

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3
Q

What is the difference between the red zone and the white zone in knee menisci? What proportion is red zone?

A

Red zone = well vascularised
–> peripheral 10-30% medial, 10-25% lateral

White zone = avascularised, receives nourishment from synovial fluid

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4
Q

Composition of menisci?

A
  • 60-70% water (higher in younger)
  • 15-25% collagen (type I)
  • 1-2% PGs
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5
Q

What is the layered structure of menisci?

A
  1. Superficial network
    - surface layer
    - random mesh-like woven matrix –> v smooth, fine fibrils
  2. Lamellar layer
    - rope-like collagen fibre bundles arranged circumferentially
    - smaller radial fibres
  3. Central layer
    - Randomly arranged collagen and PG
    - similar to hyaline cartilage
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6
Q

What are the menisci formed from and what is the timeline?

A

Menisci are formed from mesenchymal cells –> cells arise from the perichondrium and cartilage

Week 8 - distinct structrues
Weeks 8-16 - distinct alignment of cells and beginnings of ECM
Further development - cell numbers decrease and collagen matrix becomes more dominant

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7
Q

Role of the menisci (6)

A
  1. Distribute axial load
    - hoop stresses generated
    - axial load converted to tension in the circumferential fibres
  2. Reduce contact stresses
    - increase area
  3. Increase joint stability
    - acts as a wedge –> blocks tibial plateau
    - circumferential fibres have multidirectional stabilising function
  4. Contributes to joint lubrication
    - may compress synovial fluid into cartilage
  5. provides nutrition to articular cartilage
    - system of microchannels through menisci to cartilage
  6. Assists with proprioception
    - mechanoreceptors
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8
Q

How do the kinematics vary between the lateral and medial menisci?

A
  • Lateral meniscus is more mobile than the medial (11.2mm vs 5.1mm movement)
  • radius decreases with flexion
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9
Q

Meniscal tears: occurence, symptoms and types?

A

Occurence:

  • most common knee injury
  • 61 per 100,000 (medial tears 2x more common)
  • twisting on a loaded flexed knee (younger), isolation/association with other injury, degenerative process

Symptoms:

  • pain
  • swelling
  • clicking
  • giving way
  • locking

Types:

  • partial / complete
  • longitudinal (81%)
  • flap
  • degenerative
  • radial (e.g. from operative tumour)
  • horizontal
  • bucket handle
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10
Q

Meniscal repairs:

A
  • structure never fully restored –> some are also difficult to repair

Partial meniscectomy:

  • remove minimal tissue
  • ensure smoothness and stability of remaining tissue –> stops tear from propagating
  • done arthroscopically
  • results in less wear

Meniscectomy:
- leads to progressive articular wear –> higher OA risk

Replacement:

  • allograft transportation (cadaver)
  • collagen meniscal implant (meniscal implant regrows into scaffold
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11
Q

What are tendons?

A
  • dense connective tissues
  • connect muscles to bone
  • transmit tensile force from muscle to bone (allow you to move)
  • store elastic energy
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12
Q

What are ligaments?

A
  • dense connective tissue
  • connect bone to bone
  • stabilise joints
  • prevent excessive motion
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13
Q

Tendon and ligament components:

A

Cells:
- fibroblasts (rod shaped, arranged in rows –> synthesise collagen and ECM)
Matrix:
- water
- collagen (1&3)
- ground substance (PGs bind fibrils together)
- elastin

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14
Q

How is the amount of elastin varied in tendons vs ligaments and why?

A

Elastin in ligament is variable

Very little elastin in tendon
- tendons need to be still as they are transmitting force from muscle –> don’t want muscle energy going into stretching

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15
Q

How do the collagen fibres arrange in ligaments vs tendons and why?

A

Ligament:

  • smaller diameter fibres
  • collagen more randomly organised
  • -> stress in multiple directions - stability function

Tendon:

  • large parallel fibres
  • uniform insertion into bone
  • -> force from muscle to bone is a single vector - don’t need support in other directions
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16
Q

What are the three structures of a tendon?

How are tendons inserted?

A

Endotenon:

  • connective tissue - holds fascicles together
  • allows longitudinal movement of fasicles

Paratenon:

  • surrounds tendon
  • vascular connective tissue

Epitenon:

  • under paratenon at high friction locations
  • produces synovial fluid

Insertion:
Endotenon continues into bone/periosteum and perimysium

17
Q

Where does the blood supply come from in vascular and avascular tendons?

A

Vascular - surrounded by paratenon which supplies blood

Avascular - blood supply from synovial diffusion
–> compressive stresses - like cartilage

18
Q

Ligament: what is the mechanism of direct and indirect insertion?

What zones exist with direct insertion?

A

Direct:

  • superficial fibres join periosteum
  • deep fibres join bone

Indirect:

  • superficial fibres join periosteum
  • v few deep fibres

Direct insertion zones:

  • ligament
  • fibrocartilage
  • mineralised fibrocartilage
  • bone
19
Q

Vascularity in the ligament

A
  • very limited

- microvessels from insertion site provide nutrients

20
Q

Force-deformation mechanics of the tendon/ligament:

3 regions

A

(non-linear elastic behaviour –> different amounts of ‘crimp’ bear load at different points)

Toe region:

  • stretches easily
  • straightening of crimped collagen fibrils
  • reorientation of fibres in direction of loading

Linear region:
- 95% elastic strain energy recovered –> efficient, do not lose energy

Yield and failure region:

  • irreversible damage
  • unpredictable
21
Q

Ligament and Tendon:

Elastic modulus?
UTS?
UTstrain?

Tendon is ___ times stronger in tension than muscle - what is the impact of this?

A

Ligament:
E = 400MPa
UTS = 80MPa
UTs = 12%

Tendon:
E = 1.2-1.8GPa
UTS = 50-125MPa
UTs = 9-35%

Tendon - v high tensile strength –> 3x stronger in tension than muscle ==> more likely to injure muscle

22
Q

Factors affecting the biomechanics of tendons/ligaments (5):

A
  1. Specimen orientation
    - properties = highly directionally dependent
  2. Level of stress experienced - location/type
    - E flexor > E extensor
  3. Hydration (usually 60-80%)
    - decreased hydration = increased stiffness
  4. Temperature
    - increase creep (e.g. isometric contraction - tendon stretches, muscle contracts)
    - decrease stiffness
  5. Strain rate
    - viscoelastic
    - -> creep
    - ->stress relaxation
    - ->strain rate (higher = higher UTS))
    - ->hysteresis (continually decreasing stress with cyclic loading - protects ligament from fatigue failure - i.e. for same strain, get lower stress)
23
Q

What is hysteresis?

A

Energy dissipation - the difference between the loading and unloading curve = the energy lost during loading

–> more energy required in loading than unloading

24
Q

Club foot - what is it?

A

Tight tendons and ligaments prevent the foot from stretching into the right position

Casting + splinting for 3-4yrs

25
How does the loading rate effect failure of ligaments?
Slow loading rate: - bony insertion = weakest - load to failure decreased by 20% Fast loading rate: - ligament is weakest component With increased loading rate, bone increases in strength more than ligament
26
Quasilinear elastic theory: What does it describe? What is the function?
Describes time and history-dependent properties: Stress relaxation function describes stress as a function of time and elastic response in tendon/ligament: σ(t) = G(t) σ exp(ε) [MPa] G(t) = 0.86-0.05ln(t) --> component accounts for the time-dependent stress response (stress relaxation function) - decrease in stress with time σ exp(ε) = 9.7(exp(49.8ε) - 1) --> component accounts for the elastic response (dependent on strain and not on time) - creates increase in force as flexion occurs
27
Effects of ageing on ligaments/tendons (4):
- Stiffness and elastic modulus increase up until skeletal maturity - # and quality of crosslinks increase - collagen fibre diameter increases - UTload decreases (1.3-3.3x higher in younger)
28
Effects of mobilisation/immobilisation on ligaments/tendons:
Mobilisation: - increase strength and stiffness - increase in collagen fibre bundle diameter - increase collagen cross-linking Immobilisation: - decrease in modulus / ultimate stress
29
Tendon injury (5)
Tendonosis (chronic tendonitis) - chronic degradation - damage at cellular level - no inflammation Tendonitis - inflammation due to acute injury Peritendinitis - inflammation of tendon sheath Direct: Laceration - e.g. cutting Indirect: tensile overload - e.g. ruptures at junction NB: most injuries occur at muscle-tendon junction or insertion to bone (rarely mid-substance)
30
Ligament injury
Sprain | - overstretched, partially torn, completely torn
31
Repair vs Regeneration
Regeneration = normal tissue re-established Repair = structure healed - scar tissue - abnormal composition and microstructure - inferior mechanical properties
32
Extrinsic vs Intrinsic healing
Extrinsic - tough scar tissue enveloping injury - harmful effect of adhesions Intrinsic - formation of longitudinal aligned collagen fibres within the substance - minimal adhesions
33
Challenges to repair for tendon/ligament (4):
- Difficult to restore normal mechanical function - relatively avascular - not just a process of restoring continuity --> also need healed tissue to glide in tissue - most injuries occur at muscle-tendon junction / insertion to bone --> rarely mid-substance
34
Three effects of viscoelasticity
Creep: - increasing deformation under constant load - e.g. isometric contraction Stress relaxation: - reduction in stress under constant deformation Strain rate: - elongation depends on rate of force application - higher strain rate = higher UTS Hysteresis: - energy dissipation - difference between loading and unloading curve represents amount of energy lost during loading