Lecture 7 - Meniscus, Tendons and Ligaments Flashcards
What are menisci?
Fibrocartilaginous structures existing in a number of joints (e.g. knee)
Menisci in the knee: Morphology + where do they exist?
Two crescent-shaped wedges of fibrocartilage
–> wedge shaped in cross-section
Between femoral condyles and tibial plateau
What is the difference between the red zone and the white zone in knee menisci? What proportion is red zone?
Red zone = well vascularised
–> peripheral 10-30% medial, 10-25% lateral
White zone = avascularised, receives nourishment from synovial fluid
Composition of menisci?
- 60-70% water (higher in younger)
- 15-25% collagen (type I)
- 1-2% PGs
What is the layered structure of menisci?
- Superficial network
- surface layer
- random mesh-like woven matrix –> v smooth, fine fibrils - Lamellar layer
- rope-like collagen fibre bundles arranged circumferentially
- smaller radial fibres - Central layer
- Randomly arranged collagen and PG
- similar to hyaline cartilage
What are the menisci formed from and what is the timeline?
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
Role of the menisci (6)
- Distribute axial load
- hoop stresses generated
- axial load converted to tension in the circumferential fibres - Reduce contact stresses
- increase area - Increase joint stability
- acts as a wedge –> blocks tibial plateau
- circumferential fibres have multidirectional stabilising function - Contributes to joint lubrication
- may compress synovial fluid into cartilage - provides nutrition to articular cartilage
- system of microchannels through menisci to cartilage - Assists with proprioception
- mechanoreceptors
How do the kinematics vary between the lateral and medial menisci?
- Lateral meniscus is more mobile than the medial (11.2mm vs 5.1mm movement)
- radius decreases with flexion
Meniscal tears: occurence, symptoms and types?
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
Meniscal repairs:
- 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
What are tendons?
- dense connective tissues
- connect muscles to bone
- transmit tensile force from muscle to bone (allow you to move)
- store elastic energy
What are ligaments?
- dense connective tissue
- connect bone to bone
- stabilise joints
- prevent excessive motion
Tendon and ligament components:
Cells:
- fibroblasts (rod shaped, arranged in rows –> synthesise collagen and ECM)
Matrix:
- water
- collagen (1&3)
- ground substance (PGs bind fibrils together)
- elastin
How is the amount of elastin varied in tendons vs ligaments and why?
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
How do the collagen fibres arrange in ligaments vs tendons and why?
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
What are the three structures of a tendon?
How are tendons inserted?
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
Where does the blood supply come from in vascular and avascular tendons?
Vascular - surrounded by paratenon which supplies blood
Avascular - blood supply from synovial diffusion
–> compressive stresses - like cartilage
Ligament: what is the mechanism of direct and indirect insertion?
What zones exist with direct insertion?
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
Vascularity in the ligament
- very limited
- microvessels from insertion site provide nutrients
Force-deformation mechanics of the tendon/ligament:
3 regions
(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
Ligament and Tendon:
Elastic modulus?
UTS?
UTstrain?
Tendon is ___ times stronger in tension than muscle - what is the impact of this?
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
Factors affecting the biomechanics of tendons/ligaments (5):
- Specimen orientation
- properties = highly directionally dependent - Level of stress experienced - location/type
- E flexor > E extensor - Hydration (usually 60-80%)
- decreased hydration = increased stiffness - Temperature
- increase creep (e.g. isometric contraction - tendon stretches, muscle contracts)
- decrease stiffness - 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)
What is hysteresis?
Energy dissipation - the difference between the loading and unloading curve = the energy lost during loading
–> more energy required in loading than unloading
Club foot - what is it?
Tight tendons and ligaments prevent the foot from stretching into the right position
Casting + splinting for 3-4yrs
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
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
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)
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
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)
Ligament injury
Sprain
- overstretched, partially torn, completely torn
Repair vs Regeneration
Regeneration = normal tissue re-established
Repair = structure healed
- scar tissue
- abnormal composition and microstructure
- inferior mechanical properties
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
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
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
