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ANAT2012 > Synovial Jt Biomechanics > Flashcards

Synovial Jt Biomechanics Flashcards

Up to first lecture still

1
Q

Function of synovial jts

A
  • load transfer
  • allow movement
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2
Q

Features of femoral synovial jt

A
  1. graduated flexibility
  2. increased surface area
  3. variable bearing area
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3
Q

Hyaline cartilage functions

A
  • withstands and distributes loads to protect underlying bones
  • allowing motion of surfaces with minimal friction
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4
Q

Structure of hyaline cartilage

A
  • H20
  • collagen type II
  • proteoglycan aggregates
  • chondrocytes

water is free to move in response to tissue

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5
Q

Layers of hyaline cartilage

A

Upper layer - most collagen to help oppose friction
Middle layer - mesh pattern
Deep zone - aligned perpendicular to bone

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6
Q

What are proteoglycan aggregates

A

Molecules in cartilage e.g. aggrecan
A protein core with side chains of GAGs that bind to hyaluronan to form macromolecule

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7
Q

behaviour of proteoglycans

A
  • dissociate in solutions
  • expose -ve ions
  • try to expand area molecule occupies
  • attracts water into tissue “donnan effect”
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8
Q

How does PG interact with collagen

A

the figuration helps PG tension collagen to create a stiff matrix
- creates tension within fibrils
- resistant best to compression and shear

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9
Q

what are the two phases of cartilage in response to loading

A

Fluid phase > hydrostatic pressure resists 90% load
Solid phase > PG and collagen stiff matrix interact > resists further deformation

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10
Q

What determines the flow of interstitial fluid

A

Porosity = spaces in tissue
Permeability - ease of fluid
When water tries to move past solid > frictional drag

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11
Q

Outline compression of cartilage behaviour

A
  • compression
  • resisted by hydrostatic pressure of interstitial fluid
  • osmotic swelling pressure causes fluid flow out of material > generates frictional drag
  • the removal of fluid transfers the load to solid components
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12
Q

Why does hyaline cartilage have water flow into tissue

A

sulphate and carboxyl groups dissociate and expose -ve ions which draws water into the tissue

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13
Q

Creep response of HC (constant compression over time)

A
  • deformation over time until new equillibrium is reached
  • rapid rate of STRAIN and will slow down
  • this happens because of fluid leaving tissue, hydrostatic pressure and decrease of pore size
  • when new equillibrium reached when flow of fluid in and out is equal
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14
Q

Progressive slow rate of compression on HC

A
  • fluid able to adjust and redistribute around compression
  • flows out of tissue > low frictional drag bcoz slow
  • local indentation (compression localised bcoz fluid flow)
  • occurs until solid components have to resist load
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15
Q

Rapid rate of compression on HC

A
  • more resistance of tissue
  • more frictional drag bcoz of faster velocity
  • whole thing becomes stiff and causes large indentation due to fluid not being able to flow in time
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16
Q

What determines amt of frictional force

A
  1. articular surface roughness
  2. normal load
  3. static v kinetic conditions
  4. mode of lubrication
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17
Q

What is surface roughness

A

measuring avg height of asperities

  • atomic bonds between surfaces form and need to be broken to cause stress (can withstand normal shear forces)
  • higher the asperities > higher the friction
18
Q

Modes of lubrication + explain

A

Boundary-layer (high loads, low speeds)
- surfaces separated by sacrificial layer
- collagen (II) links with lubricin and hyaluronan
- low COF, worn down in friction and replenished

Fluid-film lubrication (high speed, low load)
- surfaces separated by flui-film
- load supported by pressure in fluid
- frictional resistance low

Mixed lubrication
- both of the above and occur at diff parts of the articular surface depending on aspect of surface

19
Q

Synovial fluid behaviour at rest

A

Lubricin helps HA chains to be large coils to be rigid and provide resistance to flow

20
Q

Synovial fluid during impact

A

HA chains remain coiled > reacts elastically and bears intensive load

21
Q

Synovial fluid during slow load

A

HA bonds broken and align parallel to slip past eachother
- behaves like viscious fluid

22
Q

Hyaline cartilage composition and mechanical behaviour

A
  • mainly Type II collagen, mainly water and 4-7% PGs
  • able to resist higher shear stresses due to PGs
  • PGs allow collagen to tense and resists compressive forces well
23
Q

Fibrocartilage composition and mechanical behaviour

A

Mostly Type I collagen (stronger), less PGs and moderate water

  • high tensile modulus due to the type of collagen resisting this
  • less shear resistance due to type of collagen which allows mvt
24
Q

Functions of meniscus

A
  • distribute load to decrease stress (shear forces)
  • shock absorption
  • joint stability
  • proprioception (horns have mechanoreceptors)
  • lubrication
25
Distribution of collagen in meniscus
Outer zone - most Type I collagen Inner zone - more like hyaline (more Type II) Superficial - progenitor cells (can differentiate) Periphery better at tensile strength, inside better at compression
26
How does meniscus vascularisation change throughout life
Birth - whole thing vascularised After 10yrs - 10-30% Adult - only on peripheral 10-25%
27
What part of the meniscus is innervated
Outer 1/3
28
Collagen arrangement in meniscus
Anisotropic because of arrangement Collagen fibres orient with local axis of stress Overall circumferential orientation with radial fibres present meniscus converts compressive forces into tensile (as it is better at resisting this)
29
What normal changes happen to meniscus with age
- become more opaque and yellow/brown - surface roughens (less progenitor cells) - harder and less elasticity - decreased cell density - abnormal PGs - slight increase collagen fivres - larger collagen - increased stifnness - calcification - degeneration (typically inner rim first)
30
Degeneration changes to meniscus
- abnormal cells - less PGs - separation of ECM - fraying - tears - calcification
31
Types of meniscus tears
Degenerative or traumatic - Longitudinal - Horizontal - Radial
32
Aging v degeneration
Aging = time-dependent normal changes (happens to everyone) Degeneration = structural or functional failure of tissue
33
Age-related changes to hyaline cartilage
- decrease in cell density - stops reproduction lubricin - produce inflammatory mediators - smaller and less aggrecan (old aggrecan stops new binding) - increased stiffness bcoz of collagen cross-linking - thinning - more tidemarks -calcification and accumulation of cells (no macrophages)
34
Osteoarthritis characteristics
- inflammatory whole jt disease - progressive degeneration, loss of cartilage -changes to synovium, meniscus, periarticular ligaments and bone
35
Risk factors of OA
- age - female - obesity - prev injury - genetic - diabetes - endocrine disorders
36
Pathological changes w OA
- altered lubrication > less HA and lubricin, fluid becomes less viscous - chondrocytes > clump and produce inflammation - collagen > more COF coz of degradation - less aggrecan - exposure of bone and less stiffness
37
What do different load types do to hyaline cartilage
Excessive impact > dynamic stiffening, more frictional resistance, lots of deformation to ECM Prolonged static > fluid exudation > stress onto solid components > COF increases with greater solid loading Absence of load > chondrocytes need stimuli, without can't maintain matrix Changes in rate/distribution > cartilage needs time to adapt > will be overloaded quickly
38
What are the properties of chondrocytes
- mechanosensitive - love intermittent pressure to adapt - helps them introduce aggrecan and Type II
38
Cycle of chondrocyte behaviour
Altered chondrocyte metabolism > abnormal remodelling > altered ECM collagen - PG > altered mechanical behaviour ( increased permeability, less hydrostatic pressure, load to solid, less lubrication) > more rapid deformation > abnormal chondrocyte stimuli
39
Why can HC not repair
- avascular, alymphatic and aneural - low cellular density - low metabolic activity - inability to migrate to site of injury

ANAT2012 (4 decks)

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