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Basic Science > Articular Cartilage and Lubrication > Flashcards

Articular Cartilage and Lubrication Flashcards

1
Q

What makes up hyaline cartilage?

A
  • Cells- CHONDROCYTES
  • Extracellularly matrix
    • collagen mainly type 2
    • Elastin
  • Ground glass
    • ** water**
    • **PROTEOGLYCANS and glycosaminoglycans **
      • aggrecan
      • Hyaluronan
      • decorin,byglan
    • Glycoproteins
      • cartilage oliogomeric protein ( COMP)
      • Cartilage matrix protein (CMP)
    • Degradation enzymes
    • Extracellular ions
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2
Q

What is the function of hyaline cartilage?

A
  • To distribute weight bearing forces and reduce friction
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3
Q

Describe the properties of ARTICULAR cartilage?

A
  • AVASCULAR
  • ANEURAL
  • Alymphatic
  • Almost non immunogenic
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4
Q

What is the main constituent of the extra cellular matrix?

A
  • Water 75%
    • Which is held In place by PROTEOGLYCANS (e.g.aggrecan) 10-15%
  • Collagen type 2 fibres
  • CHONDROCYTES
    • ​manufacture and maintain the extracellular matrix
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5
Q

Cent you name all the layers of the ARTICULAR cartilage?

A
  1. Superifical Gliding zone
    • collagen parallel to surface and CHONDROCYTES- resist shear forces
    • thinnest layer, highest water + collagen concentration
  2. Middle Transitional zone
    • mixture of oblique collagen fibres + CHONDROCYTES
    • protepglycan concn highest
    • transition between shearing and compression forces
  3. Deep Radial zone
    • vertical collagen fibres
    • largest part of articular cartilage
    • resists compression
  4. ​ TIDEMARK
      • boundary between calcified and uncalcified cartilage
  5. Calcified zone
    • ​​hydroxyapatite crystals anchor cartilage to bone - barrier to diffusion from blood vessels supply the subchondral bone
    • type X collagen here
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6
Q

What is the role of chondrocytes in the middle transitional zone and deep radical zone of articular cartilage?

A
  • Produce all the components of the Extracellular matrix
  • no intercellular junctions between chondrocytes, communites of 2 or more cells form chondrons
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7
Q

Where is collagen produced?

A
  • Within and outside the CHONDROCYTE
  • Polypeptide chains formed from mRNA translation within the rough endoplasmic reticulum.
  • Signal peptide is cleaved and modified polypeptide chain from a triple helical molecule.
  • Disulphides bonds determine its shape
  • Within Golgi apparatus the resultant procollagen is packed into secretory vesicles and released into the ECM via micro tubules.
  • Outside the cell the terminal ends of pro-collagen uncoil and cleaved -> Tropocollagen fibrils.
  • These combine via cross linkage of LYSINE and HYDROXYLYSINE residues -> COLLAGEN FIBRES
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8
Q

What is the type of collagen in ARTICULAR cartilage ?

A
  • Type 2 90%
  • Type X is found in calcified zone
  • The core of the collagen is formed by II and XII
  • **type IX ** found on surface of the fibre
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9
Q

What is the role of the PROTEOGLYCANS ?

A
  • Water content of the cartilage
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10
Q

What are PROTEOGLYCANS ? How does their structure allow them to function?

A
  • Large hydrophilic molecules containing chains of GLYCOSAMINOGLYCANS (GAG)- chondroitin sulphate and keratin sulphate bound by sugar bonds to a linear core.
  • The gag’s have a negative charge from attached carboxyl and sulphate groups- increasing their osmotic pressure
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11
Q

What is the most common PROTEOGLYCAN in ARTICULAR cartilage?

A
  • Aggrecan
  • which is Heavily GLYCOSYLATED with GAG components such as chondroitin sulphate and keratin sulphate
  • aggrecan interacts with hyaluronic acid , stabilised by link protein to form a large proteogylcan aggregate up to 50x106 MW
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12
Q

What are the degradation enzymes ?

A
  • Collagenases, stromelysins, gelatinases and membrane -associated metalloproteinases
  • which degrade collagen and PROTEOGLYCAN aggregates as part of normal turnover of the matrix
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13
Q

What prevented degradation of cartilage by metalloproteinases ?

A
  • Tissue induced metalloproteinases inhibitors
  • are acidic polypeptides that prevent degradation by metalliproteinases by binding to the matrix proteins
  • the avascular nature of articular cartilage is maintained by TIMPs that inhibit proteinases prodcued by migrating vascular endothelium
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14
Q

What is the ion make up in ARTICULAR cartilage?

A
  • Typically- High sodium and potassium ion content
    • the sulphate ion on the proteoglycans attract these cations.
  • Extra cellular Ca high in calcified zone
    • ​low in superifical gliding and deep radical zones
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15
Q

What is the role of glycoproteins in the cartilage?

A
  • They are in the ECM and act like ‘glue’ binding various constituent s of the matrix and CHONDROCYTE surface
    • ​ E.g. COMP ( which binds to various matrix proteins), CHONDROCALCIN
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16
Q

Where do CHRONDOCYTES originate ?

A
  • MESENCHYMAL stem cells
  • Majority of cartilage changes to bone thru ENDOCHONDRAL ossification , with growth plate and cartilaginous epiphysis persisting after birth
17
Q

What happens to CHONDROCYTES in osteoarthritis ?

A
  • chondrocytes mimic the events of endochondral bone formation by
  • CHONDROCYTE proliferation, hypertrophy and expression of type x collagen , alkaline phosphatase, matrix vesicles and matrix calcification
18
Q

What is the metabolic rate of the CHONDROCYTES in ARTICULAR cartilage?

A
  • Generally very low
  • Deep cartilage zones contain chondrocytes with decreased rough endoplasmic reticulum and increased degeneration products
19
Q

What influences CHONDROCYTES ?

A
  • Growth factors - fibroblast growth factor stimulates adult CHONDROCYTES DNA synthesis.
  • PTH and Thyroxine stimulate matrix synthesis
20
Q

What is the mania function of ARTICULAR cartilage?

A
  • Joint lubrication
  • Shock absorption - distribute joint loads and so reduce stress
21
Q

What is articular cartilage coefficient of friction?

A
  • V low - 0.002
  • X30 smoother than most joint replacements!
  • lowered by
    • fluid-film lubrication
    • elastic deformation of articular cartilage
    • synovial fluid
    • efflux of fluid from cartilage
  • increased by
    • fibrillation of articular cartilage
22
Q

What are the BIOMECHANICAl properties of cartilage?

A
  • Biphasic material that is Viscoelastic
    • which undergoes CREEP, STRESS RELAXATION, HYSTERESIS AND STRESS/strain rate.
    • these occur thru macro molecular and water movement
    • cartilage is freely permeble to water but under high compressive loads water movement is hindered by the frictional drag of moelcules- decreases flow, stiffens allowing greater resistance to higher loads
    • ANISTROPHIC- different mechanical properties depending on direction of the load
      • due to collagen arrangements, x links and collagen-PROTEOGLYCAN interactions
        • in tension cartilage pulled apart, increases water permeability and decreases the compressive stiffness
23
Q

What are the main types of lubrication?

Can you describe the 2 main types in engineering?

A
  • Fluid film
  • Boundary
  • **Hydrodynamic **
  • Squeeze film
  • Elastohydrodynamic
  • **weeping **
  • **Boosted **

​

  • Boundary
    • involves a MONOLAYER of lubricant molecule absorbed in each surface of the joint.
    • This prevents DIRECT ARTICULAR contact -
    • NB IMPORTANT AT REST/ Under load
  • Fluid film
    • a THIN LAYER OF FLUID INCREASES THE SEPARATION OF THE 2 Surfaces
24
Q

Describe the types of lubrication?

A
  • HYDRODYNAMIC
    • 2 surfaces are at an Angle to each other
    • the viscosity in the resulting wedge of fluid separates the 2 surfaces
  • SQUEEZE-FILM
    • 2 surfaces are parallel and move perpendicular to each other
    • the viscosity of the incompressible fluid maintains lubricate.
    • As the load increases the layer of fluid is forced out so a thin layer remains to prevent surface contact
  • ELASTOHYDRODYNAMIC
    • as speed increases the ARTICULAR surface creates a larger surface area when compressed by the fluid.
    • There is less dissipation of the fluid and load sustained for a longer period
    • main lubrication in dynamic movement.
  • WEEPING
    • as ARTICULAR cartilage of the joint slides under compression, fluid is exuded under and infront of the leading edge of the load , enhancing lubrication.
    • As load decreases water is once again imbibed and the ARTICULAR cartilage reforms it’s shape
  • BOOSTED
    • the solvent part of the lubricant enters the ARTICULAR cartilage which leaves behind the concentrated hyaluronic acid complex as a lubricant in trapped pools of concentrated synovial fluid.
25
Q

What happens with a Superificial laceration to ARTICULAR cartilage above the TIDEMARK ?

A
  • It doesn’t heal as completely AVASCULAR
26
Q

What happens to ARTICULAR cartilage lesions that are below the TIDEMARK ?

A
  • Results in haematoma, fibrin, clot and activation of the inflammatory response-> this acts as a scaffold for the formation of fibrocartilage
  • Produced by undifferentiated MESENCHYMAL cells that have migrated into the defect- this is different from hyaline cartilage as disorganised bundles of type I collagen - so not suitable for repetitive load bearing
27
Q

What biochemical changes happens with the aging process?

A

Water decrease - shrivel as age! Synthetic activity decrease COLLAGEN UNCHANGED PG Content decreases - length of protein core and GAG decrease PG synthesis decrease PG degradation - decrease Chondroitin sulphate- decrease KERATAN SULPHATE INCREASES CHONDROCYTE SIZE INCREASES Chondrocyte no decrease YM INCREASES

28
Q

What effect does infection have on cartilage?

A
  • Direct result of organism itself e.g. chondrocyte protease of staphylococcus aureus or due to host’s inflammatory response
  • polymorphs stimulate production of cytokines and other inflammatory products-> hydrolysis of collagen and proteogylcans
  • destruction of cells and release of lysosomal enzymes- collagenases, proteases further injures the joint
29
Q

What happens to the biochemical changes In ARTICULAR cartilage with osteoarthritis?

A
  • WATER INCREASES-90% cf n 65-80%*
  • this softens articular cartilage-> decreased Young’s M
  • reducing its ability to bear load
  • Increased permeability-> loss of lubricant-> increased interfacial wear/ fatigue wear
  • -> disruption of collagen-proteglycan matrix/ leaching out of protoglycan with large fluid movements
    • decrease in collagen but relative conc increase due to loss of proteoglycan
    • PG degradation increases significantly
  • rapid repitive high loads with no time for stress relxatn-> CP matrix damage so Chrondrocytes attempt to restore by ** SYNTHETIC ACTIVITY INCREASES
    • PG synthesis increase
    • CHONDROTIN SULPHATE - increase
    • Keratan sulphate- decrease
    • Enzymes- increase activity
    • Matrix subunits - increase levels
30
Q

What other biomechanical factors does an increase in permeability and reduction in PG concentration have on the cartilage?

A
  • Loss of lubrication-> increase interfacial wear Cartilage bearing surface deformation occurs under load with repetitive stressing leading to fatigue wear and accumulative microscopic damage
31
Q

How does fatigue wear occur?

A
  • Thru high stress and low cycle loading or low stress thru high cyclical loading
32
Q

How does fatigue wear cause damage in the osteoarthritic cartilage?

A
  • Disruption of the collagen- pg matrix with increasing age
  • Leaching out of pg by repetitive large interstitial fluid movements in the Superificial layer, leading to increased permeability and decreased stiffness
  • Rapid repeat high loading where there is no time for stress relaxation leading to collage matrix damage
  • Chondrocyes try to compensate by increasing their rate of DNA synthesis, collagen and pg- proliferate and hypertrophy initially but eventually pg decrease and chains become shorter.
33
Q

What macroscopically is seen on the surface if a damaged ARTICULAR cartilage?

A
  • Fibrillations - vertical splits then development of deep fissures
34
Q

What are the treatment options for ARTICULAR cartilage damage?

A
  • Non operative
    • physical therapy
      • loading of joint essential to allow diffusion of synovial fluid and metabolic turnover of cartilage.
      • IMMOBILSATION -> cartilage atrophy
    • Oral visco-supplementation- GLUCOSAMINE- amino-monosaccharide sugar, naturally occurring component of keratan sulphate and hyaluronate
      • ​ In vitrio studies have shown the effect of glucosamine in reversing the inhibition of PROTEOGLYCAN synthesis by IL-1 and suppressing the inflammatory response of neutrophils -v low risk of side effects ( shellfish allergy) 1500mg/day
      • INTRA-ARTICULAR visco supplementation- replace lost hyaluronate and improve Viscoelastic properties of ARTICULAR cartilage but-publication bias, poor numbers and Outcome measures
35
Q

What are the surgical options for tx?

A
  • ABRASION ARTHROPLASTY = cartilage repair from subchondral bone
    • turn defect into deep injury- undifferentiated MESENCHYMAL cells proliferate in the defect-> fibrocartilage and initially type 2 collagen but changes to type 1.
    • Contained defects < 2cm
  • Autograft/MOSAICOPLASTY
    • ​full thickness osteochondral grafts from the least weight bearing periphery of the ARTICULAR surface- superiormedial margin of the femoral notch are transplanted into the cartilage defect.
    • Most benefit medial compartment knee cf patella- small lesions < 2cm square due to donor site risks
  • Allograft -
    • caderveric cartilage usually frozen with cryoprotectant- glycerol which prevents rupture of the cell membranes during freezing process.
    • Only some CHONDROCYTES will remain after thawing.
    • Bony part of graft acts as scaffold therefore import at same size as defect
  • .>3cm defect
  • Periosteal/PERICHONDRAL MESENCHYMAL stem cell
    • Peroiosteum and perichondrium both have sig no of stem cells that could-> hyaline cartilage.
    • Periosteum ( cambrial layer) most chondrocytes positioned ) from rib sutured onto bone graft-
    • type 2 collagen and pg see in this repair
  • CHONDROCYTES from MESENCHYMAL stem cells
    • MSc located In bone marrow using tissue culture -the stromal cells inc MSC adhere and cultured.
    • Using periosteum - msc released from cambrium layer using enzymetic tx.
    • MSC placed in 3 dimensional matrix ( collagen /alginate) they differentiate into CHONDROCYTES .
    • These continue to differentiated and introduced into collagen gel which is placed into defect.
    • forms a hyaline cartilage
  • Autologous CHONDROCYTE implantation -ACI
    • A small amount of cartilage from nwb area harvested, cells grown.
    • CHONDROCYTE proliferation low in vivo,but in tissue culture CHONDROCYTES no’s expand over 4/5 wks,
    • then suspended in gel carrier and re implanted .
    • A periosteal/ collage flap sutured over the top. Can’t use In patella femoral joint OA if joint space narrowing - as need whole surround cartilage to protected aci
  • Maci- matrix induced chondrocyte implantation- growing cells of cartilage membrane and suspend in 3d hyaluron based scaffold or polymer fleece which is implanted, no need for cover
36
Q

What is the classification system for cartilage defects?

A
  • Outerbridge
  • 0= normal
  • 1-softening and swelling
  • 2-partial defect ,
  • 3- fissure diameter 1.5 cm
  • 4- exposed subchondral bone
37
Q

What happens to the biochemical changes in aging process of articular cartilage?

A
  • water content decreases - “old and wringly”
  • synthetic activity - decreases
  • collagen- unchanged
  • PG content- decrease length of protein core and GAG chains decrease
  • PG synthesis- decreases
  • PG degradation- decreases
  • Chondrotin sulphate decreases
  • keratan sulphate- increases
  • chondrocyte size increases
  • chondrocyte number decreases
  • young’s modulus- increases- stiffer

Basic Science (31 decks)

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