General Flashcards

THR implant fixation wear and osteolysis catastrophic wear prosthetic joint infections

1
Q

What does the cement in cemented THR do?

What are the indications for its use?

A
  • Interlocking fit
  • provides mechanical interlock of methylmethacrylate to the inctercises of bone ( acts as grout)
    • this is a static interface with limited remodelling potential
    • bone-cement is stronger in osteporotic/ irradiated bone ( as doesn;t rely on ingrowth)
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2
Q

How do the acetabular compotents of cemented THR fail?

A
  • Higher shear and tensional forces
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3
Q

Describe the 1st generation cementing technique?

A
  • Hand mixed cement
  • finger packed cement
  • no canal preparation or cement restrictor
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4
Q

Describe the 2nd generation cementing technique?

A
  • Cement restrictor placement
  • Cement gun
  • Femoral canal preparation
    • brush and dry
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5
Q

Describe the 3rd generation cementing technique?

A
  • Vacuum mixing to reduce cement porosity
  • cement pressurisation
  • femoral canal preparation
    • pulsatile lavage
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6
Q

What is the criteria to optimise cement fixation of prothesis?

A
  • Limit gaps
  • Limit porosity of cement
  • Create cement mantle at least 2mm thick
    • increase risk of matle fx if <2mm thick
    • for small canals in which 2mm mantle is impracticle, 2/3 of the canal should be filled by the femoral stem and 1/3 by cement
  • use stiffer femoral stem
    • increase Young’s modulus
  • Use smooth femoral stem
    • no sharp corners
  • Avoid mantle defects
    • defined as any area where the prosthesis touches cortical bone with no cement between
    • creates an area of _higher concentrated stress _& is assoc with higher loosening rates
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7
Q

What is bioloigic interdigitation?

A
  • Is a dynamic interface and there is potential for bone remodelling and a life last bond
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8
Q

Decribe the methods of bioloigcal interdigitation?

A
  1. Porous coated metallic surfaces
    • implant covered in porous covered surface that allows bone ingrowth fixation
    • extent of porous coating
      • Proximal coating only
        • adv in less distal shear stress
      • Extensively coated stem
        • disav is stress sheilding of proximal bone
        • used in tx of periprosethtic fx
  2. Grit blasted
    • implant is grit blasted creating a roughed surface that allow bony ongrowth
    • surface roughness directly proportinal to Interface shear strength
    • roughness= av distance from peak to valley
    • disadv = requires larger area of grit- blasted metal relative to porous coated metal
  3. hydroxyapatite (HA)
    • ​​an osteoconductive agent used as an adjunct to porous - coated and grit blasted surfaces
    • ​promotes more rapid closure of gaps
    • disav -> potential to delaminte from surface coating
    • success depends on
      • ​high crytsallinity
      • thickness 50um
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9
Q

What are the mechanism for porous coating?

A
  • Titanium plasma sprayed
    • often used to create pores
    • then covered with HA to supplement
  • Tricalcium phosphate
  • Ha coating
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10
Q

Can you descibe the different extent of porous coating?

A
  1. Complete vs incomplete
    • Both proximal and distal fixation important
    • trade off for fixation vs stress shielding
  2. Proximal only
    • Proximal loading of bone
    • minimise proximal stress shielding
    • more common
  3. Extensively
    • improve likelihood of solid fixation
    • Distal loading of bone
    • > proximal stress shielding
    • mainly diaphyseal spot welding
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11
Q

What are the optimal characteristics for porous coating implants?

A

Optimal values

  • Pore size 50-300um
  • Porosity 40-50% ( greater -> shear off metal)
  • Gap <50um
    ( between bone and prosthesiss
  • Micromotion <150um
    • ​anthing > 150 -> fibrous ingrowth
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12
Q

write the formula of hydroxyapetite?

A
  • Ca 10 (PO4)6 (OH)2
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13
Q

What is hydroxyapetite?

A
  • An osteoconductive agent used as an adjunct to porous coated and grit blasted surfaces
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14
Q

What is the key to uncemented fixation?

How is this achieved?

A
  • Obtain rigid fixation
    • micromotion kept <150um
    • otheriwse firbous tissue will develop-> unstable implant

Methods to obtain this

  • Press- fit technique- non porous implant
    • implant slightly larger than surrounding bone 1-2 mm
    • Bone expands around prosthesis
    • Generate hoop stresses around prothesis minimise micromotion
  • ​Line to line contact
    • mechanical strength of biological interdigitation s stronger if implant is seated against cortical bone
      • in acetabulum obtain contact between cup and cortical rim
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15
Q

What is stress shielding?

A
  • Stress shielding is the redistribution of load (and consequently stress onthe bone) that occurs when the femoral head is replaced by the femoral component of a total hip replacement;
  • as a result there is a reduction in density of bone often at proximal femur due to removal of normal stress of the bone by an implant ( femoral component of hip replacement)
  • This is because Woolfe’s law: bone in healthy person /animal will remodel in response to the loads placed upon it.
  • So if the load decreases the bone will become weaker and less dense as no stimulus for it to remodel to maintain normal bone density
  • stress on proximal 10 cm of femoral cortex is reduced, because much of the load bypasses this region and is carried in the metal stem to the isthmus of the femur
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16
Q

Where is stress shielding most common?

A
  • Proximal femur
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17
Q

What factors increase stress shielding?

A
  • larger diameter stems
  • stiffer stems
    • radius
    • young’s modulus
    • geometric shape
  • extensively porous coated stem
  • greater preoperative osteopenia
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18
Q

What factors are important in stress shielding in proximal bone?

A
  1. Stem stiffness
  • Radius
  • young’s modulus
  • geometric shape- solid round stems stiffer than stems with flutes
  1. extent of porous coating
  • proximal coating allow proximal bone loading and less stress shielding
  • extensive coating -> proximal stress shielding
19
Q

How is the extent of stress shielding evaluated?

A
  • Spot welding ( increase density) at tip of extensive porous coated stem
20
Q

What are the clinical implications of stress shielding of proximal femur?

A
  • Unknown
21
Q

What material require for uncemented THR?

A
  • Less rigidity
    • so minimising stress shielding
    • stiffness related to
      • power 4 of stem radius
      • Young’s modulus
      • solid vs slotted / flutted
  • Ti vs Colbalt chrome
    • less structurally rigid
    • lower young modulus
    • 2-3 x less stiff
  • implant size
    • as size increases the rigidity increases
22
Q

What are the signs of uncemented implant failure?

A
  • Implant migration
    • subsides and varus tilt
  • Progressive lucency on serial xrays
  • development of inferior pedestal
23
Q

What are the complications of uncemented prosthesis?

A
  • Fracture
  • infection
  • Thigh Pain
    • Instability= lack of press fit
    • tx with cerlage wire/strut grafts
  • Stress shielding
  • Osteolysis
24
Q

What are the CI to uncemented THR?

A
  • Stove pipe femur
    • measure canal at LT & 10cm below
  • inner diameter at midportion of LT divided by diameter 10 cm distal
  • must be <75% for uncemented prosthesis
    • Ratio is >0.75 so use cemented stem
    • thinning cortices on 2 views ap & lateral
25
Q

What is the wear rate of non crossed UHMWPE?

A
  • 0.1-0.2 mm/yr
  • linear wear rates of >0.1mm/yr associated with osteolysis and component loosening
  • highly crossed linked UHMWPE generates small wear particles and is more resistant to wear
26
Q

What factors increase wear in THR?

A
  • Thickness <6mm
  • maliagnment of components
  • patients <50 yrs
  • men
  • higher activity rate
  • ***Femoral head size between 22 and 46mm doesn’t influence wear rates of UHMWPE**adv as increasing femoral head size improves ROM and increases jump distance, thereby decreasig dislocation rates**
27
Q

What is the wear rate on ceramic bearing?

A
  • Lowest wear rates of any bearing combination
    • 0.5-2.5u components per yr
  • ceramic on poly varied from 0-150u
  • has a unique complication of stripe wear from lift off separation of the head gait
28
Q

What are the war rates on metal on metal prothesis?

A
  • Metal on metal lower than metal on poly 2.5-5.0 u per year
  • produce smaller wear particles- nanometres
  • better linear and volumetrix wear rates
  • achieves a steady state of wear after first year
  • Ti has high failure rate for bearing surface as Poor resistance to wear and Notch sensitivity
  • Serum ion levels higher with
    • ​cup abduction >55 degress-> more vertical cup and edge loading
    • smaller component size
  • ​METAL on metal wear stimulates LYMPHOCYTES
29
Q

What is the size of normal particle wear?

A
  • < 1 micron
30
Q

Describe macrophage activated ostoegensis and osteolysis?

A
  • MAcrophage activation
    • wear debris particles at bone/cement interface results in macrophage activation and futher macrophage recruitement
    • macrophage release proinflammatory mediators and proteolytic enzymes e.g cytokines, osteolytic factors
      • TNF-aplha
      • TGF beta
      • oseteoclast activation factor
      • oxide radicals
      • hydrogen peroxide
      • IL1/6
      • prostaglandins
  • Increase TNF alpha increases RANK
  • Increase in VEGF with UHMWPE enhances RANK and RANKL activation
  • RANKL, TNF-alpha, IL-1, IL-6, IL-17, and M-CSF mediate the differentiation of myeloid precursor cells into multinucleated osteoclasts, which release cathepsin K and acid and cause resorption lacunae;
  • Mesenchymal cells (prosthesis-loosening fibroblasts) present at the bone surface contribute actively to bone resorption.
  • Osteolysis around prothesis -> micromotion
  • micromotion-> > particle wear -> loosening
31
Q

How is the debris disseminated into the joint?

A
  • An increase in hydrostatic pressure leads to dissemination of debris into joint space
  • increase hydrostatic pressure is a result of inflammatory response
  • disseminated debris into effective joint space further propagates osteolysis
32
Q

What is measure for bone turnover and elevated in osteolysis?

A
  • N-Telopeptide urine level
  • breakdown product of type 1 collagen
33
Q

What is catastrophic wear?

A
  • Refers to macroscopic premature failure of polyethylene PE due to
    • excessive loading
    • mechanical loosening
  • ​Commonly seen in TKR cf osteolytic in THR
34
Q

What variables that lead to catastrophic wear?

A
  • PE thickness
  • Articular surface design
  • Kinematics
  • PE sterilisation
  • PE machining
35
Q

What is the thickness of PE that leads to catastrophic failure?

A
  • <8mm
    • leads to loads transmitte to localised area of PE which exceed PE’s inherent yield strength
  • Solution
    • keep thinnest part of PE>8mm
    • avoid having to use a PE <8mm by making a more generous tibial cut
36
Q

Describe the 2 types of PE inserts?

A
  1. Deep congruent joint ( deep cut PE) without rollback
    • less anatomic
    • maximise contact loads
    • decrease contact stress
  2. Flat tibial PE that improves femoral rollback and optimises flexion
    • more anatomic
    • PCL sparing
    • low contact surface area->Increase contact stress in areas of contact and catastrophic failure
37
Q

What type of PE leads to catastrophic failure?

A
  • Flat PE
  • less contact area so in areas of contact has high stress -> catastrophic failure
  • Solution
    • increase congruency of articular design
    • higher contact surface area to lower contact stress load
    • newer prosthesis design sacrifice rollback and have more congruent or dishes fit between the femoral condyle and tibal insert in both sagittal and coronal plane in order to decrease the contact stress
38
Q

What in kinematics leads to catastophic failure?

A
  • Knee alignement
    • varus alignment of knee -> C failure
  • XS Femoral rollback
    • optimises flexion at the cost of increasing contact stress and increased risk of C failure
    • dyskinetic movements of femur on tibia-> surfae cracking and wear
  • Solution
    • preform medial release to avoid varus deformity
    • decrease contact stress by Minimise femoral rollback
      • use more congrous joint design
      • increase posterior slope of tibia
      • use PCL substiting knee for incompetent PCL or dyskinetic femoral rollback
39
Q

How can PE sterilisation lead to C failure?

A
  1. o2 rich environment
    • PE becomes oxidised
    • leads to early failure by
      • subsurface delamination
      • ptting
      • fatigue cracking
  2. O2 depleted environment
    • PE becomes crossed linked
    • improved resistance to adhesive/abrasive wear
    • decreased in mechanical properties ( decreased ductility, fatigue resistance) and is greater risk of catatrophic failure under high loads
  3. pack via argon/nitrogne/ vaccum environment
  • Solution
    • ​Irradiate PE in inert gas / vaccum to minimise oxidation
    • gamma radiation is most common form of PE sterilisation
40
Q

How can PE machining effect catastophic failure?

A
  • Cutting tools can disrupt chemcial bonds of PE
  • Cause of failure
    • machining shear forces cause Subsurface region (1-2mm) stretching of PE chains
      • esp in amorphois regions>crystalline regions
    • leads to subsurface delamination and fatigue cracking
      • can show classic white band of oxidation in subsurface 1-2mm below articular surface
  • ​​Solution
    • Use direct-compression moulding​ of PE
      • preform by moulding directly from PE powder to desired product
      • results in less fatigue crack formation and propagation compared to ram bar extrusion
41
Q

How to measure wear rates between 2 diff implants?

A
  • Prospectively by radiostereometric analysis
  • Radioopaque tantalum beads ade inserted into the bone in strategic positions surrounding the implants
  • an immediate post op film records the position of the beads
  • Construct can then be followed with rpt xrays over time to evaluate the position of the components relative to the beads.
42
Q

What interacts with Rank- l to inhibit particle- induced osteolysis?

A
  • Osteoprotegrin OPG
  • binds to Rank-L to inhibit RANK which are present on osteoclast precursor cells. Normally Rank-l interacts with RANK to stimulate activation of osteoclasts
43
Q

How is highly crossed linked Pe made and what is its benefits vs disdv?

A
  • Irradiating ( 5-10 Mrad) PE which prompts free radicals fro diff polymer sections to combine and form chemical bonds between polyer chains ( x links)
  • Improved resistance to adhesive and abrasive wear
  • Decreased mechanical properties- toughness, ductility, tensile strength and fatigue strength