Ch 39 Bone biomechanics and fracture biology Flashcards

1
Q

What is the mathematical equation for a moment?

A

Applied force x moment arm

The larger the moment arm (the distance between the location of the applied force and the axis of rotation) the higher the resulting moment/rotational force

When the body is constrained such that rotational motion is not possible (Figure 39.6), or if moments are applied on opposing ends and acting in opposite directions (Figure 39.7), bending or twisting may occur. Under such conditions, the moment is called a bending moment

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2
Q

Force

A

Force can be described in terms of the time rate of change in momentum.

The rapid impulse loading associated with a trot, run, jump, or stomp can result in a ground reaction force that is greater than five times the passive body weight.

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3
Q

What are the properties of an ideal material?

A

Homogenous

Isotropic

Linear

Elastic

biological material: visioelastic (fluid and solid like properties), nonhomogenous and ansiotropic

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4
Q

What is the basic mathematical equation for stress?

A

Stress = Force/Area (N/m2)

complexity associated with describing stress of biological materials, require computational tools to deterimine stress disttributions
stress is a second order tendsro quality that varies throughout an object whne laod is applied
engineering stress is an approximation (though useful for modelling)

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5
Q

Define strain and describe the basic mathematical equation for Cauchy/engineering strain

A

Strain is a measure of the deformation of a material or structure in response to stress/a given laod

Strain = Change in length / Unloaded length

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6
Q

Strain

A

second order toensor quality and shuld be tought of as field or distribution
engineering strain is apporximation > implies material is ‘ideal’ and only under goes small deformations

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7
Q

What is the difference between a load-deformation analysis and a stress-strain analysis?

Which is most appropriate for practical applications in orthopaedics?

A

Load-deformation describes the overall changes in geometry of a sample in response to an applies load

Stess-strain analysis is conducted point-by-point within a body

Load-deformation analysis is usually most appropriate for practical applications in orthopaedics

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8
Q

Name the labelled components of the load-deformation curve

A

The toe region is unique to non-linear materials and is not a part of a stress-strain curve, therefore a load-deformation curve is more appropriate for biologic tissues

toe = low stress produces high strain (collagen uncrimp)
elastic = stress:strain relationship is linear

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9
Q

stress/strain curve

A

stiffness > linear region/young modulus, steeper the slope, stiffer the material

elastic area = material can return to prestrained state

yield point = strain exceeds material ability to recover and thus is permanently deformed
plastic deformation dt breaking of covalent bonds

ultimate failure = material can withstand no more strain and fails

ultimate strength = peak stress before failure

ductility = ability of material to deform prior to fracture

resilience = area under linear, energy that can be absorbed without damaging material

toughness = total energy absorbed before failure, area under all

brittle: exhibits very little deformation before fracturing

the transition from elastic to plastic can be difficult to determine. Can identify a “yield strength” by employing a 0.2% offset method to determine yeild strength

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10
Q

List the unique biomechanical properties of viscoelastic materials (All biologic tissues are viscoelastic)

A

Stress-strain behaviour is very sensitive to conditioning

They exhibit substantial strain rate sensitivity (The stress-strain behavious, depends on the rate at which the load is applied)

They exhibit creep-recovery behaviour (An immediate initial strain followed by a creep response to equilibrium)

They exhibit stress-relaxation behaviour (An initial spike in stress which then decreases with time as the material relaxes eg as seen with press fit femoral implants)

They exhibit hysteresis (A stress-strain relationship which differs depending on if the material is being loaded or unloaded

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11
Q

distinguishing characteristics between cortical bone and cancellous bone is the density. Cortical bone has a much higher density than cancellous bone, is much more stiff, and is much stronger. It is also very brittle compared to cancellous bone, which can withstand much higher strains

A
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12
Q

hierarchical bone structure

A

macrostructural level
composite consisting of dense cortical (compact) bone and spongy cancellous (trabecular)

microstructural level
cortical bone consists of Haversian systems (osteons) containing a central canal consisting of a neurovascular bundle surrounded by layers of concentric lamellae. Trabecular bone is also lamellar, but lamellae run parallel to a trabecular system of struts.

ultra- and nanostructural levels, bone is a composite of collagen fibers with plates of hydroxyapatite interspersed within collagen fibrils

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13
Q

What is the range of lamellar thickness in lamellar bone?

A

3-7mcm

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14
Q

List the three forms of primary bone and define each

A

Primary lamellar bone - A dense network of parallel laminar sheets with high stiffness and strength

Plexiform bone - Contains a mixture of nonlamellar bone and primary lamellar bone and contains a distinct interconnecting network of vasculature

Primary Osteons - Formed by infilling of blood vessels with lamellar bone resulting in the formation of Haversian canals. Osteons are 50-100mcm in diameter and have relative few (<10) lamellae

Primary bone is formed where bone has not previously exhisted

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15
Q

How do secondary osteons differ from primary osteons?

A

Secondary osteons are larger in size (100 - 250 mcm) and have more lamellae (20-25)

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16
Q

What is the function of Volkmann canals?

A

They link the vessels within the Haversian canals in the marrow with the vasculature in the periosteum

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17
Q

What is the cement line and what is its function?

A

Cement line is the seperation between the secondary osteons and the surrounding primary lamellar bone

It absorbs energy to prevent the propagation of microfractures

Provides a dampening function when located in cortical bone thus improving the fatigue properties

18
Q

What is the porosity of cortical and cancellous bone?

What are the benefits of the high porosity of cancellous bone?

A

Cortical - 3-5%

Cancellous - 60-75%

Porosity decreses the overall weight to facilitate locomotion, provided an enormous surface area for cellular components, and provided compliance and toughness

19
Q

List the 4 types of bone envelope and describe their basic functions

A

Periosteal envelope - Inner layer provides osteogenic precursors responsible for growth, remodelling and repair. Can form lamellar or woven bone. The osteoprogenitor cells are also capable of undergoing chondrogenic differentiation

Endocortical envelope - osteoprogenitor lining cells surrounding the marrow cavity. Important for regulation of Ca exchange between the bone and ECF

Cancellous envelope - Surfaces of trabecular struts, participate in nutrient and ion exchange

Intracortical envelope - Cells on the surface of Haversian canal systems. Regulate nutrient exchange between the vascular system and the extracellular space within cortical bone

20
Q

Define intramembranous ossification.

What types of bones are typically formed?

A

Intramembranous ossification is the direct formation of bone from progenitor cells (mesenchymal stem cells)

As cells differentiate into osteoblasts, a unique anabolic matrix is produced, which stimulates formation of primary ossification centers.
Osteoblasts become encased in mineralized matrix and transition to osteocytes.
As these centers enlarge, hypoxia and VEGF production stimulate angiogenic ingrowth to the ossification centers. Ultimately, ossification centers fuse and a complete vascular network develops throughout the bone.

Flat bones are generally formed from intramembranous ossification

21
Q

Define endochondral ossification

A

A process in which a hyaline cartilage intermediate template first forms and is subsequently replaced with bone.

condensation of mesenchymal progenitor cells (MSC) to form a primitive bone blastema.
Instead of differentiation into osteoblasts, MSC differentiate into chondroblasts. driven by local tissue hypoxia, growth factors such as (TGF-β)

chondroblasts produce an ECM containing collagen type II and proteoglycans such as aggregan.

chondroblasts are enveloped in matrix, transform into chondrocytes.

The cartilage template is surrounded by perichondrium.
Due to improved vascular supply oxygen content + matrix and growth factors, cells within the perichondrium differentiate into osteoblasts and begin to form the bone collar around the mid-diaphysis

periosteum becomes populated with osteogenic progenitor cells. The appearance of the bone collar reduces oxygen and nutrient delivery to the adjacent chondrocytes.

results in chondrocyte hypertrophy, release of (VEGF) from these chondrocytes, calcification of the pericellular matrix, and apoptosis.

results in the recruitment of a primary blood vessel to penetrate the bone collar.

pathway for osteoclasts to removing mineralized matrix. results in the creation of primary ossification center

two additional ossification centers develop at each end of the bone. These are referred to as secondary ossification centers

Occurs during skeletal development and in secondary bone healing

22
Q

List and describe the 5 classic zones of the epiphyseal growth plate (physis)

A

Resting zone - Hyaline cartilage matrix with small oval chondrocytes

Proliferative Zone - Chondrocytes undergoing mitosis in a matrix of predominately collagen type II and multiple growth factors

Hypertrophic zone - Newly formed chondrocytes begin to hypertrophy and undergo apoptosis and produce collagen type X. Collagen X induced regional hypoxia and stimulates VEGF and vascular invasion via angiogenesis. This is structurally the weakest component

Zone of calcification - Chondrocytes continue undergoing apoptosis and release ALP and other enzymes which scavenge Ca and phosphate resulting in Ca-phosphate aggregates and matrix calcification

Zone of ossification - Osteoblasts enter through vascular channels and produce woven bone on the calcified matrix. Woven bone is eventually remodelled into lamellar bone

23
Q

bone structure

A

wolffs law: bone optimises itself by forming in areas of high stress and not inareas of little stress

visoelastic: strength is depenedent on rate it is loaded (stronger when loaded rapidly)

anisotropic: mechanical properties depend on dorection of laoding and bone is better able to resist forces along axis rather than across

24
Q

How much strain can cortical and cancellous bone withstand without failing?

What axial loads can cortical bone withstand without failing in compression and in tension?

A

Cortical bone can withstand strain of approx 2%, cancellous bone can withstand approx 75%

Cortical bone can withstand compressive axial loading of >200MPa. When the axial loading is tensile, fails at closer to 100MPa

25
Q

How does a high strain rate effect cortical bone?

How does this differ from cancellous bone?

A

At a high strain rate, cortical bone exhibits higher stiffness and strength but it is also more brittle and not as tough (cannot absorb as much energy)

At a high strain rate, cancellous bone also exhibits a higher strength however it also shows an increased ductility. This allows it to function as a shock absorber

26
Q

fracture biomechanics

A

bone subject to many forces (vector, has direction and magnitude), if exceeds strength of bone, fracture occurs

axial: acts parallel to long axis, compressive and tensile

shear: act parrallel or tangential to bone surface (forces acts in opposite directions)

torsion: twist about long axis therefore creates shear stress

bending: acts to make bone convex and concave
bending forces = moments
a moment is a rendancy for a force to twist and object (torque)
1.pure bending: oposite bending moments at bone ends
2.cantilever: fixed at one point, bending moment highest at fixation, where # occurs
3.three point bending:

27
Q

fracture pattern

A

compressive: results in oblique fracture becasue bone is much weaker in shear than in compression due to osteonal/collagen arrangement, thus bone fails along shear stress (angle 30-45)

tensile: results in transverse fracture perpendicular to load. usually occurs with bending forces

bending: result sin transverse, fracture begins on side of tension

compression and bending: result sin comboned outcome, i.e. butterfly frgament with propogates from tnesion side to form fragment on compression

torsion: spiral fracture, only shear stress planes

rapid loading>high energy> comminuted

28
Q

define strain theory

A

is the effects of loading on a fracture gap

deteromeined by the equation L(change)/L1
= the change in the size of the fracture gap under loading divided by the fracture gap in the original configuration

when load is applied, small # gap will ahve more strain for a given amooutn of instability compared to a larger fracture gap wit same amouont of stability. This will affaect the function of tissue with the agp as diacted by the amout of interfrgamentart strain

fracture treatment should aim to reduce interfragmentary starin rather than just fracture gap.

29
Q

normal bone mechanisms to reduce strain? (2)

A

fracture absorption: osteoclast remove dead bone at fracture margin, increase interfragmentary distance thus reduce strain

periosteal callus: provide stability, the large it extends from gap (increased radial distance) the greater the stability/increased stiffness

30
Q

What % deformation can the following tissues withstand:

Granulation tissue

Fibrocartilage

Bone

formation @ # gap disctaed by strain amount

A

Granulation Tissue - 100%

Fibrocartilage - 10-15%

Bone - 2%

31
Q

goal of # fixation

not only reduce fracture gap

A
  1. eliminate function interfragmentary strain thrpigh anatomic recon, compression of bone ends with rigid fixation and absolute stability (no # gap therefore <2% strain)
  2. maintain low strain environment through bridging tehcniques and implants that allow relative stability (maintina larger fracture gap and therefore distribute starin accross fragments)
32
Q

Under what conditions does primary bone healing occur?

A

Occurs under absolute stability with anatomic reduction, compression and rigid internal fixation. <0.1mm gap, <2% strain

Requires the use of lag srews, cerclage wire or a dynamic compression plate for compression

33
Q

List the 2 types of healing which occue with primary bone healing and briefly describe each

A

Contact healing - Occurs when the fracture gap is <0.1mm and interfragmentary strain is functionally elimated (<2%).
primary osteonal recon occurs > osteons elongate to directly bridge gap
Cutting cones of osteoclast spear head and osteoblast tail cross the fracture gap for simultaneous resorption and formation of lamellar bone. Progresses slowly at a rate of 50-100mcm/day

Gap healing - Occurs in the small gaps between zones of contact but must not exceed 1mm.
stability provided by adjacent contact zones
Gap fills with fibrin and vascular sprouts (provisional matrix) which is rapidly remodelled with deposition of collagen type I and III.
In days to weeks, lamellar bone fills the gap in a transverse pattern in a way which mimics intramembranous ossification (mechnically weaker) > osteoblasts arrive via peristeum and deposit bone.
Overtime, remodelled into longitudinally orientated lamellar bone (cutting cones form

34
Q

List the 5 phases of secondary bone healing

A

Inflammation - Organised haematoma forms (primary haemostasis, platelet activation, cytokines/GF released, WBC recruited, secondary haemostasis results in provisional matrix), progenitor cells activated and macrophages/fibrblasts/MSC infiltrate provisinal matrix is subsequently remodeled into granulation tissue to form a reparative/external callus

Intramembranous Ossification - Thin layer of bone laid down between periosteum and cortex by differentiation of periosteal progenitor cells into osteoblasts. This is an early hard callus but is insufficient to bridge and stabilise the fracture. onfined to the space between the periosteum and cortex, results in early subperiosteal increased bone formation

Soft Callus Formation / Chondrogenesis - mature granulation tissue marks end of inflammation > transition into fibrocatilage.
due to environment (hypoxia, GF) > mesenchymal stem cells differentiate into chondrocytes and produces a matrix rich in collagen type II. This soft callus is insufficient to decrese strain to a level that permits osteoblast survival

Hard Callus Formation / Endochondral Ossification - to increase stiffness of cllus chrondrocytes hypertorpyhy and mieralise the ECM
Occurs adjacent to the intramembranous ossification and mimics the process of endochondral ossification in developing bone.
Chondrocytes upregulate collagen type X, MMPs degrade matrix, VEGF allow vascular envasion.
Mineralised cartilage further reduces strain to a level that allows osteoclast and osteoblast survival. Osteoclasts remove mineralised matrix and osteoblast deposit woven bone. Sufficient strength and stiffness for return to function

Bone remodelling - Woven bone is weaken than lamellar and so is remodelled over months to years.
Osteoclast + osetoblasts form bone multicellar unit, reabsorb woven bone and deposit lamellar bone/osteons.
regaulated by wolf law: mechniccal fores converted to biocheical sgnals through processs of mechanptrasnduction
tensile load cause increase osteoblast activity

35
Q

bone blood supply (3)

A

primary nutrient artery: supply IM cavity and diaphysis

periosteal a.: entre only at muscle/ligament attachments and supply cortex

metaphyseal a. supply metaphysis

36
Q

bone blood supply after #

A

extraosseous from surrounding soft tissue supplies callus and frgaments that lost normal blood supply

37
Q

List the unique properties of juvenile bone

A

Contains actively elongating physes

Has a developing, yet incompletely anastomosed network of medullary vasculature

Robust periosteal blood supply

Periosteal membrane which acts as an external splint

Relatively thin cortices which exhibit low stiffness and strength but increased ductility

38
Q

List the techniques which must be adhered to for elastic plate osteosynthesis (EPO)

Why is this technique useful when treating juvenile long bone fractures?

A

Minimal manipulation of the fracture haematoma and periosteal envelope

Selection of bridging plate which spans metaphysis to metaphysis while avoiding the physes

Use of 2-3 screws at each end

Placing screws in a divergent manner without tapping due to soft thin cortices of juvenile bone

The use of a plate with excessively high stiffness in comparison to soft juvenile bones results in failure at the screw-bone interface due to high stresses. By using a long, unfixed length of bone plate, plate deformation is gradual, promoting favourable micromotion at the fracture site and distributing stresses along the entire bone plate, preserving the screw-bone interface.

compliance of plate-bone construct spares weak bone-screw interface fro shear stress (therefore reduce pull out)
compliance = wroking lengt (distane between inner screws) ^3 / area moment inertia x stiffness

39
Q

What is distraction osteogenesis?

What conditions it is used for?

A

Bone formation in response to linear tensioning of the provisional fibrin matrix resulting in the deposition of collagen type II in a longitudinal manner by fibroblasts and mesenchymal stem cells forming a central radiolucent fibrous interzone (intramemberenous ossification)

On either side of this zone, adjacent to the bone fragments, there is vascular ingrowth where osteoblasts deposit osteoid along the collagen bundles.

Used for angular limb deformities, generation of de novo done in limb sparing surgeries and treatment of critical gap defects

40
Q

Fracture assessment

A

clinical factors

biology
1.age
2.soft tissue envelope (provides initial blood supply, consdier before Sx, after #, after sx)
3.# gap and interfragmentray strain (anatomic recon leads to reduced ST envolope, if not rigid, potenitl for high strain, if >15% bone not heal, consdier relative)
4.location/bone tupe (cortical longr to heal, distal radius/tibia)
5.infection
6.concurrent dz

biomechanis
1.stability (strain determine tissue type, anatoic allows primary bone healing, stability depends on load sharing and therefore reduced implant failure, bridging allows secondary healing with relative stability but reduced load sharing)
2.multiple limbs
3.pateint size and activity
4.implant type (ability to resit what forces)