Engineering in Medicine 5 Lecture Notes

Lecture 1 Introduction
1. Course Overview
The course will include:

The musculoskeletal system

Bones, fractures and healing
Biomaterials and biocompatibility
Joints and joint replacements
The spine
The hand
Tissue Engineering
Rehabilitation Engineering
Legal framework for Medical Devices

2. Assessment

3.

60% examination
o Section A Short questions (no choice)
o Section B Long questions (two of three)
40% coursework
o Task will be set in late February
o Submission due mid-April (tbc)
A few basics

The scale of biological things might not be as usual as the scale of the things that are
manmade. One of the most fascinating characteristics of biology is how it organise
matter at a molecular level.
There are four organisational levels: cells, tissues, organs and systems. Cells are
important for tissue functions, mostly how tissue is created and regenerated. Cells dont
tend to provide the mechanical behaviour but they do generate and regenerate the tissue.
Cells are therefore very important for growth and healing. Tissues are cells organised
together and coordinated to provide a particular function. The cell structures formed in
the tissue are extremely complex. Each cell has a specialist job collaborating and
communicating with each other to provide a function. Organs are the organ level of the
tissues organised together. Engineers might not be able to create an organ similar to the
human organs, but they have created machines (e.g. dialysis machine) that can perform
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the same processes. The next step is to use tissue engineering to create a new organ that
has the same functions than the natural organ.
a. A generalised Eukaryotic Cell

Most of the eukaryotic cells share the structure shown in the picture above. The
nucleolus is where the DNA is stored. The DNA can be defined as the masterplan of a
human being, containing all the information required to build the human body as well as
running it. However, not every cell in the body has a nucleolus, for example the red
blood cells have not nucleolus.
The smooth endoplasmic reticulum is where the DNA information is captured, sent out
to the cell and the information is also processed. It takes the instructions included in the
DNA to actions to be performed by the cell.
A mitochondrion is an ancient bacterium. Therefore, a eukaryotic cell is a cell that has
an ancient bacteria stuck inside. The mitochondrion can be described as the cells power
plant, little energy units. They take molecules in and convert them to molecules that the
body can use as energy. The lysosome is used by the cell to eat up things and digest it.

Lecture 2 Biomechanics of the Musculoskeletal System

1. Connective Tissue Structure

There are two types of connective tissue in the body: tendons and ligaments.
Structurally, they are really similar. Tendons attach a muscle group onto a bone and
ligaments attach a bone onto a bone. Having said that, every single tendon and ligament
has a specific set of mechanical properties tailored to their exact position and the role
they provide. There are approximately 900 in the human body.
The largest structure in the above schematic is the tendon or the ligament itself. The
ligament or tendon then is split into smaller entities called fascicles. The fascicle
contains the basic fibril of the ligament or tendon, fibroblasts, which are the biological
cells that produce the ligament or tendon. There is a structural characteristic at this level
that plays a significant role in the mechanics of ligaments and tendons: the crimp of the
fibril. The crimp is the waviness of the fibril; we will see that this contributes
significantly to the nonlinear stress-strain relationship for ligaments and tendons and
indeed for basically all soft collagenous tissues.
Outside the ligament or tendon there is a membrane, the reticular membrane. The
membrane has two main characteristics: it helps feed the ligament or tendon from the
outside and it also helps the ligament or tendon slide. It is quite interesting that
ligaments and tendons do not have blood vessels. Therefore, ligaments and tendons
have very poor blood supply. This affects the healing properties of the ligaments and
tendons. The blood comes from the insertions, i.e. where the ligaments and tendons are
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connected to bones/muscles. This blood does not reach the middle; therefore the
nutrients are obtained from the membrane. Hence, it heals very poorly.
The fascicular membrane is located between the different fascicles (typically 3 or 4
fascicles within the ligament/tendon). The fibroblasts (within the fascicles) provide the
materials needed to create the ligament/tendon. Therefore, you rely on the fibroblasts to
generate the healing. Fibrils are used to sustain the ligament, i.e. it acts like a cable
made of several small cables.

The image on the left can be a bit confusing due to the fact that the darker and clearer
bits might look like thinner and thicker. However, this effect is due to the fact that the
ligament/tendon is desiccated before analysing it, so there no thinner and thicker parts.
Collagen is protein that makes up the majority of animal stuff. All the tissues a mammal
is made from are made from collagen. Fibroblasts manufacture short spans of collagen.
Collagen molecules find other collagen molecules forming a triple helix. This structure
is then assembled in fibril structures. It is a self-assembling process. The light and dark
parts are there because of the gaps between one and another (light) and no gaps (dark).
Although the light parts might seem structurally weak, the final structure is made to
avoid putting light parts together so distributing the strain.
The collagen is hydrophilic, i.e. it needs water. They need to suck in water. Therefore, if
you stretch it, the water comes out but you relax it, it goes back in the ligament/tendon.
The motion of water the ligament/tendon is really important as a mechanical entity. The
squeezing motion of water gives elasticity to the ligament/tendon.

2. Tendon versus ligament

There are three different types of collagen: Type I, Type II and Type III. Tendons
contain collagen Type I. It is interesting the fact that collagen is the only natural thing
with hydroxyproline in it. The main thing of the picture above is the blood supply
statements.
Blood supply is quite an important characteristic for tendons and ligaments. For
tendons, you have vessels in perimysium (membrane outside the tendon), periosteal
(steal means bone and peri means close to) insertions (where the tendon joints the bone)
and the surrounding tissues. For the ligaments, they use microvascularity from insertion
points and nutrition for cell population within the structure.
3. Connective Tissue Mechanical Properties

The figure above represents force vs. length for ligaments and tendons. It looks at the
mechanical response you get from different ligaments/tendons. Most of them have a
negligible response at the start of the action of the force. This is due to the waveform of
the collagen within the tendon/ligament. There is a reasonably elastic time and then it
reaches the top, it starts to tear up and fails. Different structures have different strengths.
The force applied to a tendon is equivalent to the force applied to the muscle. We are
overall strength not the stress-strain relationship. The Fascia lata joins a muscle group
around the hip to the side of the tibia. The Gracilis tendon goes from the ischial
tuberosity (sit bone) to the medium side of the tibia. The Gracilis tendon is often
sacrificed to be use elsewhere (usually reuse it as a ligament).
The Medial Patellar tendon joins the quadriceps to the knee cap and the Anterior
Cruciate ligament is one of the ligaments that sit in the middle of the knee.

The tendon/ligament is never going to be bigger than it needs to be.

A generalised structure (shown in the figure above) is an idealised behaviour of a
tendon/ligament due to the fact there will be only one instance when the stress-strain
curve shown can be observed because of the viscoelastic behaviour of the
tendon/ligament. That is because of the water inside the collagen helix.

Soft tissues are viscoelastic. Creep occurs when you apply strain and you hold it for a
certain period of time. Stress relaxation occurs when you apply stress to a
tendon/ligament and hold it and the ligament/tendon gets a bit longer with time. The
hydrophilic structure of the material is what makes it viscoelastic; therefore, the role of
water is very important with regard to mechanical properties.
4. Ageing and Soft Tissue Properties
The results shown in the
figure on the left are obtained
from New Zealand white
rabbits at 1.5, 6-7 and 40
months old. The stiffness and
strength of both ligament and
ligament-bone attachment
increased with increasing
maturity in the femur-mcltibia complex.
Collagen content and collagen
fibril diameter tend to
increase gradually in both
sexes until sexual maturation is reached. Collagen content is significantly greater in
males than in females after sexual maturation. The production of hormones oestrogen
and progesterone decreases collagen content.
As young organisms, the strength of ligaments/tendons is lower and it gets stiffer with
age.

Woo and colleagues tested FATC from young cadaver knees with an average age of 35
and older cadaver knees with an age of 76. They found that the linear structural stiffness
of the ACL decreased both when tested at 30 degrees of knee flexion and when tested
along the axis of the ligament complex. The structural stiffness in the ligament axis
averaged 183 N/mm for the younger group but only 158 N/mm for the older group.
Tests under flexion were 150 N/mm and 129 N/mm for the younger and older group
respectively. In addition, more specimens in the older group suffered avulsion failures
than the younger group.

5. Soft Tissue Healing

The causes of injury can be
trauma, exposure to heat or
chemicals or irritation. The
cascade shown in the figure on
the left is similar in all cases but
will proceed differently. There is
not an abrupt transition from one
phase to another, instead it is
gradual.
Healing proceeds by bleeding
moments after having an injury. It
happens instantaneously and up to
a few hours or days. Indeed, for a
crush injury, it may take 24 hours.

Inflammation is a necessary part of the

process, although it was previously thought to
be disadvantageous (cold compress, etc.). The
inflammation is due to the basophil, more
correctly basophilic granulocytes, which is a
type of white blood cell, circulatory
The chemical mediators include TNF-a, IL-1
with PGE2 or leukotriene B4 in tendon
(which also stimulate pain response).
The vascular response includes swelling,
redness, heat and tissue oedema (i.e. fluid
accumulation in tissue). The cellular response
includes dead/dying cells,
debris/contaminants. The fibrin mesh and
clots need to be removed.

Proliferation is the generation of repair

material. It is usually a rapid onset (1-2 days)
but will not peak until 2-3 weeks post injury.
The more vascular the injury is the short the
time taken. This also involves scar formation
by using granulation tissue, distinct from
native issue. Scar forms early but needs time
to become a functional scar.
Fibroplasia involves fibroblasts migrating to
the injury and subsequent proliferation.
Fibroblasts produce collagen and ground
substance GAGs and PGs. Collagen
formation requires oxygen and will be constrained by its accessibility; hence
angiogenesis. The angiogenesis is controlled by chemical mediators but may be
stimulated by ultrasounds, electrical stimulation and modest exercise (e.g. weight
bearing). Scar tissue matures with lymphatic development, nerve fibre ingrowth and
mast cell invasion, which determines the collagen orientation. Scarless healing occurs in
the womb and the mouth.
Remodelling is not swift, low
key response over many months
but important nevertheless.
The initial collagen deposition
produces weak randomly aligned
structured. Over time this is
absorbed and re-deposited as
oriented tissue. After remodelling
the proportion of collagen Type
III is reduced and collagen Type I is increased. Exercise can assist in remodelling as it
will provide appropriate stress.
Several key points of healing are:

Healing will not produce a like-for-like repair but it will be functional

Healing is a normal response and does not usually require intervention
Age affects the healing process e.g. bruising is pronounced in young and old.

Lecture 3 Biomechanics of the Musculoskeletal System (Part 2)

1. Muscle Structure
Voluntary skeletal muscle (muscle you control using your brain) is under conscious
control. Each fibre is an enormous, multi-nucleate cell, formed by fusing hundreds of
myoblasts end-to-end. They show a striated patter, reflecting the regular arrangement of
sarcomeres within each cell.
Cardiac muscle (they do their own thing without brain control) is similar to skeletal
muscle, but is not under conscious control. These mono-nucleate cells are much small,
but still show a striated pattern. This muscle is not affected by fatigue.
Smooth muscle is closer to non-muscle cells. No regular striations are visible and the
contractions are much slower. Smooth muscle is found in the blood vessels, gut, skin,
eye pupils, urinary and reproductive tracts.
2. Skeletal Muscle Structure

All skeletal muscles roughly have the same structure (shown above). It can be seen that
the structure is quite similar to the hierarchical structure of soft tissue.
You have a membrane outside of the muscle, the epimysium. The purpose of the
epimysium is to allow movement of the muscle with respect to each other. The muscle
is constituted by muscle fibre (which is a single cell). When a muscle cell starts life,
cells are uni-nucleated. However, when the muscle starts growing, the cells are joined

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together to create a massive multi-nucleus cell. The myofibril represents bundles of

fibres and is responsible for the movement (contraction) of the muscle.
a. A Myoblast Cell
The figure on the left represents a
myoblast cell (muscle sample).
The myoblast is formed by infinite
uninucleate cells to form a giant
multinucleate cell.
The sarcoplasmic reticulum (SR),
from the Greek sarx (flesh), is a
special type of smooth ER found in
smooth and striated muscle. They only
structure difference between the
organelle and the SER is the medley of proteins they have, both bound to their
membranes and drifting within the confines of their lumens. This fundamental
difference is indicative of their functions: the SER synthesizes molecules while the SR
stores and pumps calcium ions. The SR contains large stores of calcium, which it
sequesters and then released when the muscle cell is stimulated/ The SRs release of
calcium upon electrical stimulation of the cell plays a major role in excitationcontraction coupling.
When the brain sends a nerve impulse to your muscle that says contract, it is the
sarcoplasmic reticulum that allows the muscle to interpret and respond to that electric
pulse. The sarcoplasmic reticulum releases calcium ions when responding to the
impulse. When the impulse requires the muscle to stop working, the sarcoplasmic
reticulum will take back the calcium. It is the release and absorption of calcium ions that
allows the muscle to respond to the message that says contract or stop contracting. For
example, cramps happen due to the lack of electrolytes or dehydration, therefore you
change the amount of calcium that is available for the muscle to respond.
The most prominent roles of the mitochondria are to produce ATP (i.e.
phosphorylation of ADP) through respiration, and to regulate cellular metabolism. The
central set of reactions involved in ATP production is collectively known as the citric
acid cycle, or the Krebs cycle. However, the mitochondrion has many other functions in
addition to the production of ATP/
A dominant role for the mitochondria is the production of ATP, as reflected by the large
number of proteins in the inner membrane for this task. This is done by oxidising the
major products of glucose, pyruvate and NADH, which are produced in the cytosol.
This process of cellular respiration, also known as aerobic respiration, is dependent
on the presence of oxygen. When oxygen is limited, the glycolytic products will be
metabolised by anaerobic respiration, a process that is independent of the
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mitochondria. The production of ATP from glucose has an approximately 12-fold

higher yield during aerobic respiration compared to anaerobic respiration.
The mitochondria are super important since they recycle ADP/ATP which are used to
generate force.
3. Muscle Contraction
The structure of actin filament is shown in the picture below (a single contracting unit).

Depending on the purpose of the muscle, they will develop differently. For example, the
thigh muscle has to be strong whereas the spine muscle only help you maintain your
posture and therefore do not need to be that strong (fatigue-resistance muscle).
In the following figures, the contracting process is explained.
a. Attached
At the start of the cycle
shown in this figure, a
myosin head lacking a
bound nucleotide is
locked tightly onto an
actin filament in a rigor
configuration (so named
because it is responsible
for rigor mortis, the rigidity of death). In an actively contracting muscle, this state is
very short-lived, being rapidly terminated by the binding of a molecule of ATP.

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b. Released
A molecule of ATP binds
to the large cleft on the
back of the head (that
is, on the side furthest
from the actin filament)
and immediately causes a
slight change in the
conformation of the
domains that make up the
actin-binding site. This
reduces the affinity of the
head for actin and allows
it to move along the filament. The space drawn here between the head and actin
emphasises this change, although in reality the head probably remains very close to the
actin.
c. Cocked
The cleft closes like a clam shell
around the ATP molecule, triggering a
large shape change that causes the head
to be displaced along the filament by a
distance of about 5 nm. Hydrolysis of
ATP occurs, but the ADP and
inorganic phosphate (Pi) produced
remain tightly bound to the protein.

d. Force-generating
A week binding of the myosin head to a
new site on the actin filament causes
release of the inorganic phosphate
produce by ATP hydrolysis,
concomitantly with the tight binding of
the head to actin. This release triggers
the power stroke the force-generating
changing in shape during which the
head regains its original conformation.
In the course of the power stroke, the head loses its bound ADP, thereby returning to the
start of a new cycle.
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e. Attached
At the end of the cycle, the
myosin head is again locked
tightly to the actin filament in
a rigor configuration. Note that
the head has moved to a new
position on the actin filament.

4. Skeletal Muscle Variation

Type 2A or fast oxidative-glycolytic fibres have a fast contraction speed and a high
myosin ATPase activity. They are progressively recruited when additional effort is
required, but are still very resistant to fatigue. Their motor neurones show bursts of
intermittent activity. These cells are thin (high surface to volume ratio) with a good
capillary supply for efficient gas exchange. They are rich in mitochondria and
myoglobin which gives them a red colour. They are built for aerobic metabolism and
can cause either glucose or fats as a source of energy. These are general purpose muscle
fibres which give the edge in athletic performance, but they are more expensive to
operate than type 1.
Type 2B or fast glycolytic fibres have a fast contraction speed and high myosin ATPase
activity. They are only recruited for brief maximal efforts and are easily fatigued. Their
motor neurones transmit occasional bursts of very high frequency impulses. These are
large cells with a poor surface to volume ratio and their limited capillary supply slows
the delivery of oxygen and removal of waste products. They have few mitochondria and
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little myoglobin, resulting in a white colour (e.g. chicken breast). They generate ATP by
the anaerobic fermentation of glucose to lactic acid. These are sprinters muscle fibres,
no use for sustained performance.
5. Contractile Properties of Muscle
a. Isometric Force-Length Relationship
The Force-Length relationship, also called the Length-Tension curve is shown in the
Figure below.

IM represents the optimal muscle fibre length. Isometric represent constant muscle
length and isokinetic is the constant rate of change of muscle length.
Muscles operate with greatest active force when close to an ideal length (often their
resting length). When stretched or shortened beyond this (whether due to the action of
the muscle itself or by an outside force), the maximum active force generated decreases.
This decrease is minimal for small deviations, but the force drops off rapidly as the
length deviates further from the ideal. As a result, in most biological systems, the range
of muscle contraction will remain on the peak of the length-tension curve, in order to
maximise contraction force. Due to the presence of elastic proteins within a muscle, as
the muscle is stretched beyond a given length, there is an entirely passive force which
opposed lengthening. Combined together, we see a strong resistance to lengthening an
active muscle far beyond the peak of active force.

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b. Force-Velocity Relationship
The Force-Velocity relationship is the rate at which a muscle is stretched or shortened.
External forces, such as load or other muscles, usually regulate this; hence, it also
affects the force it can generate. Concentric defines when the muscle shortens as it
contracts and eccentric is when the muscle lengthens as it contracts.
As the shortening velocity increases, the force it can generate compared to when
isometric decreases in a hyperbolic fashion, eventually reaching zero at some maximum
velocity. However, the reverse holds true for when the muscle is stretched force
increases above isometric maximum, until finally reaching an absolute maximum. This
has strong implications for the rate at which muscles can perform mechanical work
(power). Since power is equal to force times velocity, the muscle generates no power at
either isometric force (due to zero velocity) or maximal velocity (due to zero force).
Instead, the optimal shortening velocity for power generation is approximately one-third
of maximum shortening velocity.
6. Tetanus
The primary symptoms are caused by tetanospasmin, a neurotoxin produced by the
Gram-positive, rod-shaped, obligate anaerobic bacterium Clostridium tetani. Infection
generally occurs through wound contamination and often involves a cut or deep
puncture wound. As the infection progresses, muscle spasms develop in the jaw and
elsewhere in the body.

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a. Wave Summation and Incomplete Tetanus

If a second stimulus arrives before the relaxation has ended, a second, more powerful
contraction occurs. The addition of one twitch to another in this way constitutes the
summation of twitches or wave summation. The duration of a single twitch determines
he maximum time available to produce wave summation. For example, if a twitch lasts
20 msec (1/50 sec), subsequent stimuli must be separated by less than 20 msec a
stimulation rate of more than stimuli per second. Rather than refer to stimulation rate,
we usually use frequency, which is a number per unit time. In this instance, a stimulus
frequency of greater than 50 per second produces wave summation, whereas a stimulus
frequency below 50 per second will produce individual twitches.
If the stimulation continues and the muscle is never allowed to relax completely, tension
will rise to a peak. A muscle producing peak tension during rapid cycles of contraction
and relaxation is in incomplete tetanus.
b. Complete Tetanus
Complete tetanus is obtained by increasing the stimulation rate until the relaxation
phase is eliminated. During complete tetanus, action potentials arrive so rapidly that the
sarcoplasmic reticulum does not have time to reclaim the calcium ions. The high Ca2+
concentration in the cytoplasm prolongs the contraction state, making it continuous.
Virtually all normal muscular contractions involve complete tetanus of the participating
muscle fibres.

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Lecture 4 Soft Tissue Mechanics & Viscoelasticity

1. Langer Lines
Langer lines show the orientation in which skin will cleave
when struck with a spike. This orientation gives you the
principal orientation of collagen within the layers you can
find in that region.
This is really useful for forensic science. It also suggests
incision orientation for minimal scarring.

2. Engineering Materials
a. Linear Elasticity
Hookes Law defines linear elasticity, which is an
appropriate assumption for many materials. Many
engineering materials can be assumed to be Hookean
for small strains. In reality, all materials are nonHookean.
b. Linear Viscous Fluids
Fluids behave in a similar way,
differentiating between Newtonian fluids
and non-Newtonian fluids.

c. Comparing Elastic & Viscous Response

If we impose a step change in stress
loading in an elastic material, you
would also have a change in strain
(related to the stress).
For a perfectly elastic material, strain
will increase and decrease with the
stress. For a perfect Newtonian fluid,
the strain will reach while the load is
applied and the strain will remain after
the load is removed.

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3. Viscoelasticity
Three characteristic behaviours are observed, as shown in the figures below.

If you were to put on a

constant load, you would
get a step-like response for
the elastic part and then a
viscous response, i.e.
creep.
If you put a step
deformation and maintain
that deformation, you have
stress relaxation.
These two characteristics creep and stress relaxation, are really characteristic of
viscoelastic materials. If you put cyclical load, the material has a memory of the
previous loads applied and will behave differently.
4. Linear Viscoelasticity Constitutive Models
a. Kelvin-Voigt Solid Model

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It this case, you have a simple model of a spring in parallel with a dashpot. This can be
defined as follows:
= ! + ! (1)
= ! = ! (2) and therefore = ! = !
We also know that:
! = ! ! ! = ! !
where E is the Young Modulus. Using (1):
= ! + ! = ! ! + ! ! (3)
Combining (2) and (3):
! = ! + !
b. Maxwell Fluid Model

As shown in the figures above, the Maxwell Model is constructed by connecting a

spring and a dashpot in a series. In this case, a stress applied to the entire system is
applied equally on the spring and the dashpot ( = s = d), and the resulting strain is
the sum of the strains in the spring and the dashpot ( = s = d). Through stress-strain
analyses similar to those carried out for the Kelvin-Voigt model, a differential equation
relating stresses and strains for the Maxwell model can be derived in the form:
+ =

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c. 3-Parameter Solid Model

We know Kelvin element equation:

! = ! + ! = ! + !
where D is the differential operator for d/dt. By inspection,
= ! = ! = ! = !
Using D as an algebraic term,
! = ! + ! =

!

+

Hence,
= ! = ! =

!
!
+
+
!

as = ! = ! ,
=

+
+
!

Multiplying through by + ,
+ = +

+ =
+ 1 +
!
!
!
+ =

+ !

+
!
!

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Lecture 5 Soft Tissue Mechanics Linear and Non-Linear Viscoelasticity

1. Storage and Loss Moduli
Perfectly elastic materials occur when stress and strain are in phase. A material is
perfectly viscous fluids is when stress lag strain by 90 degrees. Normally, viscoelastic
materials lie between these two. Indeed, ALL materials lie between the two, with strain
always lagging stress.
Stress and strain in a linear viscoelastic material can be represented using the following
expressions:
= ! sin = ! sin ( + )
where is the period of strain oscillation, is the
phase lag between strain and stress and t is time.
The Elastic Modulus may be define as:
= + = 1
where the storage modulus and Loss modulus are:
! =

!
!
cos !! = sin
!
!

The same theory holds for shear moduli:

= +
2. Creep Compliance
In the case of linear viscoelasticity, the creep compliance C(t) relates the creep strain
(t) at time t with the stress increment applied at time 0, i.e. (t)=C(t) (0). In other
words, C(t) is the strain (t) at time t due to a unit stress increment at time 0, i.e.
C(t)= (t) for (0)=1.
3. Relaxation Modulus
In the case of linear viscoelasticity, the relaxation modulus G(t) relates the relaxation
stress (t) at time t with the strain increment applied at time 0, i.e. (t)=C(t) (0).
In other words, C(t) is the stress (t) at time t due to a unit strain increment at time 0,
i.e. C(t)= (t) for (0)=1.
4. Sinusoidal Load
The diagram shown in the next page shows a stress-strain curve for a linearly
viscoelastic material. The role of the phase angle or loss angle d (delta) is illustrated.
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The loss angle d, or the loss tangent tan d, may be considered as the fundamental
measure of damping in a linear material. Other measures, such as those developed
before, are often cited in analyses of viscoelastic behaviour.
5. Non-Linear Viscosity
The relaxation modulus G(t) varies
with the initial stress. Also, it can be
observed that the error bars are large,
which implies that there is an
inherent problem with empirical
work on biological systems.
The experiment shows an isochronal
curve at time 2.4s obtained from
stress relaxation tests performed on
15 Rabbit Medial Collaterals (MCL).
The graph shows the non-linear strain-stiffening behaviour found in ligaments. The
error bars represent the standard deviation.
The rates of creep and relaxation vary, as shown in the figures below.

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The figure on the left shows stress vs. rate of creep relaxation. The rate of creep is seen
to be non-linear with respect to stress. This figure represents the data pooled together
from both testing protocols (multiple stress level and repeated stress level) for creep
tests. The graph shows that the rate of creep (n) changes by an order of magnitude
through the low load region.
The figure on the right shows strain vs. rate of stress relaxation. The rate of stress
relaxation is seen to be non-linear with respect to strain. The figure represents the data
pooled together from both testing protocols (multiple strain level and repeated strain
level) for stress relaxation tests. The graph shows that the rate of relaxation (n) changes
by an order of magnitude throughout the low load region.
Additionally, the rate of creep decreases
when the stress level is increased, as can
be see in the figure on the left. Indeed, the
graph shows creep at multiple levels of
stress (Log-Log scale).

6. Fungs Quasilinear Viscosity Model (QLV), 1972

a. Superposition of effects in linear viscoelasticity
Suppose that various strain increments (i) occur at the successive time instants i,
i=1,2, etc. and that we wish to know the stress response at the later time t (t max i).
Superposing the effects of the successive strain increments, we get:

In case the strain varies smoothly with time the superposition of the effects of the
!!

elementary increments of strain at the previous times , = !! , leads to the

hereditary integral:

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Note that this means that the elementary increment of strain at the previous time
leads to an elementary increment of stress at the current time t given by:
= ( )()
The integration starting at = means that the effects of all relevant previous strain
changes must be taken into account.
Assuming that the deformation starts at =0, with (=0) for <0, and that possibly nonvanishing jump exist at = 0 0 0 = 0 , it follows from (S) and (I) that:

All the above developments show that in linear viscoelasticity the stresses depend
linearly on the strains and the stress at the current time t results from the linear
superposition of the effects of the strain changes in all relevant previous times .
b. Fungs Quasilinear Theory for bio-viscoelastic solids (1D)
Fungs theory is also based on the idea of linearly superposing at the current time the
effects from past changes in the system, and leads also to a hereditary integral. But the
theory cannot preserve the linear dependence of the stresses on the strains, since, as
already observed, the elastic behaviour of the soft tissues typically is highly non-linear.
Let T be the nominal stress, the stretch ratio, and let T(e)() denote the instantaneous
elastic response of the material, i.e. the stress instantaneously generated in the tissue
when a step stretch ratio is imposed on the tissue. In other words, T(e)() characterises
the elastic constitutive law that holds when relaxation effects are not taken into account.
T(e)() is typically a non-linear function that frequently involves exponential
contributions.
In the figure below, (t)=1, T(e)(t)=0, for t<0. At t=0, a step stretch ratio is imposed on
the tissue such that, for all t>0, (t)=(0*) and by definition of T(e)

with from (T0) and (TG), for G(0)=1:

25

Comparing these results with the linear viscoelasticity, it should be clear that:

In linear viscoelasticity G(t) has dimensions of stress, but it is non-dimensional

in quasilinear viscoelasticity.
In quasilinear viscoelasticity G(t) is normalised to be 1 at t=0.

Assuming that ()=1, T(e)( )=0 for <0, the proposed 1D quasilinear constitutive
equation for soft tissues has the form:

Consequently, this constitutive law involves linear superposition of the effects of the
instantaneous elastic stresses at all previous times. Linear viscoelasticity involves linear
superposition of strains, which is not valid in quasilinear viscoelasticity.
It is important to consider the fact that the rate of stress decreases as creep increases, as
shown in the figure below. The QLV model fails to fit experimental data at higher
initial strain levels.

7. Case Study Degloving Injury

The patient presented the injury shown in the figure. Tetanus status was unknown, but
the patient recalled that she had her series of tetanus toxoid when she was a child. She
had no allergies, no history of renal dysfunction and did not take any medication. A
detailed hand examination was carried out as part of the secondary survey. Sensation
was found to be intact the Median, and Ulnar nerve distribution. Motor function for all
three nerves was intact. There was no sensation to the radial side of the thumb, which
had a hemi-degloving type injury (see picture). Radial and Ulnar pulses were present,
26

and there was no evidence of an acute

Carpal Tunnel syndrome. There were no
injuries to the left upper extremity
proximal to the forearm.
0.5cc of Tetanus Toxoid was given, and
the patient was also given 1g of Ancef,
40mg of Gentamycin and 1.5 million
units of Penicillin. After informed
consent was obtained, the operating
room was booked for an urgent irrigation & debridement of the patients hand. Limb
salvage was considered to be possible given intact perfusion and neurological function.
A staged procedure was felt to be the best option.
There was an extensive degloving of the
distal thumb, with most of the distal phalanx
missing (see trauma room pictures on the
right). Clinical and radiographic
examination revealed that almost of the
total depth of the carpus was missing
(including articular cartilage) and that there
was massive bone loss from the distal ulna.
Finally, there was a large amount of soft
tissue loss.
First stage procedure was extensive debridement and irrigation with insertion of radioulnar pin. The second stage included removal of radio-ulnar pin and resection of ulna,
bone plates inserted from radius to 2nd and 3rd carpal and pin to immobilise thumb to 2nd
PP. The third step consisted of the transfer of free flap.

27

Postoperatively, the arm was placed in a full-length splint. Perfusion to the free flap was
monitored for one week using continuous Laser Doppler Flow (LDF) readings. The
hand and elbow were immobilised for four weeks at which time sutures and the
proximal radio-ulnar pin was removed. The wrist remained splinted but active ROM
was begun at the MCP, PIP and DIP joints of the figures and at the elbow.
At the six week mar, the pin across the MP joint of the thumb was removed, and a
removable thermoplastic splint was applied. Aggressive physiotherapy of the elbow
(flexion / extension / pronation / supination) was begun, as was active and passive ROM
of the fingers. Two months postoperatively, the patient was doing well, had regained 15 to 90 degrees of flexion at the MCP joints of her fingers, full ROM of the PIP/DIP
joints, and could pro/supinate 60 degrees each direction. The free flap remained viable
and this young woman is scheduled for debulking of the free flap approximately six
months from her last surgery.

28

Lecture 6 Bone Architecture and Hard Tissue Mechanics

1. Bone is a composite
a. At a Supra-Structure Level

The mid-section, called diaphysis, is made of cortical bone. The end-sections, i.e.
metaphysis and epiphysis, are made of cancellous bone. The physis, or growth plate,
are the start from where the bone grows.
Why do we have cancellous bone at the end and compact bone in the middle? Bending
moments are higher in the mid-section so a nice, thick tubular structure is more
appropriate (tube greater bending stiffness, 2nd moment). Also, cancellous bone is
found at the end of the bone, where bones are connected to the joints, which is a large
surface area used to transfer loads. Besides, if it were compact bone, the shell would
collapse under the loads.
Lamellar bone may be formed as a solid mass in compact (cortical) bone or as an
open, sponge-like network in cancellous (trabecular or spongy) bone. Most bones are
organised such that they have a rigid, outer cortical shell of compact bone and an inner
cancellous zone, the strength of which is provided by its connecting meshwork of
trabeculae. The spaces between trabeculae and the central medullary cavity are filled
with bone marrow where haematopoiesis (blood cell formation) occurs (red bone
marrow) or adipocytes are found (yellow bone marrow).
Lining Haversian canals and internal surfaces of the marrow cavities is the endosteum, a
layer of stem cells and inactive osteoblasts. A fibrocollagenous connective tissue layer,
the periosteum surrounds most outer surfaces of bone and contains numerous stem cells
and the neurovascular supply of the bone.
29

b. And at a Meso-Structural Level

Compact bone is organised into lengthwise bony columns (Haversian systems or

osteons) in which concentric bony lamellae surround a neurovascular central channel a
Haversian canal. Haversian canals are interconnected by perpendicular Volkmanns
canals that also bring the blood supply from the surface of the bone. Osteocytes are
trapped within the bone lamellae in spaces called lacunae. Canaliculi are tiny channels
interconnecting osteocytes in lacunae and Harvesian canals. Bone remodelling occurs
during growth and also in adult response to demands on calcium homeostasis and
changing functional stresses. O
Osteoclasts (resorb or eat bone) bore a tunnel called a resorption canal which carries
capillaries and osteoblasts (create bone) that lay down concentric layers of bone to
form a new osteon. Between osteons are interstitial lamellae that are remnants of the
previous osteons. At both the external and internal surfaces of compact bone,
circumferential bone lamellae are formed.
There is always the same rate of making bone and resorbing bone in a healthy bone:

Children skeleton is completely replaced in a year

Adults every bone is replaced every 10 years, i.e. the process slows down

In cancellous bone, the vascular function of Haversian canals is replaced by blood

sinusoids in the marrow and bone remodelling occurs at the surfaces of the trabeculae.
Finally, the cement line is the region where new osteon is bounded to old osteon.

30

c. At a Molecular Level
At a molecular level, we observe collagen and
Hydroxyapatite (Ca5(PO4)3(OH)). Collagen for bone has
become mineralised, i.e. it has embedded crystals of
calcium.
A natural composite material, protein + ceramic (matrix of
collagen) makes up the compact bone.
2. Hierarchical Bone Structure

The hierarchical bone structure gives it very anisotropic properties.

3. Cell Phenotypes in Bone

There are two paths: (A) come from tissue stem cells and (B) come from blood stem
cells. Osteoblast, osteocyte (A) and osteoclast (B) differentiation is shown in the figure
31

above. Preosteoblasts start to differentiate slowly from mesenchymal stem cell in the
bone marrow until they have the location and phenotype of osteoblasts. As the osteoid
becomes mineralised by osteoblasts, these cells become enclosed in lacuna as
osteocytes. Osteoclasts are giant multinucleate cells that differentiate from
hematopoietic cells of the monocytes/macrophage lineage in the bone marrow.
4. Mechanical Properties of Bone 1
a. Healthy Cortical

The figure on the left shows the typical stress-strain behaviour for human cortical bone.
The bone is stiffer in the longitudinal direction, indicative of its elastic anisotropy. It is
also stronger in compression than tension, indicative of its strength asymmetry
(modulus is the same in tension and compression).
The figure on the right shows the creep response of cortical bone for three different
stress levels. When a low stress is applied to the bone, the strain remains constant over
time, and there is no permanent deformation after unloading. For stress just below yield,
strains increase with time at a constant rate, and a small permanent deformation exists
after unloading. As the magnitude of the stress is increased, the rate of creep increases,
and a larger permanent deformation exists after unloading.
For bone, we know that it is stronger on compression than on tension.

32

Several points can be extracted from the figures above (dependence of UTS of human
cortical bone on volume fraction in % (ages ranged 20-100) on the left and the modulus
versus calcium content in 18 different species on the right:

Women greater bone range (density variation)

More calcium Higher Youngs Modulus in compression
The figure on the left shows the
strain-rate sensitivity of cortical
bone for longitudinal tensile
loading. Typically modulus and
strength increase only by factors 2
& 3 respectively, as the loading
rate is increased by 6 orders of
magnitude. The higher strain rates
shown here may occur in vehicular

accidents or gunshot wounds. In conclusion:

High strain bone behaves more brittly

Low strain more elastic
The figure on the left is a representation of
the viscoelastic properties of cortical bone.

33

b. Healthy Trabecular
It can be observed in the figure on
the left that the trabecular bone of
the femur is much stronger than the
trabecular bone found in the
vertebra.
For both of these, it is interesting to
see how it becomes weaker with
age, in a linear sort of way.

The figure above shows the dependence of yield stress in tension, compression and
torsion on apparent density for bovine tibial trabecular bone specimens oriented
longitudinally and transverse to the principal trabecular orientation. Overall, strength is
greatest in compression and least in shear. In compression, the strength-anisotropy ratio
[SAR = (longitudinal strength)/(transverse strength)] increases with decreasing density.
5. Bone Fatigue
The figure on the left shows fatigue and creep
behaviours for human cortical bone versus
time to failure. For fatigue loading, the
ordinate on this graph can be converted to
cycles by multiplying the time to failure by the
frequency, which is typically one cycle per
second for normal walking. Note that creep
and fatigue resistance are lower in tension,
consistent with the monotonic behaviour.
34

IF you are rigorous exerciser, there is a point where you will be exposed to fatigue
damage, really quite quickly.

The figure on the left shows the comparison of loading and reloading tensile stressstrain curves for human cortical bone. On reloading, the modulus is similar to that for
initial loading but it is quickly reduced to a value that is close to the perfect damage
modulus, the secant modulus at the unloading point. Substantial residual strains are
evident after 1 and 2 minute holds between cycles. Nf represents cycles to failure and
delta epsilon is the applied strain amplitude.
The figure on the right shows the compressive load-unload-load behaviour of human
vertebral trabecular/cancellous bone. Similar to cortical bone tested in tension, an initial
overload causes residual strains and a reloading curve whose modulus quickly reduces
from a value similar to the intact modulus to a value similar to the perfect damage
modulus.
As a general note, generic difficulty with in vitro fatigue measurements that bodys
healing processes are not occurring over the timeline. These experiments have to be
assumed to be worst-case scenarios.
6. Bone Fracture Mechanics
The figure shows the variation of
cortical bone fracture toughness Kc,
with bone density for longitudinal
slow crack growth. Solid circles are
bovine femoral data at 0.06 cm/min
and open circles are 0.003 cm/min.
Fracture toughness Kc is the
measurement of the resistance of a
35

material to fracture. Bone is interesting because it displays viscoelastic behaviour, i.e.

quite brittle a high strain rates but quite elastic at low strain rates. Therefore, it can be
suggested that there is a relationship between fatigue strength and the microstructure of
the bone.

The toughness of the bone can be increased by making it difficult for the crack to grow.
Presumably, there are many mechanisms involved in this process in bone, two of which
are illustrated above unbroken collagen fibrils bridge the crack and damage ahead of
the notch at a Haversian canal consumes energy and may cause the crack from the
growing tip to deflect.
Stress fracture by micro-cracking:

0 cracks/mm2 in the young

5 cracks/mm2 in the elderly

7. The Immature Skeleton

The fact that children renew their bones every year reduces the chances of finding
cracks in bones.
Adult have 206 bones
compared to the 270 bones
for an infant.
The process of growing
bone is shown in the figure
on the left. For certain
bones, the bones will grow
from the growth plates.
Growth plates are very
directional, i.e. it grows in
just one direction. It will lay
material behind it. It is
36

possible that bones growth at different rates.

8. The Aged Skeleton
The bone strength goes down very
significantly. That is why
fractures are highly associated
with the elderly, since bones are
much weaker and also balance is a
big issue.
The figure below shows the
change in the trabecular structures
of vertebrae.

9. Bone Remodelling
The figure on the left
represents Wolffs
Law.
This law holds that
every change in the
form or function of a
bone is followed by
adaptive changes in its
internal architecture
and its external shape.

37

10. Bone Disease Osteoporosis

Primary Osteoporosis is a metabolic bone disease characterised by low bone mass and
micro-architectural deterioration of bone tissue, leading to enhanced bone fragility and
increased fracture risk.
Secondary Osteoporosis results from a variety of chronic conditions that significantly
contribute to bone mineral loss, or from effects of medications and nutritional
deficiencies.

38

Lecture 7 Bone Fracture & Healing

1. Types of Fracture

Different types of fracture can be observed in the figure above:

Closed or simple fracture the bone is broken, but the skin is not lacerated
Open or compound fracture the skin may be pierced by the bone or by a blow
that breaks the skin at the time of the fracture. The bone many or may not be
visible in the wound
Transverse fracture the fracture is at right angles to the long axis of the bone
Greenstick fracture fracture on one side of the bone, causing a bend on the
other side of the bone. This is common in children due to the fact that their
bones are more flexible (less mineralised)
Comminuted fracture a fracture that results in three or more bone fragments,
which is interesting in terms of how to manage the healing process
Spiral fracture fracture due to torsion

39

2. Bone Healing

Primary versus secondary mineralised tissue repair. (A) When a small fracture gap
occurs and bone remains stabilised, osteoblasts deposit bone perpendicular t the bones
long axis, filling the gap and serving as a scaffold for future remodelling. (B) In primary
contact repair, fractured ends are held in direct apposition. No excess ECM is required.
Cutting cones are formed as osteoblasts absorb damaged bone, followed by osteoblasts
synthesising osteoid, which becomes mineralised to form lamellar bone. (C)
Unstabilised fractures are initially repaired through ECM production by fibroblasts and
chondrocytes arriving from the periosteum to form a stabilising soft callus. The
collagenous ECM becomes mineralised, forming woven bone, also referred to as hard
callus.
In conclusion, bone healing is not necessarily just one process.

40

Haematoma Stage Haemorrhage, clot formation (within hours to days)

o Functionally useless limb, since blood is not exactly load carrying. White
blobs show dead bone; black ones bone cells that can respond to the
damage and healing.
Inflammatory Stage Begins within 48 hours, inflammatory cells appear.
Organisation and resorption of clot
o Cleaning immune system cells come to deal with dirt, bacteria and any
foreign bodies; they also resorbs the dead cells (i.e. bits that cant
repaired)
Granulation Tissue From 2-12 days. Presence of mesenchymal cells,
fibroblasts and new capillaries
Reparative Phase
o Soft Callus One week to several months. Callus grows and bridges the
fracture site; cartilage and trabelcular bone laid down
o Hard Callus One week to several months. When callus has sealed the
bone ends. Trabecular bone
o Start to lay down collage in the wound site. But a different type to the
normal beautifully oriented one. It goes down as this random spaghetti
mass, basically gets put in the wound as soon as the body makes it. This
creates the callus. New bone is being laid down in a random sort of way,
at all places where the collagen spaghetti was laid, transforming from
soft to hard callus.
Remodelling Continues for several months: reorganisation of bone; original
cortex restored
o Once you have got the hard callus, the woven bone, you regain the
functional properties. Once youve got to the hard callus, you can walk
41

around and get release home Over the next two years, hard callus will be
gradually replaced: woven bone replaced by cortical via the osteons
moving around. The ballooning would be completely replaced under
perfect healing circumstances and become as it used to be; this is
unlikely in practice, so the callus will remain there for many, many
years. Obviously this depends on age, but such breaks are unlikely to be
encountered in young people.
a. Pagets Disease
Pagets disease of bone is a condition in which the normal cycle of bone growth is
disrupted. This can cause bones to become weakened and deformed.
After osteoporosis (brittle bones), Pagets disease is the second most common type of
bone disease.
For reasons that are unclear, Pagets disease is most common amongst people of British
descent. The condition is most widespread in the UK, and is relatively widespread in
countries that have experienced high levels of migration from the UK, such as the US,
Australia, New Zealand and South Africa.
Pagets disease is an age-related condition. It is estimated that 1-2% of white adults who
are over 55 years of age have Pagets disease. This figure rises to 5-8% for white people
who are over 80 years of age.
The causes of Pagets disease are unknown, but it has been suggested that it could be
triggered by a combination of environmental and genetic factors.
3. Mechanobiology of Bone Healing

42

The bone wants to get back to the lamella bone stage. As part of the process, we will
create woven bone. But there are different types of it and different routes to it.
If the body gets strain across the fraction (motion at the wound site) while healing, it
directs towards fibrous cells, laying down the random collagen spaghetti. If you do not
have motion (no strain) but you have hydrostatic pressure in the wound, you get tissue
more skin to cartilage laid down. Over time, it will be re-mineralised into lamella bone.

Hydrostatic pressure from swelling

Strain the stability of the fracture site

The actual route is likely to be somewhere

through the middle of these two scenarios.
Therefore, we can manage the healing process by
managing the amount of strain and pressure. This
way, you can promote the bodys self-heating
processes.
4. Mechanical Properties of Healing Fracture
The top diagram represents a
health bone. An inward callus
(middle) is less stiff than an
outward callus (bottom),
which is why biology
compensates the lower
strength of the new material
by putting the material in the
best place, strengthening the
section properties.

Axial Stiffness EA where A=pi/4(Dext Dint)

Bending Stiffness EI where I=pi/64(Dext4 Dint4)
Torsional Stiffness GJ where J=pi/32(Dext4 Dint4)
a. Rat Femoral Mid-Diaphysis Osteotomy (bone cut in two)
The figure is the schematic
representation of a callus showing the
spatial heterogeneity in indentation
modulus across the callus. Higher
modulus values were found within
the centre of the gap compared to
lower moduli found in the periphery
(P<0.05). N.M. denotes non43

measureable indents due to extremely high compliance of the tissue at those indent
locations. (B) Approximately matched CT cross-section to (A). Indentation modulus
and TMD for each of the five VOIs are also defined.
For indentation modulus, the height of each bar and of each error bar represents the
mean and standard deviation, respectively, of all indents in the VOI for both calluses
(e.g. n = 176 for the centre of the gap). In contrast, each callus yields only one value of
TMD for each VOI. Hence, for TMD, the height of each bar and of each error bar
represent the mean and standard deviation, respectively, of the average TMD values of
the two calluses (n = 2 for each VOI). Bars that are not labelled with the same number
(indentation modulus) or letter (TMD) are significantly different from one another
(P<0.05).
b. Time of Healing
The mechanical properties of the bone that will be stabilised are changing with time.
Therefore, in the best case, our stabilising material would change its properties too. The
main characteristics are:

Callus increases with time

Stiffness increases with time
Near normal stiffness after 27 days
Does not correspond to radiographs

5. Fracture Fixation External

a. Cast

Classic and simple

Relies on compression of soft tissue
o Good fit vital
Materials
o The plaster provides hydrostatic pressure,
which promotes wound healing (though it also
retards inflammation). However, you will lose
the hydrostatic pressure over time as the
swelling goes down (you put the cast on early
on); hence, the plaster will become lest tight.
Cost
Workability
o GFRP
Weight

This system is ok for simple transverse & oblique type of fracture.

44

b. External Fixator
This device was invented by Lizarov in Russia and then
used in western countries. Until recently, it was only used
for severe trauma involving soft tissue damage.
Improvements in bone screw design and insertion
techniques allied to easier mechanics of frame assembly
have widened its appeal.
There is nothing going happening on the inside. Pins are
located into the bone, which provides external support.
This technique is interesting because you really tune the
stiffness to the particular time point. As fracture heals,
you can reduce the amount of metalwork, reducing the
stiffness of the fixator as the stiffness of the callus starts
to increase.

The design gives freedom to make adjustments over time to correct skeletal deformity
and leg lengthening. Note the use of multiplanar pin insertion and circular frames.
Because you can use the external to drive the deformity, it is good for deformity
healing.
As the callus mineralisation increases so does the stiffness.
When the load taken by callus is increasing, two things must
be done:

Off loading of fixator

Pins may be removed

45

6. Fracture Fixation Internal

Different screws can be used to fix internal fractures. These
fractures are a common type of fracture in sport injuries.
Indeed, you just screw back the bit that fell off.
The figure below shows three types of screws, i.e. cortical
(left), cancellous (middle) and canulated (right).

For cortical bone, a very shallow, less open, self-tapping screw thread is used. This is
due to the fact that this screw is less likely to pull out.
The canulated has a characteristic hole in the middle. You are often not able to maintain
a good field of view in the wound (blood, etc.); hence, using these screws you can use a
guide wire to help you control the wound. This kind of screws would probably stay in
the body for good.
Many designs and sizes of bone plates
are used for myriad fracture types and
locations.
This is particularly used in fractures of
the arm as well as the face (e.g. jaw),
you would not tend to see them used in legs simply because they are not strong enough.
There are two different types, with a difference in how the head of the screw interacts
with the top of the bone plate.
a. Conventional plates Non-locking screws
In conventional plate fixation, as the
screws are tightened, and the screws
displace the bone into compression, a
compressive force is generated between the
plate and the bone. This compressive force
must be sufficient in order to generate
46

enough friction between the plate and the bone to maintain stability of the fracture. As
long as the resultant load from body weight and muscles do not exceed what the
frictional interface can support, the construct will remain stable and prevent collapse.
As you screw down, the bone is pushed to the side () due to the way the screw head is
made. This helps get the two bones closer together, promoting direct contact type of
healing. It will not be proper contact repair because the periosteum is broken. However,
no fracture is of a certain perfect type, but a mixture of the types of healing.
The big concern with this type of healing process is the fact that you have created a
huge contact stress between the bone and the plate, seriously squashing the periosteum
as well as compromising blood supply and possibly damaging the periosteum.
We must also take into consideration Wolffs Law, i.e. bone responds to its mechanical
environment. In this case, the stiff piece of metal is taking a lot of the load, so it is
possible that the bone will decide it is not need and in the long term this could lead to
resorption, i.e. a weakened bone. This is why you would usually want to take it out after
a time.
Taking a plate in/out is a very invasive operation since you need to get through nerves,
which might lead to significant risk of damage (e.g. in the arm it could be the muscles).
Therefore, plates are now reserved for special cases.
b. Locking Plates

The figure above shows the initial stress in the bone due to tightening (roughly 0).
When the bone is loaded along the axes of the bone, the bone around the screw is
compressed on the load side of the fracture.
The main difference with conventional plates is the fact that the screws have heads wit
thread in them. This system eliminates the contact between plate and bone, preserving
the periosteum and bone supply. There is also less chance for stress shielding (which
causes bone resorption). You are not trying to put the bones together.

47

c. Comparison of plates

The figure above shows the initial stress in the bone due to tightening. When the bone is
loaded along the axes of the bone, the bone around the screw is compressed on the load
side of the fracture.
As the load is increased, and the angle between the screw and the plate starts to change,
the resultant loading vector on the screw changes from pure compression to a
compressive and a tensile component. It is this additional tensile component which,
when the elastic limit of the bone is exceeded, will cause toggling and eventual collapse
across the fracture gap. On the other side, the bottom figure shows no load transfer, i.e.
a much more efficient system.
For the figure on the top, the cortical bone has a grain to it due to the osteons, so the
screws will find it easier to move along those grains. Also creep will help with the
screws moving. This reason why is not currently used in leg is because the leg is
exposed to frequent, high and continuous loads.
Regarding the plate, hardly any strain will be found on the plate side whereas more
strain will be observable on the non-plate side. This will create a bending moment. A
complex strain environment is created, which is not great for the healing process since
an ideal, controlled strain environment is preferred.

48

d. Unstable Constructs
A construct in which compression cannot be achieved across the fracture is unstable and
at risk for failure. Plates alone cannot tolerate the functional loads of a limb, and if the
fracture does not heal, the construct may eventually fail due to fatigue under cyclical
loading.
This situation may be due to:

Severe comminution consider bridge plating techniques

Bone loss
Poor quality bone
Poor screw technique
Improper choice of implants
The figure on the left shows a knee joint with a very
bad fracture to the bottom end of the femur.
This represents really bad surgery. Significant
moment will be encountered on the left side due to
the lack of support. But the main reason this will not
hold is that there is a crack running up and one of
the screws up top is not even screwed properly.
Besides, the bottom screws are screwed into mush.
Therefore, only certain screws actually carry some
load. This creates big moments, which will lead to
very poor healing.

49

e. Nails
Factors that affect the rigidity of intramedullary nailing include the cross section of the
rod, whether distal screws are used (especially to increase torsional rigidity), and the
material from which the rod is made. Although in general less stiff than either plate or
external fixation, the advantage of intramedullary nailing for femoral shaft is early
ambulation, ease of surgery, and the ability to remove rod relatively easily.
There are two types of nails:

Reamed (left)
o Early designs
o Out of favour
Unreamed (right)
o Various configurations of locking screws

Unreamed nails are pushed into the canal of the bone. Then,
the nails are screwed into place at either end.
Reamed nails require removing the canal to then put the
nail in.
Screwing the nail in will make it much stiffer at either end. The reamed one relies on the
friction between the nail and the bone to transfer the load whereas the unreamed ones
transfer the load using the screws.
This technique is good for fractures in the area of the diaphysis. Also, because the nail
is in the middle of the bone, this method provides very good strain environment for the
healing, but there is a possibility of stress shielding if you leave the nail; therefore, you
will want to take it out as soon as possible.
The figure bellow shows different nail cross sections:

The Kntscher one is based on the use of reaming and undersized slotted nail that
results in compression of nail and a force exerted on the IM canal and interference fit.
Early ones were solid. Then, they decided these were to stiff so they made them hollow.
However, they later realised they were not stiff enough and so on. They were optimised
50

over time, being the Russel-Taylor the most common at that stage. However, the most
common is the AIM, which strives for isoelasticity.
Different results of nail bending stiffness are shown in the figure below.

Different diameters for different patients

are used for these experiments, i.e.
patients with different canal sizes.
In conclusion, you cannot paly with the
external dimension of the nail due to the
fact that it is dictated by the patient.
The figure below shows bending vs.
torsional stiffness of the nail.

Slots are introduced since they make things less thick from the torsions point of view.

51

Lecture 8 Synovial Joints

1. Joint Types
Some joints just join stuff, but not really create motion (fibrous generally). For example,
joints between teeth and gums. Other types create motion primarily. Several types of
joints can be found:

Fibrous
o Gomphosis it is a joint that binds the teeth to bony sockets (dental
alveoli) in the maxillary bone and mandible.
o Syndesmosis it is a slightly movable articulation where the contiguous
bony surfaces are united by an interesseous ligament. For example,
tibiofubular syndesmosis is formed by the rough, convex surface of the
medial side of the lower end of the fibula, and a rough concave surface
on the lateral side of the tibia.
o Suture a type of fibrous joint, which only occurs in the skull (or
cranium). They are bound together by Sharpeys fibres.
o Interosseous membrane it is a broad and thin plane of fibrous tissue
that separates many of the bones of the body, e.g. in the forearm and
shank.
Cartilaginous
o Synchondrosis it is where the connecting medium is hyaline cartilage.
For example, you can find it as the sternocostal joints.
o Symphysis it is a fibrocartilaginous fusion between two bones. It is a
type of cartilaginous joint, specifically a secondary cartilaginous joint. A
symphysis is an amphiarthrosis, a slightly movable joint. For example,
the pubic symphysis and the intervertebral disc.
Synovial

Synovial

52

In the figure:

Fibrous
o (A) syndesmosis (tibiofibular);
o (B) suture (skull)
Cartilaginous
o (C) symphysis (vertebral bodies);
o (D) synchondrosis (first rib and sternum);
Synovial
o (E) condyloid (wrist)
o (F) gliding (radioanular)
o (G) hinge or ginglymus (elbow)
o (H) ball and socket (hip)
o (I) saddle (carpometacarpal of thumb)
o (J) pivot (atlantoaxial)

2. Synovial Joints
There are several different types of synovial joints, as it can be observed in the figure
below.

(1) Ball in socket (enarthrosis)

it has a huge range of motion. Used for,
for example, hip &glenoidohumeral;
(2) Ellipsoidal (condylar)
characteristic of the knee replacement;
(3) Saddle Use for
sternoclavicular and carpometacarpal
modest in the orthogonal direction
(4) Hinge (ginglymus) used
for the elbow
(5) Pivot (trochoid) it is suitable for shaky movements, with rails in the head
for nodding. Used for the proximal radioulnar joint & atlas-axis joint

53

3. Generalised Synovial Joint

When considering joints, you take into
consideration not only motion but also
distribution of loads. The structure of the
synovial joint includes:
Articular cartilage it coats the ends
of the bones, acting as a bearing surface. It
also acts as a capsule which encases the
following element
Synovial fluid this is manufactured
by the next element of the structure
Synovial membrane manufactures
synovial fluid
o Synovium
Ligaments wrap the outside to provide structural integrity.
4. Articular Cartilage Structure

The superficial or tangential zone contains the highest collagen content, about 85% by
dry weight. In addition, the collagen fibrils are oriented parallel to the joint surface,
54

indicating that the purpose of this may be primarily to resist shear stress. The amount of
collagen decreases in each zone moving closer to the tidemark, dropping to 68% in the
middle zone.
Cartilage is slivery due to the fact there is no blood supply. It also des not have any
nerve cells because you would not want it to feel pain.
The bone at the bottom of the first picture is impervious (from the tidemark) so nutrients
cannot pass. The top right figure shows the collagen fibre orientation, which, as can be
seen, changes with how close it is to the bone.
Cartilage is not stiff, as it has no mineral crystals like bones do. The collagen only has
strength in tension, where as it is basically always in compression. Cartilage collagen
fibres form hoops, which are in tension because the water absorbing molecules inflate
the space like a balloon. So this explains how the fibres in tension transferred
compression.
Chondrocytes manufacture the collagen constantly. All their nutrients come through the
synovial fluid since there is no blood supply. The synovial joint is also where the water
comes from. Additionally, the top surface has all these molecules that act as lubricant.
The figures at the bottom show the relation between water molecules (proteoglycans)
and the collagen molecules. This is another example of how hierarchical structures lead
to the different abilities and functions.
a. Composition
The composition of the articular cartilage is shown in the table and figure below.

Of the three major

components, the most
prevalent is water. About
30% of the total water
exists within the
intrafibrillar space of
collagen. The collagen fibril
diameter and the amount of
water within the collagen is
55

determined by the swelling pressure due to the fixed charge density (FCD) of the
proteoglycans. In other words, the proteoglycans have strong negative electric charges.
The proteoglycans are constrained within the collagen matrix. Because the
proteoglycans are bound closely, the closeness of the negative charges creates a
repulsion for that must be neutralised by positive ions in the surrounding fluid. The
higher concentration of ions in the tissue compared to outside the tissue leads to
swelling pressures. The exclusion of water raises the density of fixed charge, which in
turn raises the swelling pressure and charge-charge repulsion. The amount of water
present in turn raises the swelling pressure and charge-charge repulsion. The amount of
water present in cartilage depends on (1) the concentration of proteoglycans, which
determines FCD and swelling pressure, (2) the organisation of the collagen network,
and (3) the stiffness and strength of the collagen network. The collagen network resists
the swelling of the articular cartilage. If the collagen network is degraded, as in the case
of OA, the amount of water in the cartilage increases, because more negative ions are
exposed to draw in fluid. The increase in fluid can significantly alter the mechanical
behaviour of the cartilage.
The third major components of cartilage are the proteoglycans. Proteoglycans are large
biomolecules that consist of a protein core with glycosaminoglycan side chains. These
molecules normally occupy much larger space when compacted by a collagen network.
The compaction of the proteoglycans affects swelling pressure as well as fluid motion
under compression. This also allows for better holding of the water particles.
b. Mechanical Properties

As perhaps can be gleaned from the previous sections, there are three major factors that
contribute to articular cartilage mechanical behaviour. First, there is the swelling
pressure due to the ionic affects in the tissue. Second, there is the elastic behaviour of
the solid matrix itself. Third, there is the fluid-solid interaction in the cartilage under
compressive load.
As you squeeze the cartilage, the water can only go sideways. This creates the fluidsolid interaction, i.e. the viscosity of the fluid and the fluid interacting with the solid
matrix.
56

This theory (figure above) captures the basic behaviour of cartilage under compression.
As an example, the behaviour of cartilage under compression is shown above.
In this case, cartilage is subjected to a fixed displaced at point (B). Because the fluid
cannot immediately leave, it carries a good portion of the load. As the fluid leaves the
cartilage, load is shifted to the solid matrix and stress is reduced. The spike at (B) in the
graph is due to the fact that a finite amount of time is needed for the fluid to move
initially.
Two key material properties in biphasic theory are equilibrium modulus and
permeability. Equilibrium modulus is the stiffness of the cartilage as all the fluid flows
out.
5. Synovial Fluid
Synovial fluid is produced by the synovial membrane. The main outcome is to dialysate
(ultrafiltrate) the blood. No cells are found and it is stripped of high Mw proteins.
The protein encoded by this gene is a large proteoglycan specifically synthesised by
chondrocytes located at the surface of articular cartilage, and also by synovial lining
cells. This protein contains both chondroitin sulphate and keratin sulphate
glycosaminoglycan. It functions as a boundary lubricant at the cartilage surface and
contributes to the elastic absorption and energy dissipation of synovial fluid.
The synovium adds particular biomolecules to the synovial fluid, i.e.:

Hyaluronan (hyaluronic acid)

57

o Viscosity modifier
Lubricin
o A.k.a. PRG4

A controversy is whether the lubricin actually exists, since it is considered more like a
cluster of different molecules coming together to form these lubricant ball bearings at a
Nano scale.
a. Viscosity
The synovial fluid is a non-Newtonian fluid, i.e. has pseudo-plastic, shear thinning
properties. It is however not known how the biomolecular components achieve this.
The figure on the left shows the shearrate-dependent-viscosity of the CACPhSF, BSF (normal synovial fluid), ETBSF, UHA and UHA with added
lubricin measured in the rheometer.
After the addition of lubricin, the zeroshear viscosity of UHA decreased
considerably. An increase in zero-shear
viscosity was also noted in BSF after
digestion with trypsin. The onset of
power-law behaviour (between arrows)
at greater shear rates in the CACP-hSF
sample may be attributable to a wider range in the molecular weight distribution of HA.
Captodactyly-arthropathy-coxa vara-pericarditis (CACP) syndrome is cased by
truncating mutations in the gene PRG4, leading to no lubricin expression.
In conclusion, the graph shows that:

Low shear rates (slow velocities) thicker fluid

Higher shear rate thin liquid (for quick movements)

6. Lubrication
Considering a day in your day, you could observe a vast range of tribological
conditions. You stand around or lie around amounts of time and then within an instant
when you start to move you want perfectly frictionless, perfectly mobile joints. You
also want to keep the same friction over, for example, the entire 4 hours of running a
marathon.
There are several types of lubrication. However, nature achieves a better type of
lubrication by combining all lubricants simultaneously.

Hydrodynamic
58

Squeeze film
Boosted
Weeping
Boundary
a. Hydrodynamic
You do not want to have
the two sides touching
each other. Lubricant is
entrained in the front end.
This results in fluid
pressurisation and load
support.
b. Squeeze Film

No sliding motion, just the

two sides coming together,
e.g. as happens when you
jump and land. Squeezing of
the fluid causes
pressurisation and load
support.

c. Boosted vs. Weeping

These two types are
contradictory hypotheses.
For the boosted one, the
lubricant viscosity is
enhanced by fluid uptake by
cartilage. In general terms,
you squeeze fluid out of the
lubricant into the cartilage,
boosting the viscosity of the lubricant in the contact area.
For the weeping one, the lubricant volume is supplemented by exudation from cartilage.
As the cartilage is squeezed, the cartilage weeps lubricant into the contact area (water
leaks out of the cartilage).

59

d. Boundary

This method allows the surface of the cartilage to hold to water better. The body can use
different modes or combinations of lubrication.
7. Diseases Osteoarthritis
This disease is attributed to wear &
tear. It is a traumatic event related to
obesity. Indeed, 8.5 million Britons are
affected.
In this disease, cartilage becomes
thinner. It also loses strength as well as
increases the amount of calcification.
The pain comes late in the process
when cartilage is severely degraded.
Regarding the synovial fluid, the
viscosity is reduced but the volume is
increased.
The reduction of tensile strength is shown in the table below.
The concept of fibrillation is
the initial degenerative
changes in osteoarthritis,
marked by softening of the
articular cartilage and the
development of vertical clefts
60

between groups of chondrocytes.

Whereas the permeability increases, the equilibrium modulus decreases. This leads to
less rate of load shared by the fluid phase.
8. Diseases Rheumatoid arthritis
Rheumatoid arthritis is a chronic inflammatory disorder that can be found in any age
range. 350,000 Britons are affected
by this disease, with three times
more women.
Due to this disease, the cartilage
becomes thinner and also loses
strength. The joint hurt for two
reasons:
Never endings are irritated
by the chemicals produced by the
inflammation
The capsule is stretched by
the swelling of the joint
The synovial fluids viscosity is reduced whereas its volume is increased.
Four kinds of drugs may be used to treat rheumatoid arthritis:

Analgesics
Non-steroidal anti-inflammatory drugs (NSAIDs)
Disease-modifying anti-rheumatic drugs (DMARDs)
Corticosteroids

Synovectomy and viscosupplementation can also be considered for the treatment.

9. Diseases Osteochondritis Dissecans
Due to this disease, the cartilage separates from the subchondral bone, as shown in the
figure below.
This is a rare disorder affecting
the knee, there are 3-6 cases per
10,000 adult population, mainly
males. It most commonly affects
the knee joint (75% cases). About
85% of knee lesions are on the
medial and femoral condyle.

61

The elbow and ankle are the next most common joints affected. In the elbow, it affects
the capitellum of the humerus and, in the ankle, it affects the talar dome.
In conclusion, 5% of OA suffered have had OD.

62

Lecture 9 Total Hip Replacement

1. The Hip Joint

The hip joint is supplied with blood from the medial circumflex femoral and lateral
circumflex femoral arteries, which are both usually branches of the deep artery of the
thigh (profunda femoris), but there are numerous variations and one or both may also
arise directly from the femoral artery. There is also a small contribution from a small
artery in the ligament of the head of the femur, which is a branch of the posterior
division of the obturator artery, which becomes important to avoid avascular necrosis of
the head of the femur when the blood supply from the medial and lateral circumflex are
disrupted (e.g. through fracture of the neck of the femur along their course).
The hip has two anatomically important anastomoses, the cruciate and the trochanteric
anastomoses, the latter of which provides most of the blood to the head of the femur.
These anastomoses exist between the femoral artery or profunda femoris and the gluteal
vessels.
a. Huge Range of Motion
Lateral or external rotation
(30 degrees with the hip extended, 50
degrees with the hip flexed)
Medial or internal rotation
(40 degrees)
Extension or retroversion (20
degrees)
63

Flexion or anteversion (140 degrees)

b. Avascular Necrosis

Avascular necrosis is a disease resulting from the temporary or permanent loss of the
blood supply to an area of bone. Without blood, the bone tissue dies and the bone
collapses. If avascular necrosis involves the bones of a joint, it often leads to destruction
of the joint articular surfaces, or Osteochondritis dissecans.
c. Congenital (or developmental) Dysplasia of the Hip
The cause for this is unknown. However, there are several risk factors:

Genetic factors may play a role

Low levels of amniotic fluid during pregnancy
Being the first child
Being female
Breech delivery
Family history of the disorder

This case occurs in about 1 out of 1,000 births. Several treatments for CDH are
available, depending on when it is caught:

If caught during infancy

o Pavlik harness or Frejka pillow/splint
If adolescent
o Contracture release
o Splinting
If untreated can lead to OA in adults
o Arthroplasty
64

2. Reconstructive Surgery of the Hip

Methods for reconstructing the hip have been changed and improved over the years:

Carnochan, New York, 1840

o Wooden block
Auguste Stanislas Verneuil, Paris, 1850
o Soft tissue
Lopold Ollie, Lyon, 1885
o Adipose tissue
Vitezlav Chlumsky (1867-1943), Breslau
o Muscle, celluloid, silver plates, rubber struts, magnesium, zinc and wax
Marius Smith-Peterson, Boston, 1925
o Glass (1925), celluloid (1925), Perspex (1928), CoCr (1933)

3. Hemiarthroplasty
Different options are available:

Gluck, Berlin, 1890

o Ivory, zinc plated screws
Delbet, 1919
o Rubber
Judet, Paris, 1938
o PMMA

High-density polyethylene is the most common polymer for total hip arthroplasty.
4. Total Hip Arthroplasty
It is important to consider how the cup is located in the pelvis; indeed, it is meant to be
about 45 degrees and neutral (not open or closed orientation). They are often put in too
vertically leading to it being much easier to dislocate. If it is to open, no many problems
65

are encountered. On the other hand, if placed to closed-oriented (i.e. hole facing the
back), the neck of the other part of the replacement will hit the rim of the cup, easily
leading to dislocation. Additionally, it is really not possible to fix misplaced joints.
Philip Wiles worked out a replacement based on stainless steel against itself, with screw
and bolt fixation. The weight of the replacement does not matter (100 g does not make a
difference for the full body weight).
Bone cement was developed by Haboush in the 1940/50s. Joint replacements are held in
place by bone cement or interference fit with spaces in metal to which the bone can
grow into. The process starts with the replacement being hammered inside a bit, and
then stopping to let the bone creep, then hammering it again achieving initial
interference fit.
There was a general concern called cement disease due to the fact that an
inflammation was detected and was thought to be caused by cement particles.
Mc-Kee-Farrar introduced the metal on metal design and Charnley introduced the metal
on polymer one, as it can be observed in the figures below.

McMinn introduce the resurfacing method (BHR) with a metal-on-metal. This process
was the result of efforts to minimize amount of bone being taken out. This involves:

Do not cut femoral head. Instead, reshape it. The pin fits in the head but it does
not go all the way down.
The cup is metal because the cup is too thin to use plastic.
5. Ostelolysis
Osteolyis, also called aseptic loosening is a lesion that is considered
the principal cause of long-term failure for the hip replacement. This
happens to 10% of THR at 10 years time. This disease was first seen in
the 60s but not really recognised. This is observable in the figure on the
left.
66

A survivor analysis is shown in the figure on the

right.
If a joint fails within the first year, the
replacement was either badly positioned or there
was an infection. An infection is very bad in
joint replacements; bacteria can hide from the
body due to the scrapping out of the tissue that
naturally had blood supply when the joint was installed. Therefore, it is difficult to get
antibiotics there, etc. These days, bone cement is loaded with antibiotics to prevent
infection, called septic loosening.
The problem with osteolysis is that happens after many years; hence, when the patient
starts having symptoms it is too late. In the x-ray, the osteolysis is the gap between the
metal and the bone. Indeed, the component loses its fixation and starts to move a little
which is what the patient feels. At this point, the bone has been substituted by a kind of
fibrous bone that provides no support (but not an empty space).
The only way to treat osteolysis is to take out the joint and put in a new one. But, as
mentioned before, it is hard to take out the joint (due to the bone cement). Therefore, the
bone is compromised so the 2nd joint is going to last less long. In conclusion, with the
increasing of life expectancy, it is very important to delay the first surgery as much as
possible to avoid having to do 2+ revision surgeries.
Nowadays, titanium is used because it has a lower Youngs modulus, which leads to
less stress shielding in the bone so it is less likely for the bone to break/crack.
There are two hypotheses that explain this process.
a. Hypothesis 1
This theory is probably the most
favourable. Particles are released
from wear. The wear particles
are about the same size as
bacterial cells.
When you have a big lump of
something that will not rust or be
toxic, like bullets, the body just
encases it in fibrous tissue and
leaves them be. However, tiny
particles are attached by
macrophages and eaten. When the macrophages eat a lot, more macrophage join in,
which need space to move so the body creates space by removing bone. Additionally,

67

macrophages die once its too full (it cant digest plastic compared to bacteria),
releasing all those wear particles all over again.
Cytokine release represents the signal that is sent to other macrophages to come in. The
severity of response depends on:

Material
Number of particles
Size/volume of particles
Morphology of particles
b. Hypothesis 2
Per Aspenberg suggested a cyclical hydraulic erosion of the
joint due to use. The osteolytic cavity created due to the
hydraulic pressure. The debris gets in by accident.
It was found that bigger debris stays near the joint whereas
small debris travels far away, even to your brains.
Macrophages cannot wrap around things over 5 microns,
but they can join to form bigger cells to deal with these.
Only at sizes of ~millimetres are ignored by the body
system.

An ex vitro assessment of debris dissemination was carried out:

104 tissue samples from 33 revision procedures

17 Charnley, 4 Howse, 2 Muller, 10 other

Tissue harvest location ranked according to remoteness from articular region.

6. THR Wear
The data gathered is from ultra high molecular weight PE data, but it is not really used
anymore.
68

Engineers are looking at an alternative bearing technologies to

reduce the particle problems. Once you have done the replacement,
you still have synovial fluid to lubricate, although it might be a little
more watery. Indeed, friction is not the problem, wear is. Therefore,
we want to reduce wear.
In joints, a mix of all wear modes is observed. Polyethylene is what wears mainly.
When considering implanted surface finish, a lot of height differences straight from
machining are observed. Over time, it becomes very smooth though.
When you zoom in, you can see the ripples, which lead to the creation of wear
particles. Finally, the age of the joint is important since polyethylene over time becomes
brittle due to oxidation. This is also why these things are now packaged in inert gas
instead of air.

69

Lecture 10 Failure of Total Joint Replacement

1. Amontons Law
This theory states that friction is independent of contact area.

In this equation, is the coefficient of friction. For dry contacts, this coefficient is 0.10.4. For lubricated contacts, 0.001-0.1.
Friction is independent of the contact
area between two surfaces. The
reason that force is the same in either
case is due to the differences
between the apparent area of contact
and the actual area of contact.
Surfaces are generally wavy and
bumpy, even at microscopic level.
Therefore, two adjacent surfaces, as
shown in the figure on the left, are
never in total contact. The upper
body is supported by the lower body surface at the top of roughness irregularities, called
asperities. Under load, these asperities bend and deform until the load is fully supported.
At that point, less than 1 part in 10,000 of the apparent area is usually in contact.
Friction is indirectly proportional to the real area of contact. Since this is almost always
a small portion of the total area, friction is effectively independent of the apparent area
of contact.
2. Coulombs Law
Coulombs Law states that friction is independent of velocity. Both Amontons and
Coulombs laws only apply to dry contacts.
3. Tribological Contacts
It is mandatory to explain the difference between friction and wear, since these terms
are often confused. Indeed, low friction is not necessarily low wear, e.g. early PTFE
THR low friction but high wear. On the other hand, non-lubricated steel has high
friction but low wear.
Wear is the erosion of material from a solid surface by the action of another solid. Four
main were processes are found.

70

a. Modes of wear

Abrasive wear this happens when the material is removed by contact with
hard particles. The particles may either be present at the surface of a second
material or exist as loose particles between two surfaces. Abrasive wear can be
measured as loss of mass.
Adhesive wear it is also known as scoring, galling or seizing. It happens when
two solid surfaces slide over one another under pressure.
Fatigue wear it is a process by which the surface of a material is weakened by
cyclic loading, which is one type of general material fatigue
Three-body wear the removal of material is due to the inclusion of a third
material between the two layers.
b. Archards Wear Factor
Archards wear factor is defined
in the formula below, with the
variation of Archards constant k
shown in the figure on the right.
=
where W is load and S is the
sliding distance.
There are two ways to minimise
wear; you can make the patient
lighter or reduce the sliding
71

distance (by walking less or reducing head radius).

4. Polyethylene Wear
There are many wear mechanics when considering polyethylene:

Vary with position within contact region

Vary with head roughness
Vary with joint age

5. Metal Wear
Metal wear occurs as it occurs with polyethylene, adding fretting and corrosion.

72

Lecture 10b Failure of Total Joint Replacement Engineering Solutions

1. Lubrication
The main purpose is to maintain fluid film between counterfaces. Hydrodynamic
systems vary pressure profile as the joint moves. On the other hand, hydrostatic do not
provide that and therefore cannot be used for hip joint.

2. Stribeck Diagram Lubricated Contacts

The main idea is to operate joints in full
fluid film side because wear is minimal.
Changing viscosity is not a practical
solution, left with changing radius and
sliding velocity.
The more the sommerfeld is increased,
the better the lubricating regime is. The
friction factor depends on the nature and
size of the joint. If the load is very high,
or the viscosity is low, you get high friction.
As you increase viscosity, the ability of the
lubricant to support load increases. Friction
losses due to excess viscosity are why the
profile goes up again after the middle line.
In the figure on the right, u represents the
sliding velocity.

73

3. Metal-on-Metal
Metal-on-metal was a good bearing combination, which was popular in early days. For
this system, the hydrodynamic lubrication is increased, which will provide tight radial
clearance with large diameters. Hard material are also used (CoCr alloy), e.g.
Birmingham Hip Resurfacing (BHR). This type of joint is better when operated in full
fluid film to make the joint float.
a. BHR Effect of Radial Clearance

The effect of radial clearance is shown in the two graphs above. The title of the graphs
determines the diameter of the femoral head. If R is smaller, you are reducing the wedge
angle, which provides a greater area to support but less pressurisation. The graphs show
the predicted separation between the two sides of the joint.
For the graph on the left, the optimal radial clearance will be at 20 microns, which is
very hard to get. This is the main reason to explain the unsuccessful use of metal-onmetal. For the graph on the right, the diameter of the head is increased, which reduces
the manufacturing challenge. This increases the chances of getting it right.
b. BHR Stribeck Curves
The graph on the left shows the results for a
pre-wear friction test, right as they were
taken out of packaging. It can be observed
that, as cycles of wear are applied (1, 2 and 3
million), the joint matures and performs
better. After 1 million, the joint is still in
mixed lubrication. After 2 and 3 million, the
joint moves towards full fluid film
lubrication. The viscosity was changed
74

during the experiments.

4. Soft-Layer (Cushion-Form)
The figures shown below represent the different soft-layers used for knee joints.

For the figure on the far right, two different materials are used. A stiffer polymer is
placed at the bottom, which is clipped into the base plate that goes into the bone. A
softer polymer is placed on top. The idea is to try and mimic the real behaviour of the
biological joint. However, it has never been used in humans.
Two main characteristics are applicable to this technique: biomimetic and
elastohydrodynamic lubrication.
The contact area increases if you have soft
material. Indeed, once the joint starts rotating,
the contact area increases, as it can be seen in
the figure on the left.

The figure on the right tries to explain the

phenomenon called
microelastohydrodynamic lubrication.
The side of the polymer, which was casted,
is rough. When pushed down, the softer
surface becomes flatter due to the pressure
of the lubricant.
a. Stribeck Curve
The graph shows very low friction
factor, with full film lubrication. They
are not used; trials on sheep were
carried out but performed as well as
conventional joints. Therefore, it is not
worth it, moneywise, for companies.

75

5. Why is Surface Roughness Important?

It has been said that if you
increase roughness, you decrease
wear. This statement is not
always true.
Making joints smoother increases
wear because you want to have
depression, which act as fluid
reservoirs. Therefore, you are
changing the mode of wear. You
have abrasive wear at one end, transitioning then to adhesive wear.
6.

Highly Cross-Linked UHWMPE Reduction in Wear Factor

Higher radiation, higher cross-linked
polymers are desirable, since this locks the
structure of the polymer diminishing wear.
UHWMPE is semi-crystalline, which
makes it a bit hard. They make good
bearing surface but the wear process can
realign their structure. It is also susceptible
to wear if the movement is transversal
because the molecule chains are aligned
side by side.

7. Lubrication vs. Wear

Wear has evolved over the years with the application of different materials:

Conventional (~50nm particle) 240,000 particles/stride

Metal/Metal (~25nm particle) 57.7x106 particles/stride
XLPE/Ceramic (~50nm particle) 4.8x106 particles/stride
Ceramic/Ceramic (~20nm particle) 37.5x106 particles/stride

As can be extracted from the data above, particle size comes down, but particle number
increases. These particles diffuse out in your body because the immune system does not
detect them due to their size. There is a general concern regarding its side effects in the
long-term because they are still unknown.
8. Problem Solved?
Several issues are encountered:
76

Conventional (~50nm particle)

o Phagocytosis, foreign body generation. Large particles tend to stay close
to the joint whereas small joints will travel around.
Metal/Ceramic/XLPE <25nm particle
o Pinocytosis
Membrane pore transfer, nuclear access
o Systemic dissemination

9. Problem Created?
XLPE is prone to fatigue, although wears very little. Sequential cross-linking &
annealing can give good wear and improved fatigue performance.

77

Lecture 11 Host Responses

1. Toxicity & Hypersensitivity
These two main aspects are considered when analysing host responses:

Toxicodynamic considerations
o Release of toxic compounds
Ions from metal corrosion, leachates from polymers
Hypersensitivity
o Allergy and intolerance
o Allergy Types I to IV
Type I mediated by IgE
Type IV delayed type (>12 hours to develop)

2. Measuring Biocompatibility

Assay methods
o Direct contact test
Material placed directly on the cells
o Agar diffusion
Cells grown in agar, biomaterial placed on top
o Elution
Solvent used to extract
Record cell death / health

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3. Natural Materials

Grafts bone, ligament, etc.

o Autograft skin graft from same individual, vein graft for bypass
surgery
From within an individual
o Allograft e.g. bone grafts
From within species (can come from a different individual)
o Xenotypic (e.g. heart valve from a pig into a human heart)
Across Species
Also processed materials are used

4. Case Study Sulzer Recall

Sulzer Orthopedics developed the Inter-Op acetabular shell. These were manufacture
during or after October 1999 but a limited number were produced as early as June 1997.
Approximately 25,000 units of Inter-Op acetabular shell were manufacture of which
17,500 were implanted.
Sulzer recommends patients and surgeons to be aware of the following symptoms:

Sedimentation rate, C-reactive protein and aspiration show no evidence of

infection preoperatively
All cultures at surgery are negative and an arthrogram does not show dye around
the shell
No reason to believe that the joint would fail because of infection at the time of
surgery

Up to 6 weeks post-op, the following should be observed:

The patient may be progressing well, or may be reporting pain in the groin or
anterior trochanteric area
Patient may have increase thigh pain
Patient may have significant pain when starting to walk, or buttock pain after
rising from seated position
X-ray may show possible migration of the component

From 6 weeks to 3 months post-op:

Significant pain with weight-bearing, possibly requiring a cane or crutch

Patient cannot exert resistance in straight-raised leg test or side-lying abduction
test

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At 3 months post-op:

A line around the acetabular component and possible migration can be seen
sometimes only on Lauenstein lateral x-ray, not AP x-rays

What sort of immune reaction was this? How could that help direct you to the cause?
Mineral oil leakage was found into coolant for machinery. The contamination was not
removed at the solvent wash stage. This residue causes DHT.

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Lecture 12 Polymer Biomaterials

1. Common Polymeric Biomaterials
The table shown below provides the properties of several polymeric biomaterials,
highlighting polyethylene and polymethyl-methacrylate.

2. Ultra-High Molecular Weight Polyethylene (UHMWPE)

UHMWPE is the most commonly used polymer material in orthopaedic applications.
UHMWPE is a linear polymer, as shown in the figure below.

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a. Manufacturing Processes
Four different types of Consolidation process are used to manufacture UHMWPE:

Compression moulding this process takes polymer fibre, squeeze it together

and add heat. This is then compressed into sheets of polymer and then cut it so
as machine the final product.
Ram extrusion the material is extruded in die, obtaining a long bar of
polymer. This bar is then cut to make the desired component.
Hot isostatic pressing This process is a variation of the compression
moulding process. A constant pressure is applied for a certain time to obtain the
part.
Direct compression moulding the finish good is mould directly to the shape
you want to manufacture. This process cannot be used for complex shapes since
the compression method limits the geometries you can achieve.
The first two methods are the most commonly used nowadays.
The figure on the left shows the cross-section through a
consolidate piece of UHMWPE.

The molecular process that UHMWPE follows is shown below. It

is a semi-crystalline material, where the polymer chains folds back on itself, although
there are inefficiencies in the folding due to the length of the chains. Additionally,
lamelia provides a worm-like feature (see figure below).

The mechanical performance goes up with

molecular weight. It is important to maintain
high crystallinity but this is difficult to achieve
with long polymer chains. It also has a lower
density that HDPE, with much better
strength/toughness.

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The graph below shows the different steps of the manufacturing process for UHMWPE.
You can vary pressure and temperature during the consolidation process. This will
modify the degree of crystallinity produced. Manufacturers usually change these two
parameters to differentiate their products.
b. Surface Properties
Hydrophobic surface
Differing roughness depending on
manufacture
Surface may be passivated (not clinically
applied)

c. Biostability

Essentially inert
o No biodegradation
o Limited oxidation (more dependent on shelf-life)
Immune response is muted
o Fibrous encapsulation
Only for bulk material
d. Sterilisation

Normally, high-pressure steam will be used to sterilise an object. However, this is not
appropriate for polymers. Several methods are available:
Ethylene Oxide gas (ETO) has been a commercially available sterilisation method
since the 1980s. Highly toxic, ETO neutralises bacteria, spores and viruses. UHMWPE
is a good candidate for ETO sterilisation because it contains no constituents that will
react with or bind to the toxic gas.
Low-temperature gas plasma is relatively a new commercially available sterilisation
method that was applied to UHMWPE in the 1990s. Gas plasma is a surface sterilisation
method that relies upon ionised gas for deactivation of biological organisms. Two
plasma methods are used: peracetic acid gas plasma or hydrogen peroxide gas plasma.
Starting in the 1960s, UHMWPE components for joint replacement have been stored in
air-permeable packaging and gamma sterilised with a nominal dose of 25 kGy (2.5
Mrad)(see graph below). Although the packaging of orthopaedic implants has evolved
during the past 30 years, gamma sterilisation of UHMWPE components remains an
industry standard today. Historically, UHMWPE components have received a dose
ranging between 25 and 40 kGy during sterilisation. Two methods are available:
83

In air
In inert gas this breaks the links of the different polymer fibres (see figure
below)
o Nitrogen, argon

This final sterilisation process is called XLPE, which will reconnect

the polymer fibres by applyind a warm irradiated annealed melt
(WIAM) process.

3. Polymethyl-methacrylate (PMMA)
This is a widely used polymer material in many applications, such as bone cement,
intra-ocular lenses and dentures & dental moulds. The table shows the properties of
different PMMA polymers.

Bone cement is a thermosetting

polymer with free radical
polymerisation. It also has a linear
structure and amorphous (i.e. not
crystallised). Viscosity and porosity
are two parameters of bone cement that
are very important, since we want no
air at all in the bone cement.
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4. Polyesters Biodegradable Polymer

Widely used polymers for low strength orthopaedic applications, sutures and drug
delivery. There are several options for biomaterial applications:

Poly-lactic acid (PLA), semi-crystalline

Poly-glycolic acid (PGA), highly crystalline
Poly -caprolactone

a. Biostability
These materials are biodegradable, following a hydrolytic process:

PLA slow, due to its hydrophobicity

PGA rapid, more hydrophilic

Regarding melting temperatures:

PLA, Tg 50-80C, Tm 173-178C

PGA, Tg 35-40C, Tm 225-230C

We often use a copolymer, which involves putting different monomers into a polymer
chain.
b. Mechanical Properties
Mechanical properties change
over time due to the degradation
of the polymer. The flex-strength
can be up to 200-250 MPa with a
modulus of 12-15 GPa. The graph
on the left shows the strength and
mass of the polymer over time. It
is clear that strength declines
faster than mass. The hydrophobic nature means that it tends to degrade from the
surface so you maintain a strong core.
An example of copolymer is shown in the left. Once
screwed, you tear off the head. It is used to screw bits
of bones (e.g. hand bone) that do not get huge amount
of load. The plastic would lose strength as bone heals,
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giving stable fixation early in the healing process. It is also used in birth control
implants.
5. Case Study Implanon
Implanon is a single-rod implant, with a length of 4cm and a diameter of 2mm. It
contains 68mg of etonogestrel. It is basically an Ethylene Vinyl Acetate (EVA) carrier,
i.e. low Youngs modulus, flexible and less palpable. The manufacturing process is as
follows:

The polymer is dissolved in an organic solvent;

Powdered drug and filler (typically an inert sugar) are added to the liquid
solution and rapidly mixed to obtain homogeneous mixture;
The drug-filler-polymer mixture is then casted into a mould at -80C and freezedried until it solidifies;
Slowly release drug over time. While the polymer is not biodegradable within
the body, it is inert and causes little or no reaction following implantation.

86

Lecture 13 Metallic & Ceramic Materials

1. Metallic Biomaterials
The following table includes the main metallic materials used for biological
applications.

It is important to remember that the mass difference is not important in most medical
cases for the components (i.e. in terms of body weight). The next table provides
properties of several metallic biomaterials.

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When considering surface properties of metals, the main factors to be considered is the
hardness / ductility. Hardness is important when you are making smooth components
(e.g. femur head). For different materials:

SS: HV 275-300
Ti-6Al-4V: HV 360-400
CoCr: high carbon HV 450-470, low carbon HV 430-460

The picture on the left represents the femur head as it was put in and the right figure is
an image of the same femur head taken out later with the scratches due to the service.
Since the metal is a ductile material, it can self-heal to some
extent because the metal keeps moving. The two bumps
represented in the figure on the left are damaging the other
part (non-smooth surface), but they will wear away with
time.
To provide a harder surface to the metal biomaterial, several options are available:

TiN
Diamond-like Carbon (DLC)
Oxinium

This protection must be persistence at surface.

The figure on the right represents the use of DLC to cover the
metallic biomaterial. A thin layer of crystalline carbon, meant to be
scratch resistant. The big challenge is getting good interface
(strength of the bond) between the ceramic coating and the metallic
surface. If it is not well integrated, the ceramic will chip off upon
scratching which can be very damaging to the joint.
The figure on the left is a material covered with Oxidium. The process includes
manufacturing the metallic part to
then oxidize it. There is no problem
with the interface since the bond is
naturally strong. There is no
distinctive boundary between metal
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and ceramic, as seen in the figure below. The Au part is there because you need some
conductivity to help in surgery, but it is not part of the bearing surface.
a. Biostability and Biocompatibility
All the metallic biomaterials form thick, stable, oxide
layers. Hence, biocompatibility is good. Indeed,
Titanium alloys deemed to be osseointegrative, as it can
be seen in the figure. In the figure, the bone (pink) can
go all the way into the titanium (black) in a way it could
not when using other alloys.
Several osseointefration technologies are available:

Texturing encourages bone to grow into the material, e.g. the knee joint has
below this porous coating so bone can grow into it
o Porous coating, sintered beads
o Wire mesh coating
Hydroxyapatite coating
Titanium wires used to create a metallic mesh, since you
cannot do beads with titanium because of its welding
properties. There are problems with both the beads and the
mesh since they have lower strength. Therefore, you get
more degradation, with the possibility of the material
chipping away.

Elficks recommendation for the hip joint replacement is

using a cemented femoral component and a cementless cup part. The femoral
component will be ceramic whereas a cross-linked polyethylene will be used for the
cup.
2. Ceramic Biomaterials
Several options are available when considering ceramic biomaterials for replacements:

Tissue attachment bioceramics these will degrade with time, promoting tissue
growth
o Hydroxyapatite coating
o Bioactive glass
o Tricalcium phosphates
Articular bioceramics
o Composition
Zirconia, ZrO2
Alumina Al2O3
Alumina matrix composite
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a. Tissue Attachment Bioceramics

This product is part of a niche market at the moment.

Hydroxyapatite Coating this material can coat onto metallic components

o Intimate ingrowth of bone
Bioactive glass this material will resolve over time and bone will grow in its
place
o Surface reactive ceramics (Na2O-CaO-P2O5-SiO2)
Bone will bond to bioactive glass
Tricalcium phosphates this material will resolve over time and bone will grow
in its place
o Will be resorbed and replaced by bone

The rate of biodegradation of calcium phosphate ceramics increases as:

I.
II.
III.
IV.
V.

Surface area increases (powders > porous solid > dense solid)
Crystallinity decreases
Crystal perfection decreases
Crystal and grain size decrease
There are ionic substitutions of CO32-, Mg2+ and Sr2+ in HA

The following table shows the surface reaction stages.

b. Articular Bioceramics
In the 1970s, early alumina ceramics were used. This design shown poor quality and
design flaws. Indeed, brittle failures were very common, up to 15%. This is not a
surprising to an engineer since ceramic material will have brittle failure under this kind
of load.
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The following material used was Ceramtec, De. In fact, 2.5 million alumina femoral
head were manufactured. In the old days, the cup had 90-degree edges; nowadays you
have radii. This is difficult to manufacture because you cannot machine a ceramic after
it is made. Therefore, you need to improve the manufacturing processes completely.
Using biolox femoral heads, the percentages of fail rates were:

0.026% for first generation alumina

0.014% for second-generation alumina
0.004% for femoral heads manufactured after 1994

In the last 40 years, engineers have come a long way; ceramics nowadays are very
unlikely to fail brittly. This is due to improvements in both manufacturing processes and
design.
Contemporary ceramic biomaterials are currently used. Zirconia was introduced in the
mid 1980s as part of the new era, with a hardness of HV1270. Zirconia properties
decline due to the sterilisation process. Even in the short time, the sterilisation process
reduces its performance.
Alumina 3rd generation had a hardness of HV2000
and a grain size of 1.8 microns. The graph on the left
shows the impact of the sterilisation onto three
materials: biolox delta (alumina matrix composite),
zirconia and biolox (alumina).

Phase instability was found in Zirconia, which leads to surface roughening. When you
manufacture zirconium, whole grains can change structure. The figure on the left shows
zirconia as manufactured. The right one shows the same material after some wear,
where the change in grain structure can be observed.

Zirconia ceramics have three phases of crystal structure, which transform according to
temperature. The monoclinic phase transforms into a tetragonal phase at less than
1100C, while the tetragonal phase transforms into the cubic phase at 2370C. Since the
tetragonal phase is unstable, but shows the greatest mechanical strength of the three
phases, Y-TZP was used for the surgical grade zirconia ceramics. Transformation from
the tetragonal phase into the monoclinic phase brings a 3% increase in the volume of
91

ceramics. While this phase transformation plays an important role in increasing the
mechanical strength of Y-TZP, when it occurs extensively it may cause an increase in
the surface roughness. Phase transformation in Y-TZP is induced at a relatively low
temperature in the presence of water and pressure. Therefore, sterilisation of Y-TZP in
an autoclave is contraindicated.
4th generation Alumina was an alumina matrix composite is called Biolox delta,
consisting of ~75% alumina, 24% zirconia and other trace elements. The pink colour is
due to the chromium oxide (Cr2O3), with a hardness of HV 1950. This material is very
tough because of the grain structure. Plate-like grains help bind all the grains together.

When considering ceramics as bearing materials, it is important to take into

consideration its benign scratch morphology. In ceramics, material is removed rather
than replaced. On the plus side, you do not get the top bumps you get on metal, but on
the minus side, it releases bits to its environment. However, modern ceramics do not
really scratch much.
3. Sterilisation
Both metals and ceramics are sterilised using:

ETO
Gas Plasma
Autoclaving (pressurised steam at 170C)

92

Lecture 14 Basic Biomechanics

1. Motion, Action & Control

2. What Contributes to Joint Force?

The figure on the left shows the reaction around the knee, as it
happens when you climb the stairs. The forces represent the
summation of:

External forces
Inertial forces
Gravitational forces

3. Body Segmental Dynamics

Mass
Length moment of arms
Position of centre of mass
Distribution of mass radius of gyration

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4. Gait

Flat is most efficient but demands more knee flexion. Gait is compromise to minimise
effort required.

Gait analysis includes 3D motion tracking systems, reaction plates and goniometers.

94

Lecture 15 The Hand

1. Bone Anatomy
There are 23 bones in the hand, with 8
carpal bones and more than 20 synovial
joints. The hand has lots of synovial joints;
therefore, it is prone to arthritis,
specifically rheumatoid arthritis due to the
fact that there is not that much wear and
tear as in osteoarthritis.
As an example, the hip joint has large,
cyclical loads with movement, getting
motion and load at the same time. At the
hand joints, there are much smaller loads.
Additionally, when the joint is under load there is no motion. Motion and load happen
discreetly, which is a big difference. This explains why osteoarthritis is less likely.

In some hand positions, the red-circled bones are

closer together and in others they are spaced
apart. When your hand bends closed packed
(bottom); you get a compression fracture (e.g.
fall snowboarding). On the right, the top figure
shows the hand straight and the bottom one
represents the movement of bending the hand.
The green star shows the location where the
compression fracture occurs. In children, the
space between bones is bigger so this fracture is
really unlikely. Between the distal and
intermediate phalanges you find the distal
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interphalangeal joint; and between the proximal and the intermediate phalanges you find
the proximal interphalangeal joint.
2. Circulation / Innervation of Hand
The thumb is very
important because of
its functionality.
However, the hand
feels due to the huge
amount of nerves.
The most important
part that you don not
want to damage is
the bottom middle
part of your palm,
since that is where
your median nerve is.
The yellow line going through the middle of
the arm is the nerve that goes through the
carpal tunnel whereas the yellow line on the
left of the arm is the nerve that goes around it.
Regarding the muscles of the thumb, most of
these muscles come down from the arm. That
is why you can feel them in the arm when
moving your thumb.
3. Ligaments of the Finger

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The ligaments in the hand act much more like actual hinges. The side-to-side movement
of the fingers is restricted by the collateral ligaments, especially in the proximal and
distal interphalangeals.
The bollar ligaments (acting as cables in a bridge) and groove help to keep the volar
ligament in place. This system allows the finger to flex and bend.
4. Muscles & Tendons of the Hand

5. Wrist Motion
The motion of wrist can be divided into:
Flexion / extension
Adduction / abduction
Supination / pronation (figure on the left) it is
interesting to see that when you flip your hands, the
bones in the arm go from parallel to crossed.

97

6. Grips

7. Tendon Biomechanics

98

8. Finger Forces
Retinacular ligaments and tendon sheats
are responsible for the forces in the
fingers. Tendon sheats are the membrane
that act as a guide of the tendons,
although it also lubricates so the tendon
can slide easily (A-1). The retinacular
ligament is represented by C-1.

9. Cumulative Trauma Disorders

Several disorders are encountered:

Carpal tunnel syndrome

Vibration white finger
Repetitive strain injury
o Tendonitis
o Epicondylitis
a. Carpal Tunnel Syndrome

Is the carpal tunnel syndrome an anatomical design problem?

The symptoms include swelling in the region of the carpal tunnel. You get numbness
and pain, and maybe also tingling/needle sensation. This syndrome is associate with
repetitive injury to your hand.
10. DeQuervains Tenosynovitis
This is the inflammation of the abductor pollicis longus and extensor pollicis brevis
tendons. The predisposing factors for this disease are:
99

Repetitive action
o Grip, squeeze, wringing
o Force >4kg
o Cold, gloves
o Vibration

11. Rheumatoid Arthritis in the Hand

This disease is an autoimmune disease leading to characteristic deformities of the hand,
with fingers pointing away from the body as a classic deformation (swan neck
deformity).
Swelling pushes out ligaments, stretching them; therefore, they do not work as well
anymore, allowing fingers to move to the sides. This leads to resting forces that are on
the joints and case these deformations. The stretch volar plate allows hypertension of
the top of the thumb.

The condylar structure of the MP joint, which permits motion in 2 planes, makes the
MP joint inherently more unstable than the IP joints; therefore, the distorting effects of
RA are more pronounced. The classic deformities associated with RA of the MP joints
are ulnar drift, which is made up of ulnar shift and ulnar deviation, and volar
dislocation. The cumulative effects of various factors contribute to these deformities.
Initially, the MP capsule and ligamentous structures are stretched by the proliferation of
the synovium, which loosens the collateral ligaments and decreases joint stability.
Normally, in the flexed position, minimal lateral movement occurs at the MP joint, but,
100

with increased laxity of the collateral ligaments, up to 45 degrees of lateral deviation

occurs in this position.
With loss of MP stability, other forces on the MP produce the characteristic ulnar drift.
For example, wrist collapse contributes to ulnar drift. Weakened radiocarpal ligaments
cause radial rotation of the metacarpals and carpus on the radius, which results in ulnar
deviation of the MP joint via the Z mechanism. This phenomenon describes the
consequence of an imbalance of opposing forces at a joint; when a particular joint is
continuously angulated in one direction, the joints on either side of it will adopt the
opposite position if no physical impediments are present.2 Moreover, the extensor
tendons can be shifted or dislocated in the ulnar direction and contribute to the ulnar
drift. The normal ulnar shift of the fourth and fifth extensor tendons during flexion of
the MP joints is exaggerated when the radial side of the transverse lamina fibers
stretches as a result of synovial proliferation.
Volar dislocation or subluxation is also caused by weakening of the collateral ligaments
and by weakening of the dorsal extensor mechanism when the extensor tendons are
dislocated between the metacarpal heads. As a result, no force counters the extrinsic and
intrinsic flexors, and a flexion contraction at the MP joint occurs, which is evident by
prominent metacarpal heads.
Conservative treatment is advised for RA of the MP joints to see if control can be
gained with medication therapy alone.2 Recurrence is always a possibility
postsynovectomy, and approximately 30-50% of patients may undergo spontaneous
remission. Synovectomy is indicated in the RA patient who is refractory to 6-9 months
of medical treatment and has persistent MP joint synovitis with minimal joint deformity
and minimal radiographic evidence of RA. Additionally, extensor tendon relocation
with synovectomy is indicated for an RA patient who also has early volar subluxation
and ulnar drift, especially if the patient is young and the disease is not rapidly
progressing. Subluxed extensor tendons fall into the ulnar gutters of the MP joint. The
patient may not be able to extend this finger once it is in the flexed position. However,
the finger can maintain extension if passively placed into this position.
The arthroplasties of the MP joint can incorporate reconstruction of the soft tissues only
or involve complete joint replacement. Soft tissue arthroplasty usually incorporates an
element of synovectomy with MP joint stabilization, such as reconstruction of the radial
collateral ligament or tendon realignment. Joint replacement is indicated for MP joint
deformity or subluxation when pain is not controlled or function is impaired. Various
MP joint implants are available for joint replacement.
The MP joint replacement procedure involves making either a transverse incision across
the entire dorsum of the hand at the MP level or individual longitudinal incisions over
each MP joint. Less chance of interference with the lymphatics and venous outflow
occurs with the individual longitudinal incisions, but the transverse incision is most
commonly used for ease of access. The dissection is carried down to the paratenon
level. An incision is made on the ulnar aspect of the extensor tendon, and the tendon is
101

reflected radially. Care is taken to not breach the integrity of the capsule at this time. An
incision is made longitudinally in the capsule of the MP joint. Using a periosteal
elevator, the metacarpal head is freed of any soft tissue attachments to the metaphyseal
flare.
Using an oscillating saw, a true cut is made, maintaining 90 in line with a long access
of the metacarpal and in the coronal plane. The metacarpal head is then discarded. An
electrical burr or a Christmas-tree type of rasp can be used to ream the medullary canal.
The medullary canal of the proximal phalanx is then identified through a burr hole on
the articular surface of the base of the phalanx. Osteophytes are removed from the
proximal phalanx at this time with a rongeur. The intramedullary canal of the proximal
phalanx is reamed. Care is taken so that the rectangular opening for both the metacarpal
and the proximal phalanx are square in line with the axial direction of both the
metacarpal and phalanx. Appropriate sizes are then placed inside the medullary canals.
Using a no-touch technique, the definitive prosthesis is then introduced. The capsule is
repaired, and the extensor tendon is subsequently aligned. Some authors prefer to
reconstruct the collateral ligaments at this time. Care is taken at the initial dissection to
preserve as much of the collateral ligament as possible. The skin is then closed using
nylon suture, and a splint is applied with the fingers in extension and in a neutral
position.
Approximately 4-5 days after the procedure, the patient is fitted for a dynamic outrigger
splint that maintains extension in an appropriate anatomical position of the fingers while
the patient undergoes active flexion exercises. Night splints are manufactured to
maintain the fingers in extension. Splinting is required for the next 4-8 weeks. Followup radiographs are obtained to confirm the appropriate positioning of the implants.
Crossed intrinsic transfer of the extensor tendons from the ulnar side to the radial side of
the adjacent finger to increase stability is another surgical option. Intrinsic release to
alleviate intrinsic tightness eliminates the dorsal digital expansion tightness that is one
of the subluxing forces on the MP joint. Finally, MP joint arthroplasties can provide
long-term relief. A patient with good hand function in the absence of pain is not a
candidate for arthroplasty, even if obvious MP joint deformity is present, because
surgery may not improve the hand function and could decrease grip strength.

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12. One Piece MCP Replacement

The Swanson design provides flexure not articulation. Made of
rubber, it was firstly used in 1969, with more than half a million
implanted to date. PIP and DIP are a possibility when considering
this replacement.
The main source of failure was not at flexure but stem, like when you
snap the fingers.
The development of Swanson model lead to
metallic grommets-like reinforcements with
improved performance, this could take
scissor-like stresses much better.

a. Performance Testing for MCP

The MCP joint was tested using the Durham finger function simulator. The purpose of
the simulator is to mimic the motion, no load and load no motion behaviour of the
joints. This was used to improve the performance of the joint.

Pinch grip, 100N for 45 seconds

Motion cycle, 10-15N, 1.5Hz, 3000 cycles
Repeated for >5million cycles
RoM 50-90 degrees

The simulator successfully recreated the failure mode observed in the Swanson MCP
joint.
b. Two-piece MCP joint
A two-piece replacement was introduced, with
resurfacing prostheses and made of ascension,
PyroCarbon material.
The characteristics of this model are show in the table below.

103

Lectures 18 & 19 Tissue Engineering

1. Lecture Overview

The Tissue Engineering Paradigm

Stem or pluripotent cells
o Their power & origins
o Ethical dimensions
Growth factors
Tissue Engineering scaffolds

2. Tissue Engineering Motivations

The desire is to recapitulate biological material such as:

Cartilage, bone & tendon

Alternative to grafting

Tissue Engineering is all about encouraging the body to repair/heal itself. Instead of
replacing something with a big intervention, we repair a patch by growing a new piece
cartilage.
It also helps reduce the scarcity of organ donors (skin, heart, kidney, liver, etc.).
3. Tissue Engineering Origins
The First Generations (1950s) goal was Bionertness, which means trying to create a
man-made material that you can put into the body and that the body will just integrate.
There will a minimum reaction from the body to the presence of the biomaterial.
The Second Generations (1980s) goal was Bioactivity, i.e. materials that can be
integrated in the body, and the body will grow around and in it and, after, the
biomaterial will be replaced by actual bone. This include resorbable materials that will
have a controlled reaction with physiological environment.
The Third Generations (2000s) goal is regenerate functional tissue. The concept of
re-growing tissue is main concept including in this third generation. There is a lot of
optimism but it still remains as an ambition rather than a real thing (very few products).
These Third Generation materials main characteristics are: biointeractive, integrative,
resorbable; stimulate specific cell response at molecular level.
4. Tissue Engineering Paradigm
There are three approaches to the use of tissue engineering:

Cell injection method You can just inject stem cells into a damage part of the
body and the cells will manage the healing process better.
104

Closed system method you have the cells encapsulated in something. The
encapsulation process is a process of bidirectional trafficking of small
molecules, but protect cells from effector agents of immune system
(complement).
o Extravascular capsules
o Macrocapsules
o Microcapsules
Tissue Engineering using scaffold biomaterials hard-core version of tissue
engineering.

5. Scaffold Paradigm
To use scaffold
materials, there are two
things you need: cells
and scaffold.
A scaffold is a three
dimensional piece of
material which you can
saw cells into. Cells like
to grow on surfaces;
they like to be attached
to something. IF you
take those cells and you
try to grow them in the
lab, they are much
happier if they grow on
something, the scaffold. From an tissue engineering point of view, were going to take
the scaffold and we are going to make it into a piece of new tissue. The scaffold is going
to form part of the device we are going to implant. You manufacture the scaffold to be
the right kind of thing for the thing we want to do. For example, to re-grow cartilage,
we need scaffold that has the right architecture, etc.
We will then put the stem cells into the scaffold and hope that ultimately they become
cartilage cells. We need to make sure that the cells get all the right signals to turn them
from stem cells into cartilage cells.
The signals we are interested in are mechanical properties, right biological reactions,
right architecture, right nutrients, etc. Ultimately what we want to happen is that our
scaffold with the cells on it, over time, will no longer be there. It will be a natural piece
of cartilage. Therefore, the scaffold needs to be resorbable, i.e. replace by natural
materials.

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Maturation in bioreactor refers to taking scaffold and cells and letting them grow in the
lab.
The tissue engineering market is very significant, with $1.5 billion in 2008. It is
projected to grow at a 16.2% compound annual rate from 2008 through 2013, therefore
approaching $3.2 billion by 2013. This market is driven by the expectations that tissue
engineering will be able to replace many of the things that are currently manufactured
and used as devices.
6. Stem Cells
Stem cells are those cells are able to
generate other types of cells. It is a
vey basic type of cell but also a very
powerful type of cell. These cells are
highly used for tissue repair and
tissue maintenance.
At first, there was some ethical
controversy due to the fact that stem
cells had to be taken from the
embryo. Two options are available:
you can take it from the embryo or
you can make them in the lab.

a. Embryonic Stem Cells

Some workers have taken very early human embryos (a few days old), allowed the
embryo to develop a few more days, and removed the inner cells destined to form the
embryo; these cells in culture form embryonic stem cells or ES cells. Because they
are derived so early in development, they are said to be totipotent, i.e. totally potent to
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form any specific cell type in the body, or sometimes termed pluripotent, i.e. able to
form many potential specific cell types.
While this is a tantalising source of stem cells, it is perhaps because of this unlimited
potential and the numerous development signals needed to become a specific cell type
that it is also may be a less controllable source. A study with mouse embryonic stem
cells indicates that at times, these cells, when injected into mice, form tumours
(teratocarcinomas).
Another source of human embryonic stem cells is later human embryos, from 5-9 weeks
old. The primordial germ cells from these embryos (cells destined to form the egg or
sperm cells in the adult) also can form embryonic stem cells in culture. However, use of
these cells for treatment of disease or organ generation, as well as the use of embryonic
stem cells from early human embryos as proposed by NIH, faces a major hurdle
immune rejection. Even early embryonic cells already have the molecules on their
surface that lead to an immune response in the host, or even a response of the transplant
against the host (graft vs. host disease).
Thus, use of embryonic stem cells for tissue regeneration faces the same problem as
normal organ transplants. The body of the person receiving the embryonic stem cells
will reject them, unless large doses of toxic immunosuppressive drugs are used. One
way to avoid this problem might be to form a clone of the pation (but of course this
procedure is also highly controversial); the embryonic stem cells from this procedure
would not be rejected.
b. Adult (somatic) Stem Cells
Other stem cells are found in somatic tissues and are called either somatic stem cells or
adult stem cells. These stem cells are multipotent, i.e. they are committed to give rise to
cells that have a particular function. Examples of somatic stem cells include:

Hematopoietic stem cells, which give rise to all blood cells;

Mesenchymal stem cells, which give rise to tissue such as bone, tendon, muscle,
cartilage, nerve tissue, etc.;
Stromal stem cells, which generate bone, cartilage, fat, connective tissue, etc;
Brain stem cells, which can generate both non-neuronal and neuronal cells in the
brain.

Most if not all tissues and organs contain a small number of undifferentiated cells that
can differentiate into the major cell types of the tissue or organ.
Induced pluripotent cells (iPSCs) push them backwards in time to become more basic
and powerful.
The tissue engineering process using iPSCs is shown in the figure below.

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7. Scaffolds
There are several factors that affect the degradation rate:

Polymer chemistry
o Composition, structure, molecular weight, chain motility,
impurities/additives
Scaffold structure
o Density, shape, size, surface texture, surface to volume ratio, pore size,
wettability, sterilisation
In vitro
o pH, temperature, ionic strength, mechanical loading, etc.
In vivo
o Vasculature, tissue, mechanical loading, enzymes, etc.
a. Materials

Several bio-resorbable polymers are used:

Poly (-hydroxy esters)

Poly (propylene fumarate)
Polyhydroxyalkanoate
Polydioxanone
Polyphosphates and ployphosphozenes
Pseudo-poly (amino-acids)
b. Structures
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There are several structure requirements:

Open scaffold
o Cell seeding cells can get into it
o Nutrient perfusion nutrients can then get into it
o Control of resorption rate (surface-volume ratio)
Mechanical properties
o Bulk properties
o Time dependency

Figure 1 - Scaffold Structures

Several strategies are available with regard to cell seeding:

Static culture
Spinner flask culture
o Scaffolds suspended in media, mixed by stirrer bar
Rotary vessel culture
o Media is mixed by rotating whole vessel
Perfusion culture
o Continuous media flow pumped through scaffold
o

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3D Printing
The structures are based on the solid freedom fabrication concept:

3D printing
Stereolithography
Selective laser sintering

It is a very long process although it provides a high degree of structure control.

Salt leach
You get your polymer; you melt it and mixed it with salt. You then let it cool and put it
in water so as to dissolve the salt, which leaves a whole in the structure. It is compatible
with compression mould, extrude and solvent casting. It is cheap and rapid although it is
difficult to control the structure and to ensure open pore structure.
HIPE High Internal Phase Emulsions
It is a rapid and more complex process although it has solvent pairing constraints.
Gas Foaming
No solvent is required for this procedure, which is good if chemokines are incorporated.
It is also non-porous, which can be changed to porous by adding salt leaching step. The
porosity rate is 45-84% with a pore size of 50-200 micrometres.
Electrospun Fibres
Electrospinning involves the application of a high voltage electric field to a polymer
solution or melt, so that mutual charge
repulsion on the surface of the liquid
overcomes the surface tension and causes a
thin liquid jet to be ejected. As the jet
travels towards a collector (at a different
electric potential), electrostatic repulsion
from charges on the surface causes the jet
diameter to narrow. Often, instabilities in
the electric field cause the jet to enter a
whipping mode, which stretches the jet and further narrows its diameter. Sometimes, the
electrostatic repulsion can cause the jet to split into even narrower jets.
Continuous solid polymer fibres are formed as the jet dries or cools, which accumulate
on the collector to form a non-woven material. These fibres can typically possess
diameters between 10 nm and 10 micrometres, resulting in materials with very high
surface areas.
A simplified schematic of the electrospinning process is shown in the figure above. A
polymer solution held in a syringe (A) is fed to a metal needle (B). A high voltage
supply (C) is connected to the needle, producing a fine jet of polymer solution (D). This
dries out in transit, resulting in fine fibres, which are collected on an earthed target (E).
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