me471-1

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Prepared By: S. Ehtesham Al Hanif (Hridoy) [0510035

BIO (BIO-MEDICAL) ENGINEERING – BONE

ME 471- BIO-ENGINEERING / BIO-MEDICAL

TOPICS: BONE

Prepared By,

S. EHTESHAM AL HANIF (HRIDOY)

STUDENT ID: 0510035

E-MAIL: [email protected]

MOBILE: 88-01670839383

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Bone

Structural support of the body

Connective tissue that has the potential to repair and regenerate

Comprised of a rigid matrix of calcium salts deposited around protein fibers

• Minerals provide rigidity

• Proteins provide elasticity and strength

Shape Long, short, flat, and irregular

• Long bones are cylindrical and “hollow” to achieve strength and minimize weight

Microstructure of the Bone

Composition of Bone: Cells

Osteocytes (mature bone cells)

o Bone forming

o Synthesize collagen

o Deposit hydroxyapatite into collagen matrix

Osteoblasts (form bone)

o Bone resorbing

o Large multinucleated

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o Ruffed edge

o Secret calcium

Osteoclasts (resorb bone)

o Mature bone cell

o Most numerous

o Relatively dormant

o Osteoblastic cells that no longer produce collageno Reside in lacunae

o Communicates with processes through canaliculi

Controlling Factors of osteoclasts and osteoblasts

Hormones

• Estrogen

• Testosterone

• Cytokines

Growth factors,

Interleukins (1, 6, and 11), Transforming growth factor-b

Tumor necrosis factor-a

Macrophage

• Phagocytose invading pathogens

Cell alters shape to surround bacteria or debris

Process: Chemotaxis, adherence, phagosome formation, phagolysosome

formation

• Secrete Interleukin-1

(IL-1)

• Involved in bone resorption

Composition of Bone: Matrix

Cortical/ Compact Bone

Cancellous/ Trabecular/ Spongy Bone

Cortical Cancellous

Physical Description Dense protective shell Rigid lattice designed for

strength; Interstices are filled

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with marrow

Location Around all bones, beneath

periosteum; Primarily in the

shafts of long bones

In vertebrae, flat bones (e.g.

pelvis) and the ends of long

bones

% of Skeletal Mass 80% 20%

First Level Structure Osteons Trabeculae

Porosity 5-10% 50-90%

Circulation Slow circulation of nutrients andwaste

Haversian system allowsdiffusion of nutrients and waste

between blood vessels and cells;

Cells are close to the blood

supply in lacunae

Strength Withstand greater stress Withstand greater strain

Direction of Strength Bending and torsion, e.g. in the

middle of long bones

Compression; Young’s modulus

is much greater in the

longitudinal direction

Stiffness Higher Lower

Fracture Point Strain>2% Strain>75%

Properties of Cortical and Cancellous Bones

Load Type Elastic modulus (109N/m2) Ultimate stress (106N/m2)

Bone Type Cortical Cancellous Cortical Cancellous

Tension 11-19 ~0.2-5 107-146 ~3-20

Compression 15-20 0.1-3 156-212 1.5–50

Shear 73-82 6.6+/-1.6

Bone Remodeling

BonRemodelinge

Bone structural integrity is continually maintained by remodeling

• Osteoclasts and osteoblasts assemble into Basic Multicellular Units (BMUs)

• Bone is completely remodeled in approximately 3 years

• Amount of old bone removed equals new bone formed

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BMU Remodeling Sequence

Load Characteristics of Bone

Load characteristics of a bone include:

Direction of the applied force

• Tension

• Compression

• Bending

• Torsion

• Shear

Magnitude of the load

Rate of load application

Material Properties Comparison*

Material

Cortical

Compressive Strength (MPa)

10-160

Modulus (GPa)

4-27

Trabelcular 7-180 1-11

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Concrete ~ 4 30

Steel 400-1500 200

Wood 100 13

*Variability of Properties

Material properties listed may vary widely due to test methods used to determine them

Variances of the following can effect results:

Orientation of sample

Bone and wood are elastically anistropic; steel is not

Condition of sample

Dry or wet with various liquids

Specifics of sample

Bone: age of donor, particular bone studied

Wood: species of tree Steel/Concrete: preparation methods, components

Function of Bone

Mechanical support

Hematopoiesis

Protection of vital structures

Mineral homeostasis

Fatigue of Bone

Microstructural damage due to repeated loads below the bone’s ultimate strength

• Occurs when muscles become fatigued and less able to counter-act loads during continuous strenuous

physical activity

• Results in Progressive loss of strength and stiffness

Cracks begin at discontinuities within the bone (e.g. haversian canals, lacunae)

• Affected by the magnitude of the load, number of cycles, and frequency of loading

3 Stages of fatigue fracture

• Crack Initiation

Discontinuities result in points of increased local stress where micro cracks form

Often bone remodeling repairs these cracks

• Crack Growth (Propagation)

If micro cracks are not repaired they grow until they encounter a weaker material surface and

change direction

Often transverse growth is stopped when the crack turns from perpendicular to parallel

to the load

• Final Fracture

Occurs only when the fatigue process progresses faster than the rate of remodeling

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Process to Fatigue Failure

Road to Failure: Region 1

1. Crack initiation

2. Accumulation

3. Growth

Characteristics:• Matrix damage in regions of

High stress concentration

Low strength

• Relatively rapid loss of stiffness

• Bear less load

• Absorb more energy ( can sustain larger deflections)

• Cracks develop rapidly

May stabilize quickly without much propagation

• Cracks occur first in regions of high strain

Accumulate with either• Increased number of cycles

• Increased strain

• Cracks develop perpendicular to the load axis


1. Crack growth

2. Coalescence

3. Delamination and debonding

Characteristics:

• After a crack forms

Interlamellar tensile and shear stresses are generated at its tip

Tend to separate and shear lamellae at the fiber-matrix interface

• Secondary cracks may extend between lamellae in the load direction

• Cracks tend to grow parallel to the load

• Delamination along the load axis

Elevated and probably unidirectional strain redistributions

• Along the fibers parallel to the load axis

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• Stiffness declines rapidly

• End of a material’s fatigue life

• Fiber failure

Coalescence of accumulated damage

Crack propagation along interfaces

• Rapid process• Ultimate failure of the structure

Stress Fractures

Stress fractures are

• Partial or complete fractures of bone

• Repetitive strain during sub-maximal activity

There are two main types:

• Fatigue fracture

• Insufficiency fracture

Fatigue Fracture

A fatigue fracture may be caused by:• Abnormal muscle stress

Loss of shock absorption

Strenuous or repeated activity

• Torque

bone with normal elastic resistance

• Associated with new or different activity

Abnormal loading

Abnormal stress distribution

Fatigue Micro Damage

Insufficiency Fractures

Due to normal muscular activity stressing the bone

Seen in post-menopausal and/or amenhorroeic women whose bones are

• Deficient in mineral

• Reduced elastic resistance

Occurs if osteoporosis or some other disease weakens the bones

Signs and Symptoms

Pain that develops gradually

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Increases with weight-bearing activity

Diminishes with rest

Swelling on the top of the foot or the outside ankle

Tenderness to touch at the site of the fracture

Possible bruising

Causes of Stress Fractures

There are two theories about the origin of stress fractures:1. Fatigue theory

2. Overload theory

Fatigue Theory

• During repeated efforts (as in running)

Muscles become unable to support during impact

Muscles do not absorb the shock

Load is transferred to the bone

As the loading surpasses the capacity of the bone to adapt

A fracture develops

Overload Theory Certain muscle groups contract

• Cause the attached bones to bend

After repeated contractions and bending

Bone finally breaks

Risk Factors for Stress Fractures

Age:

• The risk increases with age

• Bone is less resistant to fatigue in older people

Training errors:

• Sudden, drastic increase in running mileage or intensity

• Running with an unequal distribution of weight across the foot

• Intense training after an extended period of rest

• Beginning training too great in quantity or intensity

Fitness history:

• Sedentary people entering a sports program are prone to injury

• Gradual increase in training loads is important

Footwear:

• Only significant factor is the condition of the running shoe

• Newer shoes lead to fewer fractures

Endocrine status:

• Women athletes suffering from amenorrhea are at especially high risk

• Heavy endurance training may also compromise androgen status in men

Nutritional factors:

• Recommended calcium intake in post-puberty is 800mg/day

• Stress-fracture patients are encouraged to consume 1500mg of calcium daily

Biomechanical factors:

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• Incidence of stress fractures* are due to

• Tibial torsion (twisting/bending)

• Degree of external rotation at the hip

• When neither were present

• Incidence was 17%

• When both were present

• Incidence was 45%

• Other factors include:

• High arched foot

• Excessive pronation of foot (turning inward)

• Excessive supination of foot (turning outward)

• Longer second toe

• Bunion on the great toe

Prevention of Stress Fractures

Avoid abrupt increases in overall training load and intensity

Take adequate rest

Replace running shoes

Tend to lose their shock-absorbing capacity by 400 miles

Bony alignment may be modified to some extent by the use of orthotics

Women athletes should pay careful attention to

Training

Hormonal status

Nutrition and eating disorders

Treatment of Stress Fractures

Discontinue the activity

Rest Ice

Elevate the affected part

Non-impact aerobic activity (e.g. swimming and cycling)

Cast (if necessary)

Crutches

Osteon

Major structural unit of cortical bone

• Concentric cylinders of bone matrix around haversian canals

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HaversianCanal

Periosteum

Capillary-rich, fibrous membrane coating exterior bone surface

• Responsible for nourishing bone

Osteoclasts

Located in lacunae Derive from pluripotent cells of the bone marrow

Responsible for bone resorption

• Bind to bone via integrins

• Enzymes digest bone matrix

• Controlled by hormonal and growth factors

Identifying traits

• Large size

• Mulitple nuclei

• Ruffled edge

Location of active resorption

Osteoblasts

Bone forming cells

• Line the surface of the bone

• Surrounded by unmineralized bone matrix

• Derived from osteoprogenitor cell line

Produce type I collagen

• Secretion is polarized towards the bone surface

Attract Ca salts and P to precipitate to mineralize the bone

Upon completion of bone formation,

• Remains on the surface of bone

• Covered by non-calcified osteoid

Identifying traits:

• Outer membrane surface coated in alkaline phosphates

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• Polarized (nucleus away from bone surface)

• Basophilic stains

Osteocytes

Osteoblasts surrounded by mineralized bone matrix

• Most numerous bone cell

Positioned between lamellae in a concentric pattern around the central lumen of osteons

Regulate extracellular concentration of calcium and phosphate Mechanosensory cells

• Respond to deformation

• Flow of interstitial fluid through the osteocyticcanalicular network

Directed away from regions of high strain

Initiates electrokinetic and mechanical signals

Growth Facors (intercellular signal molecules)

• Insulin-like growth factor, IGF-1,

• Prostaglandins G/H synthase

• PGE2 and Nitric oxide

(a) First Level

Hydroxyapatite crystals embedded between collagen fibril

(b) Second Level

Fibrils are arranged into lamellae

a. Sheets of collagen fibers with a preferred orientation

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(c) Third Level

Lamellae are arranged into tubular osteons

Basic Multicellular Units

“The Basic Multicellular Unit (BMU) is a wandering team of cells that dissolves a pit in the bone surface and then

fills it with new bone.”

• BMUs are discrete temporary anatomic structures organized as functional unit

Osteoclasts remove old bone, then osteoblasts synthesize new bone

• old bone is replaced by new bone in quantized packets

A photomicrograph of bone showing osteoblasts and osteoclasts together in one Bone Metabolic Unit

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Activation

Occurs when bone experiences micro damage or mechanical stress, or at random

A BMU originates and travels along the bone surface

• Differentiated cells are recruited from stem cell populations

• Pre-osteoclasts merge to form multi-nucleated osteoclasts

Bone Resorption

Newly differentiated osteoclasts are activated and begin to resorb bone

• Minerals are dissolved and the matrix is digested by enzymes and hydrogen ions

secreted by the osteoclastic cells

• Move longitudinally on bone surface

This process is more rapid than formation, though it may last several days

Reversal

Transition from osteoclastic to osteoblastic activity

Takes several days

Results in a cylindral space (tunnel) between the resorptive region and the refilling region

Forms the cement line

Bone Formation Following Resorption, osteoclasts are replaced by osteoblasts around the periphery of the

tunnel

Attracted by cytokines and growth factors

Active osteoblasts secrete and produce layers of osteoid, refilling the tunnel

Osteoblasts do not completely refill the tunnel

Leaves a Haversian canal

• Contains capillaries to support the metabolism of the BMU and bone matrix

cells

• Carries calcium and phosphorus to and from the bone

Mineralization When the osteoid is about 6 microns thick, it begins to mineralize

Formation of the initial mineral deposits at multiple discrete sites (initiation)

• Mineral is deposited within and between the collagen fibers

• This process, also, is regulated by the osteoclasts

Mineral maturation

• Once the cavity is full the mineral crystals pack together, increasing the density of the

new bone

Quiescence

After the tunneling and refilling

• Some osteoblasts become osteocytes

Remain in bone, sense mechanical stresses on bone

• Remaining osteoblasts become lining cells

Calcium release from bones

Period of relative inactivity

• Secondary osteon and its associated cells carry on their mechanical, metabolic and

homeostatic functions

Mechanical Support

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Provides strength and stiffness

Hollow cylinder: Strong and light

Have mechanisms for avoiding fatigue fracture

Hematopoiesis

Development of blood cells

• Occurs in the marrow of bone These regions are mainly composed of trabecular bone

• (e.g. The iliac crest, vertebral body, proximal and distal femur)

Protection of Vital Structures

Flat bones in the head protect the brain

Protects heart and lungs in chest

Vertebrae in the spine protect the spinal cord and nerves

Mineral Homeostasis

Primary storehouse of calcium and phosphorus

Trabecular bone are rapidly formed or destroyed

• In response to shifts in calcium stasis without serious mechanical consequences

Fatigue Curve

Structural Support of the body:

Connective tissue that has the potential to repair and regenerate

Comprised of a rigid matrix of calcium salts deposited around protein fibers

o Minerals provide rigidity

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o Proteins provide elasticity and strength

Bone’s Mechanical Functions:

Support & shape

Lever system for force transduction

Protection

Sound transduction (overshadowed hearing)

Bone’s Physiological Functions:

Hematopoiesis in the marrow

Mineral homeostasis (Ca, P)

Acid-base balance (alkaline salts)

Detoxification

Fat storage

Growth factor storage

Bone as a Composite Material:

Bone is a composite of collagen (Cn) and hydroxyapatite (HA)

Cn is rather like a p that it comes in fibres

HA is very like polymer material

o except a reinforcing ceramic in the form of elongated crystals

The photo shows the Cn fibres without the HA

Sheets of composite material (lamellae) are stacked together

Fiber orientation may vary from sheet to sheet and the sheets may be flat

The effect of Density:

The density of bones varies (but only slightly) due to porosity

Cancellous is just a framework of struts and plates made from (essentially) the same material as compact bone

its density and properties vary greatly

The figures below show plots of E and UTS as a function of bone density

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Strain Rate Effect:

Bone is viscoelastic and so its properties vary with the speed of loading, showing up as an effect of strain rate in

the stress/strain curve and an effect of frequency in fatigue tests

For the same reason there is a temperature dependence, much the same as in polymers

However, as graph were shows, the effect is quite small – much smaller than in soft tissue, so it is not a major

concern provided we take care to carry out our tests at a similar rate to that experienced physiologically

Aging:

Bone changes with age, becoming relatively weak and brittle in old people

This graph shows how the fracture toughness drops considerably over time

Osteoporosis:

Bone disease:

o Often associated with aging, especially women

o Bone resorption > bone deposited

o Reduced bone mass

o Matrix chemical composition maintained

o Cortical bone, thinner, less dense

o Trabecular bone: less trabeculae, thinner

Most vulnerable

Examples: wedge fractures of vertebra, femoral neck fractures

o Prevention: adequate Ca, fluoride, exercise

Mechanical Properties of Bone:

Properties of bone depends on:

o Types of bone

o Structure

o Type of load

o Direction of load

o Age

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Anisotropy of Bone:

Effect of loading type and direction:

Effect of bone type and apparent density:

Apparent density:

Apparent density: =

o Where, ≡ tissue density (e.g., density of individual trabeculae)

o ≡ volume fraction of bone present in bulk specimen (e.g., = 0.05 for porus trab bone = .60 fo

dense trab bone)

For trabecular bone: = 0.05 − 1.0 /

o ∝

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Effect of age:

Effect of age on trabecular bone:

Viscoelectric behaviour of cortical bone:

Effect of strain rate:

Creep:

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( )

Creep to failure:

Trabecular bone:

Individual trabeculae may have similar creep and fatigue behaviour as cortical bone

Continuum trabecular bone (machined specimens) do not appear to be strain rate sensitive

May sustain up to 50% strain before yielding

Large capacity for energy storage because of porous structure

Demonstrates stress relaxation during compressive loading

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