Prepared By: S.

Ehtesham Al Hanif (Hridoy) [0510035]

ME 471- BIO-ENGINEERING / BIO-MEDICAL

TOPICS: BONE

Prepared By,

S. EHTESHAM AL HANIF (HRIDOY)

STUDENT ID: 0510035
E-MAIL: SEAHHRIDOY@GMAIL.COM
MOBILE: 88-01670839383

BIO (BIO-MEDICAL) ENGINEERING – BONE

 Prepared By: S. Ehtesham Al Hanif (Hridoy) [0510035]
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 collagen
o 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
BIO (BIO-MEDICAL) ENGINEERING – BONE
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with marrow
Location Around all bones, beneath In vertebrae, flat bones (e.g.
periosteum; Primarily in the pelvis) and the ends of long
shafts of long bones bones
% of Skeletal Mass 80% 20%
First Level Structure Osteons Trabeculae
Porosity 5-10% 50-90%
Circulation Slow circulation of nutrients and Haversian system allows
waste diffusion 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 Compression; Young’s modulus
middle of long bones 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 Compressive Strength (MPa) Modulus (GPa)
Cortical 10-160 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

Road to Failure: Region 2

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

BIO (BIO-MEDICAL) ENGINEERING – BONE

 Prepared By: S. Ehtesham Al Hanif (Hridoy) [0510035]
Road to Failure: Region 3
• 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

BIO (BIO-MEDICAL) ENGINEERING – BONE

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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:

BIO (BIO-MEDICAL) ENGINEERING – BONE

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

BIO (BIO-MEDICAL) ENGINEERING – BONE

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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

BIO (BIO-MEDICAL) ENGINEERING – BONE

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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

BIO (BIO-MEDICAL) ENGINEERING – BONE

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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 for
dense trab bone)
 For trabecular bone: = 0.05 − 1.0 /
o ∝

BIO (BIO-MEDICAL) ENGINEERING – BONE

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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

BIO (BIO-MEDICAL) ENGINEERING – BONE