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Bone Structure and Physiology Fatigue Properties of Bone and

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									Bone Structure and Physiology
              &
Fatigue Properties of Bone and
       Stress Fractures
                      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
                              www.sirinet.net/ ~jgjohnso/skeleton.html
   Osteon

Periosteum

                                                                   Cancellous
                                                                   Bone




                      Cortical Bone
    Bone Physiology. Courtesy Gray's Anatomy 35th edit Longman Edinburgh 1973
      Microstructure of the Bone




(a)           (b)        (c)
Microstructure of Bone (Cont’d)
Composition of Bone: Cells

           Osteocytes


           Osteoblasts


           Osteoclasts
       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
                     Controlling Factors
                                        of osteoclasts and osteoblasts
         Macrophage
             • Phagocytose invading pathogens
                           Cell alters shape to surround bacteria or debris
                           Process: Chemotaxis, adherence, phagosome
                            formation, phagolysosome formation

             • Secrete Interleukin-1
                           (IL-1)                                Nuclei
                                                                             Bacterium


             • Involved in bone
               resorption                                                  Ingested
                                                                           bacterium

http://saints.css.edu/bio/schroeder/macrophage.html
http://academic.brooklyn.cuny.edu/biology/bio4fv/page/phago.htm
http://www.allsciencestuff.com/mbiology/research/osteoporosis
      Composition of Bone: Matrix


   Cortical/ Compact
    Bone


   Cancellous/
    Trabecular/ Spongy
    Bone
                 Cortical                 Cancellous
                                        Rigid lattice designed for
 Physical
              Dense protective shell    strength; Interstices are
Description                             filled with marrow


              Around all bones,
                                        In vertebrae, flat bones
              beneath periosteum;
 Location     Primarily in the shafts
                                        (e.g. pelvis) and the ends
                                        of long bones
              of long bones

  % of
 Skeletal              80%                        20%
  Mass
                Cortical              Cancellous
First Level
                   Osteons                 Trabeculae
Structure

 Porosity           5-10%                   50-90%


                                    Haversian system allows
                                    diffusion of nutrients and
              Slow circulation of   waste between blood
Circulation   nutrients and waste   vessels and cells; Cells
                                    are close to the blood
                                    supply in lacunae
                   Cortical                Cancellous
 Strength      Withstand greater stress Withstand greater strain

                                          Compression; Young’s
                 Bending and torsion,
Direction of                             modulus is much greater
                 e.g. in the middle of
 Strength                                   in the longitudinal
                      long bones
                                                 direction

 Stiffness              Higher                   Lower


 Fracture
                     Strain>2%                Strain>75%
   Point
  Properties of Cortical and Cancellous Bones

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




http://www.orthoteers.co.uk/Nrujp~ij33lm/Orthbonemech.htm
Bone Remodeling
                              Bone Remodeling
         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
http://www.elixirindustry.com/resource/osteoporosis/jilka.htm
         BMU Remodeling Sequence
www.ifcc.org/ejifcc/ vol13no4/130401004n.htm




             Osteocytes


                                      Activation


 Quiescence
                                                   Resorption




  Formation &                                      Reversal
  Mineralization
    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*
                              Compressive                              Modulus
   Material
                             Strength (MPa)                             (GPa)
    Cortical                         10-160                                4-27

Trabelcular                           7-180                                1-11

  Concrete                              ~4                                   30

          Steel                   400-1500                                  200

      Wood                              100                                  13
Pink:      http://www.engineeringtoolbox.com/24_417.html
Yellow:    http://www.brown.edu/Departments/EEB/EML/background/Background_Bone.htm
Green:     http://ttb.eng.wayne.edu/%7Egrimm/BME5370/Lect3Out.html#TrabecularBone
                    *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
http://silver.neep.wisc.edu/~lakes/BoneAniso.html
         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
                       Fatigue of Bone (Cont’)
          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
http://www.orthoteers.co.uk/Nrujp~ij33lm/Orthbonemech.htm
Simon, SR. Orthopaedic Basic Science. Ohio: American Academy of Orthopaedic Surgeons; 1994.
    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
Process to Fatigue Failure (cont’d)

  • Relatively rapid loss of stiffness
  • Bear less load
  • Absorb more energy ( can sustain larger
    deflections)
  • Cracks develop rapidly
       May stabilize quickly without much
        propagation
Process to Fatigue Failure (Cont’d)
  • Cracks occur first in regions of high
   strain
       Accumulate with either
            Increased number of cycles
            Increased strain
  • Cracks develop perpendicular to the
    load axis
Process to Fatigue Failure (cont’d)
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
Process to Fatigue Failure (cont’d)
  • 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
Process to Fatigue Failure (Cont’d)
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:
    1. Fatigue fracture
    2. 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
       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
Risk Factors for Stress Fractures (Cont’d)

       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
Risk Factors for Stress Fractures (Cont’d)

       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
Risk Factors for Stress Fractures (Cont’d)
                  Biomechanical factors:
                  • 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%


* - Gilati and Abronson (1985)
Risk Factors for Stress Fractures (Cont’d)
         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
The End
                   Osteon
                                                Haversian Canal

   Major structural
    unit of cortical
    bone
    • Concentric
      cylinders of bone
      matrix around
      haversian canals




                            http://www.nd.edu/~humosteo/OsteonModel.gi
                Periosteum
   Capillary-rich, fibrous membrane
    coating exterior bone surface

    • Responsible for nourishing bone
                          nuclei


The osteoclast
is a large cell   cytoplasm
 with multiple
    nuclei
                 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
           Osteoblasts (Cont’d)
   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
          • 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
            Osteocytes (Cont’d)
   Mechanosensory cells
         • Respond to deformation
         • Flow of interstitial fluid through the osteocytic
           canalicular 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
            • Sheets of collagen
              fibers with a preferred
              orientation
(c) Third Level

           Lamellae are
            arranged into
            tubular osteons
Osteoclast
Osteocytes
Osteoblast
       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.”      http://uwcme.org/site/courses/legacy/bonephys/physiology.php




    • 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
     Basic Multicellular Units (cont’d)




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

http://uwcme.org/site/courses/legacy/bonephys/physiology.php
                                     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




http://uwcme.org/site/courses/legacy/bonephys/physiology.php
                              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


http://uwcme.org/site/courses/legacy/bonephys/physiology.php
http://www.britannica.com/ebc/article?tocId=41887
              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


http://uwcme.org/site/courses/legacy/bonephys/physiology.php
                                     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


http://uwcme.org/site/courses/legacy/bonephys/physiology.php
                                             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



http://uwcme.org/site/courses/legacy/bonephys/physiology.php
      Mechanical Support
   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


      Probability of Injury

								
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