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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
   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
   Long, short, flat, and irregular
    • Long bones are cylindrical and “hollow” to
      achieve strength and minimize weight



                      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

             • Involved in bone
               resorption                                                  Ingested
      Composition of Bone: Matrix

   Cortical/ Compact

   Cancellous/
    Trabecular/ Spongy
                 Cortical                 Cancellous
                                        Rigid lattice designed for
              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%
                Cortical              Cancellous
First Level
                   Osteons                 Trabeculae

 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

 Stiffness              Higher                   Lower

                     Strain>2%                Strain>75%
  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
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
         BMU Remodeling Sequence vol13no4/130401004n.htm




  Formation &                                      Reversal
    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
                             Strength (MPa)                             (GPa)
    Cortical                         10-160                                4-27

Trabelcular                           7-180                                1-11

  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
   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
                         • 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
Simon, SR. Orthopaedic Basic Science. Ohio: American Academy of Orthopaedic Surgeons; 1994.
    Process to Fatigue Failure
Road to Failure: Region 1
 1.Crack initiation

 • 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
  • Cracks develop rapidly
       May stabilize quickly without much
Process to Fatigue Failure (Cont’d)
  • Cracks occur first in regions of high
       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
  3.Delamination and debonding
  • 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
          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
   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
   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
     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
     • 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

       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
        •   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
    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
                                                Haversian Canal

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

   Capillary-rich, fibrous membrane
    coating exterior bone surface

    • Responsible for nourishing bone

The osteoclast
is a large cell   cytoplasm
 with multiple
   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
   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
          • Polarized (nucleus away from bone surface)
          • Basophilic stains
   Osteoblasts surrounded by mineralized bone
         • 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
(b) Second Level

           Fibrils are arranged
            into lamellae
            • Sheets of collagen
              fibers with a preferred
(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
     Basic Multicellular Units (cont’d)

                 A photomicrograph of bone showing osteoblasts and osteoclasts
                              together in one Bone Metabolic Unit
              Occurs when bone experiences micro damage
               or mechanical stress, or at random

              A BMU originates and travels along the bone

                   •     Differentiated cells are recruited from stem cell

                          •    Pre-osteoclasts merge to form multi-nucleated
                              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
 Transition from osteoclastic to osteoblastic

 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
                    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

                          • 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
                   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
      Mechanical Support
   Provides strength and stiffness
   Hollow cylinder: Strong and light
   Have mechanisms for avoiding fatigue
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

   Protects heart and lungs in chest

   Vertebrae in the spine protect the
    spinal cord and nerves
    Mineral Homeostasis
   Primary storehouse of calcium and
   Trabecular bone are rapidly formed
    or destroyed
    • In response to shifts in calcium stasis
      without serious mechanical
Fatigue Curve

      Probability of Injury

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