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Slide 1 - Bone Structure and Physiology&Fatigue Properties of Bone and Stress Fractures
Slide 2 - 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
Slide 3 - Shape www.sirinet.net/ ~jgjohnso/skeleton.html Long, short, flat, and irregular Long bones are cylindrical and “hollow” to achieve strength and minimize weight
Slide 4 - Bone Physiology. Courtesy Gray's Anatomy 35th edit Longman Edinburgh 1973 Cancellous Bone Cortical Bone Osteon Periosteum
Slide 5 - Microstructure of the Bone (a) (b) (c)
Slide 6 - Microstructure of Bone (Cont’d)
Slide 7 - Composition of Bone: Cells Osteocytes Osteoblasts Osteoclasts
Slide 8 - Controlling Factors Hormones Estrogen Testosterone Cytokines Growth factors, Interleukins (1, 6, and 11), Transforming growth factor-b Tumor necrosis factor-a of osteoclasts and osteoblasts
Slide 9 - 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 Controlling Factors of osteoclasts and osteoblasts 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 Bacterium Nuclei Ingested bacterium
Slide 10 - Composition of Bone: Matrix Cortical/ Compact Bone Cancellous/ Trabecular/ Spongy Bone
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Slide 14 - Properties of Cortical and Cancellous Bones http://www.orthoteers.co.uk/Nrujp~ij33lm/Orthbonemech.htm
Slide 15 - Bone Remodeling
Slide 16 - 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
Slide 17 - BMU Remodeling Sequence Activation Resorption Reversal Quiescence Formation & Mineralization www.ifcc.org/ejifcc/ vol13no4/130401004n.htm Osteocytes
Slide 18 - 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
Slide 19 - Material Properties Comparison* 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
Slide 20 - *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
Slide 21 - Function of Bone Mechanical support Hematopoiesis Protection of vital structures Mineral homeostasis
Slide 22 - 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
Slide 23 - 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.
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Slide 25 - Process to Fatigue Failure Road to Failure: Region 1 Crack initiation Accumulation Growth Characteristics: Matrix damage in regions of High stress concentration Low strength
Slide 26 - 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)
Slide 27 - 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
Slide 28 - Road to Failure: Region 2 Crack growth Coalescence 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)
Slide 29 - 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)
Slide 30 - 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
Slide 31 - 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
Slide 32 - 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
Slide 33 - Fatigue Micro Damage
Slide 34 - 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
Slide 35 - 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
Slide 36 - Causes of Stress Fractures There are two theories about the origin of stress fractures: Fatigue theory Overload theory
Slide 37 - 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
Slide 38 - Overload Theory Certain muscle groups contract Cause the attached bones to bend After repeated contractions and bending Bone finally breaks
Slide 39 - 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
Slide 40 - 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)
Slide 41 - 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)
Slide 42 - 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% Risk Factors for Stress Fractures (Cont’d) * - Gilati and Abronson (1985)
Slide 43 - 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 Risk Factors for Stress Fractures (Cont’d)
Slide 44 - 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
Slide 45 - 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
Slide 46 - The End
Slide 47 - Osteon Major structural unit of cortical bone Concentric cylinders of bone matrix around haversian canals http://www.nd.edu/~humosteo/OsteonModel.gi Haversian Canal
Slide 48 - Periosteum Capillary-rich, fibrous membrane coating exterior bone surface Responsible for nourishing bone
Slide 49 - The osteoclast is a large cell with multiple nuclei nuclei cytoplasm
Slide 50 - 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
Slide 51 - 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
Slide 52 - 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
Slide 53 - 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
Slide 54 - 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
Slide 55 - (a) First Level Hydroxyapatite crystals embedded between collagen fibril
Slide 56 - (b) Second Level Fibrils are arranged into lamellae Sheets of collagen fibers with a preferred orientation
Slide 57 - (c) Third Level Lamellae are arranged into tubular osteons
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Slide 59 - Osteoclast
Slide 60 - Osteocytes
Slide 61 - Osteoblast
Slide 62 - 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
Slide 63 - 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
Slide 64 - 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
Slide 65 - 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
Slide 66 - 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
Slide 67 - 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
Slide 68 - 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
Slide 69 - 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
Slide 70 - Mechanical Support Provides strength and stiffness Hollow cylinder: Strong and light Have mechanisms for avoiding fatigue fracture
Slide 71 - 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)
Slide 72 - 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
Slide 73 - 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
Slide 74 - Fatigue Curve Probability of Injury
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