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Bone Structure & Dev: Readings. Frankel and Nordin, Chapter 2 Frost, H.M. (2000) Muscle, bone, and the Utah paradigm: A 1999 overview. Medicine & Science in Sports & Exercise , 32:5 , pp 911-917. - PowerPoint PPT Presentation
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Bone Structure & Dev: Readings
– Frankel and Nordin, Chapter 2– Frost, H.M. (2000) Muscle, bone, and the Utah
paradigm: A 1999 overview. Medicine & Science in Sports & Exercise, 32:5, pp 911-917.
– Turner, C.H. and Robling, A.G. (2003) Designing exercise regimens to increase bone strength. Ex & Sp Sci Rev, 31:1 pp 45-50.
– Modlesky, C.M. and Lewis, R.D. (2002) Ex & Sp Sci Rev, 30:4 pp 111-176.
– Humphries, B., et al. (2000) Effect of exercise intensity on bone density, strength, and calcium turnover in older women. Medicine & Science in Sports & Exercise, 32:6, pp 1043-1050.
Bone Structure & Dev Outline
• Outline– Structure and architecture – Development and growth
• Process – continuous remodeling
• Factors affecting bone density and strength
– Mechanical properties – Osteoporosis
Bone Gross Structure, Architecture and Development
Long Bone Structure
Bone Micro-Structure, cont’dProjections of osteocytes are
thought to be cite of strain
sensing, which
stimulates bone to form
Bone Composition & Structure• Material Constituents:
– Calcium carbonate and Calcium phosphate• 60-70% bone weight• Adds stiffness• Primary determinant for compressive strength.
– Collagen• Adds flexibility• Contributes to tensile strength
– Material Constituents– Water
• 25-30% bone weight• Contributes to bone strength• Provides transportation for nutrients and wastes.
Bone Composition & Structure• Structural Organization
– Bone mineralization ratio specific to bone
– Two categories of porous bone:
• Cortical bone(70-95% mineral content)
• Trabecular bone (10-70% mineral content)
– More porous bones have:
• Less calcium phosphate
• More calcium carbonate
• Greater proportion of non-mineralized tissue
Bone Composition & Structure
• Cortical Bone– Low porosity– 5-30% bone volume is non-
mineralized tissue– Withstand greater stress but less
strain before fracturing
Bone Composition & Structure
• Trabecular Bone– High porosity– 30 - >90% bone volume is non-mineralized
tissue– Trabeculae filled with marrow and fat– Withstand more strain (but less stress) before
fracturing
Bone Composition & Structure
• Both cortical and trabecular bone are anisotropic – stress/strain response is directional
• Bone function determines structure (Wolff’s law)
• Strongest at resisting compressive stress
• Weakest at resisting shear stress
Bone Growth & Development
• Longitudinal Growth– at epiphyses or epiphyseal plates– Stops at 18 yrs of age (approx.)
• can be seen up to 25 yrs of age
• Circumferential Growth– Diameter increases throughout lifespan– Most rapid growth before adulthood
• Periosteum build-up in concentric layers• Endosteal growth• Internal remodeling
Bone Growth & Development
• Osteoblasts – bone building cells• Osteoclasts – bone absorbing cells• Osteocytes – mature bone cells, embedded in bony
matrix in circular pattern• Adult Bone Development
– Balance between oseoblast and osetoclast activity
– Increase in age yields progressive decrease in collagen and increase in bone brittleness.
• Greater in women
lamella
Bone Growth & Development
• Women– Peak bone mineral content: 25-28 yrs.
– 0.5%-1.0% loss per year following age 50 or menopause
– 6.5% loss per year post-menopause for first 5-8 years.
• Youth – bones are vulnerable during peak growing years– Bone mineral density (BMD) is least during peak growing
years
– Growth plates are thickest during peak growing years
Bone Growth & Development
• Aging– Bone density loss as soon as early 20’s– Decrease in mechanical properties and general
toughness of bone– Increasing loss of bone substance– Increasing porosity– Disconnection and disintegration of trabeculae
leads to weakness
Bone loading modes: Compression – pushing together Tension – pulling apart Torsion – twisting Shear – cutting across
Cutting across
Load-deformation relationship:
Stress-strain curve:
Repetitive vs. Acute Loads
• Repetitive loading
• Acute loading
• Macrotrauma
• Microtrauma
I: bone vs glass and metal
II: Anisotropic behavior of bone
Comparison of tendon andligament
Bone Response to Stress
• Wolf’s Law– Indicates that bone strength increases and decreases as the
functional forces on the bone increase and decrease.
• Bone Modeling and Remodeling– Mechanical loading causes strain– Bone Modeling
• If Strain > modeling threshold, then bone modeling occurs.
– “conservation mode”: no change in bone mass– “disuse mode”: net loss of bone mass
• Osteocytes – projections sense strain, or pressure, beginning remodeling process
Bone Response to Stress
• Bone mineral density generally parallels body weight– Body weight provides most constant
mechanical stress– Determined by stresses that produce strain on
skeleton– Think: weight gain or loss and its effect on
bone density
Frost’s mechanostatTheory of bone’s Response to stress
What factors mightChange thresholdLevels?
Bone Hypertrophy
• An increase in bone mass due to predominance of osteoblast activity.
• Seen in response to regular physical activity– Ex: tennis players have muscular and bone hypertrophy
in playing arm.
• The greater the habitual load, the more mineralization of the bone.– Also relates to amount of impact of activity/sport
Bone Atrophy
• A decrease in bone mass resulting form a predominance of osteoclast activity– Accomplished via remodeling– Decreases in:
• Bone calcium
• Bone weight and strength
• Seen in bed-ridden patients, sedentary elderly, and astronauts
Osteoporosis
• Website on osteporosis: http://www.nof.org National Osteoporosis Foundation• A disorder involving decreased bone mass and
strength with one or more resulting fractures.• Found in elderly
– Mostly in postmenopausal and elderly women– Causes more than 1/2 of fractures in women, and 1/3 in
men.
• Begins as osteopenia
Osteoporosis
• Type I Osteoporosis = Post-menopausal Osteoporosis– Affects about 40% of women over 50– Gender differences
• Men reach higher peak bone mass and strength in young adulthood
• Type II Osteoporosis = Age-Associated Osteoporosis– Affects most women and men over 70
Osteoporosis
• Symptoms:– Painful, deforming and debilitating crush
fractures of vertebrae• Usually of lumbar vertebrae from weight bearing
activity, which leads to height loss– Estimated 26% of women over 50 suffer from these
fractures
Osteoporosis
• Men have an increase in vertebral diameter with aging– Reduces compressive stress during weight
bearing activities– Structural strength not reduced– Not known why same compensatory changes
do not occur in women
Position Statement of ACSM on Osteoporosis
• Weightbearing physical activity is essential for developing and maintaining a healthy skeleton
• Strength exercises may also be beneficial, particularly for non-weightbearing bones
• An increase in physical activity for sedentary women can prevent further inactivity-related bone loss and can even improve bone mass
• Exercise is not an adequate substitute for postmenopausal hormone replacement
• Ex programs for older women should include activities for improving strength, flexibility, and coordination, to lessen the likelihood of falls
Osteoporosis Treatment
• Hormone replacement therapy• Estrogen deficiency damages bone• Increased dietary calcium• Lifestyle factors affect bone mineralization• Risk factors for osteoporosis:
– Smoking, alcohol– Inactivity– Low body fat– White, female, postmenopausal
Osteoporosis Treatment
• Future use of pharmacologic agents– May stimulate bone formation
– Low doses of growth factors to stimulate osteoblast recruitment and promote bone formation.
• Best Bet:– Engaging in regular physical activity involving weight
bearing and resistive exercise
– Avoiding the lifestyle (risk) factors that negatively affect bone mass.
Common Bone Injuries• Stress Fractures
– Begin as small disruption in continuity of outer layers of cortical bone.– Occur when there is no time for repair process (osteoblast activity)
• Injuries to articular cartilage (osteoarthritis)• Epiphyseal injuries
– Injuries to cartilaginous epiphyseal plate• Acute and repetitive loading can cause
– Premature closing of epiphyseal junction and termination of bone growth– Osteochondrosis
• Disruption of blood supply to epiphyses• Associated with tissue necrosis and potential deformation of the epiphyses.
– Injuries to tendon-bone junction, the apophysis• Apophysitis
– Osteochondrosis of the apophysis– Associated with traumatic avulsions.
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