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Fall 2014 > KIN 429 Midterm 1 > Flashcards

KIN 429 Midterm 1 Flashcards

1
Q

Functions of bone?

A

Supports body structures, protection of internal organs, movement (along with muscles), mineral homeostasis, blood cell production (hemopoiesis in red bone marrow), triglyceride storage (in yellow marrow)

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2
Q

Types of bone

A

1) Long: tube-like, length > width, medullary cavity, limbs 2)Short: cube like, carpal and tarsal bones 3) Flat: broad, thin, scapula, skull bones, pelvic bones 4) Irregular: vertebra, mandible 5) Seasmoid: patella

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3
Q

Macrostructure to sub-nanostructure of cortical bone

A

Cortical bone (macrostructure) –> osteon –> lamella and Haversian canal –> collagen fiber –> collagen fibril –> collagen molecule and bone crystals

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4
Q

What is the functional unit of cortical bone?

A

Osteon

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5
Q

In trabecular bone, how are the lamellae arranged?

A

In irregular layers, they are not arranged like osteons

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6
Q

Are osteons in trabecular bone?

A

No

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7
Q

What are other names for trabecular bone?

A

Cancellous or spongy bone

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8
Q

Where is trabecular bone found in long bones?

A

On the end of the long bones

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9
Q

What is a Haversian system?

A

An osteon in cortical bone –> rings of lamellae around a circular canal

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10
Q

What is a central canal?

A

Centre of osteon, blood vessels and nerves

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11
Q

What are lamellae?

A

Rings of mineralized inorganic matrix (collagen and minerals)

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12
Q

What are osteocytes?

A

Bone cells

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13
Q

What are lacunae?

A

Spaces that contain trapped osteocytes that project via cellular processes

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14
Q

What are canaliculi?

A

Projection from osteocytes, facilitate cell to cell communication

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15
Q

Where are bone cells in trabecular bone?

A

No true osteons, bone cells on surface

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16
Q

What percentage of trabecular bone is calcified?

A

15-25%, the rest is bone marrow, blood vessels and connective tissue

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17
Q

How are lamallae arranged in trabecular bone and what is found between them and withiin them?

A

Lamellae are arranged in irregular lattices of thin columns (trabeculae/rods and plates). Between trabeculae is red bone marrow, and within trabeculae are osteocytes in lacunae.

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18
Q

Where is trabecular bone commonly found?

A

In most short flat and irregular bones and in the epiphysis of long bones

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19
Q

Where do areas of fracture commonly occur? Why?

A

Fractures occur most at sites with high trabecular bone because trabecular bone is list first and fasted, so areas with high trabecular bone fracture first, such as the distal radius, spine, and rib. Trabecular bone is next to red marrow so it has a lot of bone cells, so it is more metabolically acctive and is therefore lost first during bone loss

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20
Q

What is a VOlkman’s Canal?

A

Canals parallel to the central canal and allows for blood vessels to branch out and form connections/network with other vessels

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21
Q

What is the periosteum?

A

Connective tissue on the outside of bone

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22
Q

What is the endostieum?

A

Connect tissue on the inside of the bone; lines medullary cavity and trabeculae; where you find bone cells

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23
Q

What does an osteon consist of?

A

A central canal and lamelae in cortical bone only

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24
Q

Where is marrow found in long bones?

A

Red marrow is in the epiphysis, and yellow marrow is in the diaphysis

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25
Q

What are the two surfaces in contact with soft tissue? Where would they be?

A

Periosteum is in contact with muscle, and endosteum is in contact with red marrow

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26
Q

What is bone made of?

A

Matrix (osteoid, 35%) and Mineral Salts (65%) and Cells

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27
Q

What is matrix made of?

A

Collages (Type I) for 10% and Non-collagenous proteins (osteocalcin and alkaline phosphatase), water for 25%

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28
Q

What are the mineral made of?

A

Hydroxyapatite (Ca2+ and phosphorus) deposited between collagen

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29
Q

What cells make up bone?

A

Osteoblasts (bone building), osteoclasts (chew up bone), and osteocytes (bone cells that sit in the spaces in lacunae)

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30
Q

What type of collagen is matrix primarily made of?

A

Type I

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31
Q

What does collagen do for the bone?

A

Provides flexibility and tensile strength…helps absorb energy and deform…provides toughness…it the bone doesn’t have collagen, it is considered brittle

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32
Q

How is collagen arranged in cortical bone? Trabecular bone?

A

Compact is lamellae and trabeculae is arranged at random

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33
Q

What is woven bone?

A

Bone that is put down during growth or repair and is evenetually replaced with bone organized into lamellae, which has aligned collagen fibers to resist tensile forces

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34
Q

What is the gene for Type I collagen, what are the characteristics of Type I collagen?

A

COL1A1 (collagen type I alpha I); involved in the creation of collagen; produces pro-alpha(1) chain; two pro-aplha(1) side chains and pro-alpha(2) chain (produced by COL1A2) combine to make a molecule of Type I procollagen ; most abundant collagen, present in tendons and bones

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35
Q

What is the gene for type II collagen, what are the characteristics?

A

COL2A1, provides instructions for the production of pro-alpha(II) chain tpye II collagen. Type II collagen found primarily in cartilage, the vitreous, the inner ear, and nucleus pulposus, procollagen formed with 3 pro-alpha (II) side chains, processed by enzymes in the cell, arranged into long, thin fibrils that corrlink to one another in hte spaces around the cells –> Type II collagen

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36
Q

What % of the matrix do non-collagenous proteins account for?

A

5%

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37
Q

What is alkaline phosphatase, and what is it a marker of?

A

Bone specific form can be used as a biomarker, may be involved in bone mineralization; deficienct = defective mineralization; blood measure of bone formation

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38
Q

Osteocalcin? What is it a biomarker of?

A

Secreted during bone formation, incorporated into matrix, binds calcium. Biomarker of bone remodelling or turnover…good marker for people who turn bone over really fast….may shift activity from osteoblastic to osteoclastic?

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39
Q

Why does bone need to be remodeled?

A

Repair fatigue damage, reshape bone during growth or in response to mechanical loading, release calcium from bone

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40
Q

What are the the steps in bone remodeling?

A

1) Osteoblastic resorption: ruffled border seals off section, release acids to dissolve mineral, lysosomal enzymes digest organiz matrix (`2 wks in humans) 2) Reversal 3) Proosteoblastic migration and differentiation into osteoblasts 4) Osteoblastic matrix (osteoid formation) 5) Mineralization

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41
Q

How long does bone formation take?

A

2-3 months

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42
Q

How much bone is replaced each year?

A

10%…25% cancellous bone and 3% cortical

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43
Q

How long after matrix deposition does primary mineralization occur?

A

5-10 days and lasts <100 days

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44
Q

How does mineral contribute to bone strength?

A

Provides the stiffness and rigidity

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45
Q

How does collagen contribute to bone strength?

A

Collagen fibers provide the ductility and ability to absorb energy (deform).

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46
Q

What would happen if you had much less mineral relative to collagen in your bones?

A

Super deformable bones

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47
Q

What would happen if your osteoclasts stopped working?

A

Bone would become brittle

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48
Q

What is bone strength determined by?

A

Bone strength is largely determines by tissue mass and stiffness, which is determined by the mineral phase, whereas the collagen matrix contribute mainly to bone toughness. With age, the properties of the mineral and the collagen change, altering the material properties of bone tissue. The different role of collagen in the mechanical properties of bone is exemplified by in vitro studies showing that ionizing radiation that damages bone collagen results in decreased bone toughness w/o modification of Young’s Modulus.

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49
Q

What is osteopetrosis?

A

Rare congential disorder –> failure of osteoclasts to resorb bone (carbon anhydrase II deficiency –> required for osteoclast and renal tubular cells to excrete H+ and acidify their environment. Absence of this enzyme = osteoclasts can’t solubilize and resorb matrix and blocks acidification of urine by renal tubular cells). Bones appear more dense on x-rays but are brittle, more likely to fracture. Adult onset, infantile, intermediate forms.

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50
Q

What determines fracture risk?

A

Bone strength + applied load

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51
Q

What are the 3 major calcium pools in the body?

A

Intracellular calcium, calcium in blood and extracellular fluid, and bone calcium (99% of calcium in bone is in the mineral phase, the remaining 1% is in a pool that can exchange with extracellular calcium)

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52
Q

What are the 3 areas calcium is absorbed or resorbed from?

A

Small intestine (calcium is absorbed from ingested food and enters the blood), bone (bone resorption releases calcium and phosphate into blood, supressing resorption allows calcium to be deposited in bone), kidney (reabsorption of calcium back into blood, which preserves blood calcium levels, if tubular reabsorption of calcium decreases, calcium is lost by excretion)

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53
Q

Where is calcitonin produced? What does it do?

A

Produced by the thyroid gland, secretion stimulated by increased in extracellular calcium. Serves to decrease blood calciu, by supressing renal tubular reabsorption of calcium and inhibits bone resorption.

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54
Q

What is PTH, where is it produced, and what does it do?

A

Parathyroid hormone, produced by the parathyroid glands. Serves to increase blood calcium by increasing Ca2+ uptake in kidneys, increasing bone resorbtion, and increases calcitriol (active vitamin D3). Secretion is stimulated by a decreased in extracellular calcium, phosphate, and active D3 can also modulate secreition. Activity mediated by PTH/PTH-related peptide (PTHrP) receptor

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55
Q

What is 1,25(OH)2D, what does it do?

A

Active form of vitamin D (calcitriol), produced in the kidney, serves to increased blood calcium by facilitating absoprtion of calcium from the small intestine nand enhancing the fluxes of calcium out of bone

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56
Q

What is primary hyperthyroidism?

A

Parathyroid gland disease most often caused by a tumor –> secretes PTH without proper regulation. Chronic increase of blood [calcium], kidney stones, and decalfication of bone

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57
Q

What is secondary hyerthyroidism?

A

Disease outside of the parathyroid gland. Kindney disease –> kidneys can’t reabsorb calcium, blood calcium decreases, stimulating continual secretion of PTH to maintain adequate blood calcium (a lot is lost in urine). Can be caused also be inadequate nutrition of calcium or vitamin D, or excessive phosporus

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58
Q

What is cholecalciferol?

A

Naturally occurring form of vitamin D, sometimes called vitamin D3, made in large quantities in your skin when exposed to UVB, can also be taken as a supplement.

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59
Q

What is calcidiol?

A

25 hydroxy vitamin D3. A prehormone in your blood made in the liver from cholecalciferol. Only blood test that can be drawn to test for deficiency

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60
Q

What is calcitriol?

A

1,25 dihydroxy-vitamin D3. Made from calcidiol in both the kidneys and other tissues. Active form of D (helps with Ca2+ absorption), most potent steroid hormone derived from cholecalciferol.

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61
Q

What are natural and artificial sources of vitamin d?

A

Natural are egg yolks, fatty fish, and fish liver oils. Artificial are milk, margarine, cereals, although, vitamin D levels vary widely in fortified milk

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62
Q

KNOW THE CALCIUM REGULATION BY PTH AND VITAMIN D DIAGRAM

A

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63
Q

What enzyme converts cholecalciferol to calcidiol in the liver?

A

Vitamin D-25-hydroxylase

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64
Q

What enzyme conversts calcidiol to calcitriol in the kidney?

A

1 alpha hydroxylase

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65
Q

Actions of vitamin D in the intestine?

A

Absorption of calcium and phosphate

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66
Q

Actions of vitamin D on bone?

A

Activation of bone remodeling, needed for normal mineralization of bone, synthesis of collagen, non-matrix proteins.

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67
Q

Actions of vitamin D on kidney?

A

catabolism of 1,25 (OH)2 D

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68
Q

Action of vitamin D on parathyroid glands?

A

Suppression of PTH synthesis

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69
Q

What form of vitamin D is measured in the blood?

A

Calcidiol

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70
Q

WHy isn’t calcitriol levels indicative of vitamin D levels?

A

Its synthesis is tightly regulated by PTH, calcium, and phospahte, and levels may even be normal in severe Vitamin D deficiency

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71
Q

What are some diseases that cause fat malabsorption, and therefore vitamin D deficiency?

A

Pancreatic enzyme deficiency, Crohn’s disease, cystic fibrosis, celiac disease, liver disease, and surgical removal of part or all of the stomach or intestines can impair digestion and absorption of many nutrients

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72
Q

What is osteomalacia?

A

A metabolic bone disease where there is defective mineralization of osteoid at sites of bone remodeling, or periosteal or endosteal apposition. Essentially bone is forming but it isn’t becoming mineralized

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73
Q

What are are some vitamin D related causes of impaired mineralization?

A

Vitamin D deficiency (don’t eat it or go out in sun), impaired calcidiol production (liver disease, impaired liver enzymes), impaired calcitriol production (kindey disease or impaired 250hydroxy vitamin D 1alpha hydroxylase…pseudovitamin D deficiency rickets), and impaired vitamin D receptor (hereditary vitamin D resistant rickets)

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74
Q

What is the clinical presentation of osteomalacia?

A

Diffuse bone pain, muscle weakness, waddling gait (later stages), fragility fractures (ribs, vertebrae, long bones), radiographic evidence (decreased bone dnesity, non-specific thinning of the cortex and looser pseidofractures), trabeculae of vertebral bodies appear less clear, concavity of vertebral bodies can occur

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75
Q

Lab findings of osteomalacia?

A

Hypocalcemia or normal serum calcium, hypophosphatemia or normal, elevated PTH, elevated alkalin phosphatase (marker of bone formation), low serum 25 (OH) D if due to deficiency (may have normal vit D if the osteomalacia isn’t caused by a vitamin D deficiency)

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76
Q

How is vitamin D supplement usually given?

A

Given as cholecalciferol, however, in individuals with renal or hepatic failure, calcitriol should be used.

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77
Q

What is the recommended vitamin D intake for adults

A

400-1000 IU and 800-2000 IU

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78
Q

WHo might need vitamin D supplement?

A

Older people, breastfed infants, vegans/dieters/fat malabsorbers, dark skin, people with no sun, obese individuals because they can’t mobilize the vitamin D3 from their fat

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79
Q

Calcium intake recommended for 19-50, 50+, and pregnant/lactating women according to osteoporosis Canada?

A

1000 mg, 1200 mg, 1000 mg. Largely from diet is best, but if it is a supplement form, calcium carbonate or citrate is best

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80
Q

What is bone tissue formation called?

A

Osteogenesis or ossification

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81
Q

When the embryo is < 8 weeks old, what is the skeleton made of?

A

Hyaline cartilage and mesenchymal stem cells

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82
Q

What are the 2 types of bone formation?

A

Intramembranous and endochondral ossification

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83
Q

What is intramembranous ossification? What bones are formed from this?

A

Ossification from the mesenchyme; skull, mandible…flat bones

84
Q

What is endochondral ossificaiton? What bones are formed from this?

A

Replaces hyaline cartilage…most bones, especially long bones

85
Q

Overview of steps in intramembranous ossification?

A

Mesenchymal cells become osteogenic cells then osteoblasts –> osteoblasts produce matrix, become osteocytes –> matrix turns into woen bone –> woven bone is eventually remodeled into trabeculae –> blood vessels incorporated between trabeculae will form red marrow –> mesenchyme condenses as periosteum at the bone surface –> superficial layers of spongy bone are replaced with compact bone

86
Q

What is hyaline cartilage, and what is it made of?

A

Connective tissue that is made of ECM, electrolyte fluid, and cells (chondroblasts and chondrocytes)

87
Q

What are chondroblasts?

A

On the surface near perichondrium, produce matrix, become embedded in lacunae

88
Q

What are chondrocytes?

A

Found within cartilage, less active. Mature chondroblasts that are trapped.

89
Q

What is the ECM made up of in hyaline cartilage?

A

Large proteogylcans, noncollagenous prpteins, small proteoglycans, collage

90
Q

2 ways cartilage growth occurs

A

Appositional (from surface, chondroblasts) and Interstitial (growth from within, chondrocyte growth)

91
Q

What is appositional cartilage growth?

A

Takes place deep to the perichondrium (outer edge of cartilage), chondroblasts produce matrix at the outer edge of the cartilage, chondroblasts become trapped in lacunae, and become chondtrocytes. As matrix grows, the chondrolbasts are buried beneath the new growth so they are below the surface and become chondrocytes

92
Q

What does appositional cartilage gain?

A

Width

93
Q

What is interstitial cartilage growth?

A

Takes places within the cartilage, chondrocytes divide and produce matrix and are pushed AWAY from each other, increases the total volume of cartilage, growth from within

94
Q

What does interstitial cartilage growth gain?

A

Volume/length

95
Q

Overview of steps in endochondral ossification

A

Mesenchyme condenses, differentiate into chondrocytes. Perichondrium forms periosteum, formation of bone collar, chondrocytes hypertrophy and die. Invasion of blood supply with bone cells, primary ossification center, osteoblasts form bone. Bone remodeling and then lamellar organization with marrow space. Secondary ossification centers form in epiphysis, separated from primary by growth plate

96
Q

What is a growth plate?

A

Location where bone growth occurs (growth in length). Held together by tough fibrous tissue (weak link). Area of bone containing proliferating chondrocytes. Chondrocytes mature and calcify. Calcified cartilage is resorbed and new bone is formed in its place.

97
Q

When does the epiphyseal plate close?

A

Between ages 18-25

98
Q

How does bone growth in width occur?

A

Bone growth via more periosteal apposition than endosteal resorption. Larger increases in boys than in girls.

99
Q

Hormones involved in growth plate proliferation of cartilage?

A

GH, IGF, and androgens

100
Q

Hormones that promote growth plate closure

A

Thyroid hormone and estrogen

101
Q

What does the prognosis of growth plate injuries depend on ?

A

Severity of injury, age of child, bone/growth plate that is injured and type of injury.

102
Q

When do you stop making bone, and when do you start losing it?

A

Stop around 25 and start losing it around 40. ~26% of adult mineral is accrued during the 2 years around peak bone mineral content velocity, which is 11.5-13.5 for girls and 13.1-15.1 for boys

103
Q

What could cause defective bone mineralization?

A

Vit D abnormalities (most common), hypophosphatemia (genetic disorders, aluminum, kidney disease, tumors). Toxcicity (fluoride, chronic etidronate), hypophosphatasia (deficiency in alkaline phosphatase, alkaline phosphatase cleaves pyrophosphtase, pyrophosphtase inhibits mineralization)

104
Q

What is VDDR?

A

Defect in renal tubular 1alpha hydroxylase, so there is an increased circulating level of calcitriol

105
Q

What is PVDR/VDDRII?

A

Defect in intracellular calcitriol receptor, so there is Vitamin D resistance, leads to increased circulating levels of calcitriol

106
Q

Clinical presentation of rickets

A

Muscle weakness, bowing deformity with weight bearing, kyphosis, lordosis –> wassling gait, prominence of costochondral junciton, “rachitic rosary,” indentation of lower ribs (Harrison’s groove), increases incidence of pneumonia/difficulty breathing, diffuse bone pain

107
Q

Role of thyroid hormone in bone

A

Necessary for growth and maturation of the skeleton, controls metabolism. Hyperthyroidism results in increase in osteoclastic bone resorption, which can cause bone loss. Involved in the fusion of the epiphyseal plate.

108
Q

Role of GH in bone

A

Produced by pituitary gland. Stimulates production of IGF-1 by liver, skeleton, and other tissues. Stimulates differentiation and proliferation of chondrocytes –> important for longitudinal growth and bone formation. Increases osteoblast function. Important for muscle growth and metabolism.

109
Q

Categories of steroid hormones

A

Glucocorticoids, mineralcorticoids, gonadal steroids (estrogens, androgens, progesterone)

110
Q

What do estrogens facilitate in bone?

A

The decline in number and rate of chondrocytes proliferating, number and size of hypertrophic chondrocytes, height of growth plate and density of columns of chondrocytes –> cessation of growth in long bones. Help regulate bone formation and bone resorption rates. Levels decrease after menopause. Deficiency increases osteoclastic resorption.

111
Q

What is menopause?

A

Cessation of menstruation. Average age is 52, but can occur between 42-56. A woman has begun her menopause when she hasn’t had a period for a full year. Decrease in ovarian hormone is gradual and starts several years before last period.

112
Q

Estrogen’s effect on osteoclasts

A

Decreases osteoclasts and precursors, decreases RANKL, decreases cytokines that stimulate OC differentiation, recruitment and activity. Increases apoptosis. Essential, decreases the number of them, their activity, and their lifespane

113
Q

Estrogen effect on osteocytes and osteoblasts

A

Decrease apoptosis. Essential increases how long bone can be made for.

114
Q

What happens to calcium metabolism in menopause, which may contribute to bone loss?

A

Decreased intestinal absorption, increased urinary calcium loss (reduced renal absorption)

115
Q

What does a deficiency in androgens or estrogens do to bone?

A

They are both necessary for bone strength, so a deficieny in either one results in osteoporosis. Aromatization of androgens into estrogens is important for skeletal homeostasis…people on aromtase inhibitrs have an increased fracture risk.

116
Q

What is a glucocorticoid (GC), and what is the main one?

A

It is a class of steroid hormones that is distunguished from mineralocorticoids and sex steroids by specific receptors, target cells, and effects. Cortisol is the most important human GC, essential for life.

117
Q

Where is cortisol produced, and what is its role?

A

Produced in the adrenal cortex, receptors are found in cells of almost all tissues, anti-inflammatory and immunosuppressive, important in normal immune and stress repsonse, effects on fetal development, important for maintaining blood glucose levels

118
Q

Pharmacological use of GC

A

Hydrocortisone, prednisone, dexamethasone (some more portent than cortisol). Used to suppress carious allergic, inflammatory (e.g. arthritis) and auto-immine disorders, post-transplantory immunosuppressant to prevent the acute transplant rejection, graft-versus-host disease

119
Q

GC use side effects

A

Muscle breakdown and weakness, decreased bone density and altered bone structure, decreased intestinal Ca2+ absorption, increaed Ca2+ and P loss in urine, decreased gonadal steroid hormone production, anovulation, irregularity of menstrual periods, growth failure, pubertal delay, increased gluconeogensis, insulin resistance and impaired glucose tolerance, increased visceral and trunkcal fat deposition, stim. appetite, increased hepatic glycogen synthesis, excitatory effect on CNS

120
Q

% of people who will develop OP on chronic GC therapy

A

30-50%

121
Q

What impact does chronic GC use have on fracture risk?

A

Fractures at higher BMD than women with bone loss after menopause. Predictor of fracture independent of BMD. GCs may alter bone strength in a way that cannot be measured by BMD. As little as 2.5 mg/day of prednisone increases risk.

122
Q

GC excess effect on osteoclasts

A

Decreases OPG (inhibts osteoclast differentiation) and increases RANKL and survival. Leads to increased bone resoprtion.

123
Q

GC excess effect on osteocytes

A

Increased apoptosis and decreased viability. Leads to decreased bone quality.

124
Q

GC excess effect on osteoblasts

A

Decreased proliferation of precursors (stromal cells), increased apoptosis, decreased IGF synthesis/binding, all of this leads to decreased osteoblast number, and therefore, decreased bone formation

125
Q

When do fractures occur?

A

When applied load (balance and falls, reaction time, shock absorption) is greater than bone strength (structural properties and material properties)

126
Q

What determines bone strength?

A

Structural properties (size/shape/mass, microarchitecture/cortical thickness/porsoity/trabecular thickness, number, separation, microcrack accumulation) and Material properties (minerals (BMD and mineral:matrix), crystal size, collagen (type and cross-links), proteins

127
Q

What can alter bone strength?

A

Chaning bone mass, changing the distrubution of mass in bone (strucutre), changing the material properties of bone

128
Q

What is stiffness?

A

Slope of the stress-strain curve: defines the relationship between applied load and resulting deformation

129
Q

Yield point?

A

Elastic limit or point where damage begins to occure

130
Q

Ultimate load/strength

A

Point at which bone breaks

131
Q

Stess?

A

Force applied or load per unit area

132
Q

Strain?

A

Deformation…percentage change in length

133
Q

KNOW WHAT A STRESS/STRAIN CURVE LOOKS LIKE FOR OSTEOPOROSIS, NORMAL, AND OSTEOMALCIA!

A

sljslfgsofe

134
Q

When is bone strength reduced?

A

When bone becomes brittle: decreases in collagen content and increases in mineralization

135
Q

Why do older people have a higher fracture risk that younger people?

A

Older people have higher mineralization and less collagen, so there bones are brittle. Younger people have lower mineralization and more collage, so there bones are more ductile.

136
Q

Assessment of fracture risk is based on?

A

History or prior fracture, risk factors (GC, aromatase inhibitor, etc), bone density. >65

137
Q

Bone density testing is done to?

A

Predict fracture risk and monitor therapy

138
Q

How does DXA work?

A

Measures amount of X-rays attenuated. Uses attenuation profiles to divide into bone and soft tissue, determine mass. Attenuation profiles of soft tissue pixels can be compared to callibration material to determine fat-free and fat masses

139
Q

Why does there appear to be an increase in BMD in the lumbar spine during aging?

A

Increases due to arthritic changes and bony growth that show up in the DXA machine as bone

140
Q

What happens to bone with aging?

A

Decreased volume, decreased trabecular thickness, decreased trabecular number, and decreased connectivity

141
Q

Where does loss in trabecular structure usually occur?

A

Loss tends to occur in trabecular components that are the least loaded, typically the horizontal struts and plates. May preservie normal strength during normal activity, but a fall to the side may be catastrophic

142
Q

The strength of a vertical vertbrae is inversely proportional to what?

A

Inversely proportional to length squared (shorter = stronger). A loss of a single cross tie will typically affect two trabeculae, increasing their unsupported length

143
Q

In bone, what is a stress riser?

A

Area of resorption that procudes local weakness. Vertical trabeculae slightly bow when loaded. Therefore, when stress risers occur, there is a smaller cross-sectional area to bear load. This leads to an increase in fragility that often precedes appreciable loss in bone mass.

144
Q

Trabecular bone strength is reduced when?

A

The total number of trabeculae to bear load (bone volume) is reduced. Vertical struts become weaker due to thinning, due to perforation of horizontal struts, due to points of weakness created by resoprtion pits or microdamage

145
Q

Axial stiffness?

A

ability to resist being compressed or elongated in response to an axial force

146
Q

How does the distribution of bone impact the long bone strength?

A

The more bone that is distributed away from the central bending axis, the greater the strength. Wider bones can withstand greater loads than skinnier bones.

147
Q

Cross sectional area and distribution of mass from the bending axis and impact on load?

A

The more material there is in the cross-section, the better it will resist applied loads. The farther the material is distributed from the axis of bending, the better it will resist bending. The farther the material is distributed from the central axis, the better it will resist torsion or shear. Essentially, the amount of material and where it is matters for bone strength.

148
Q

What are the age-related changes in long geometry?

A

The distribution of mass is changed. In women there is a greater loss of bone on the inside than is added to the outside. Essentially, there is an increase in cortical porosity

149
Q

Fractures can be

A

open or closed (simple or compound), stable or displaced, fractured along different lines, traumatic or non-traumatic

150
Q

Overview of fracture healing?

A

1) Inflammatory response 2) Endochondral formation (soft callus) 3) Primary bone formation (hard callus) 5) Secondary bone formation (remodeling)

151
Q

What is the inflammatory response in fracture healing?

A

Bleeding, tenderness swelling. Activated platelets release a variety of procuts (fibronectin, platelet derived growth factor, transforming growth factor beta), triggers influx of inflammatory cells. Cytokine cascade brings cells needed for repair (fibroblasts, endothelial cells, and osteoblasts) into the fracture gap

152
Q

Endochondral formation in fracture healing?

A

Characterized by the formation of connective tissues, including cartilage, and formation of new capillaries from pre-existing vessels (angiogenesis). Mesenchymal stem cell recuitment, skeletal cell differentiation, formation of cartilage and bone

153
Q

What is primary bone formation in fracture healing? Secondary bone formation?

A

Starts within a week or two. Osteoblasts can form woven bone rapidly to bridge fracture. Secondary bone formation is when woven bone is remodeled into stronger, lamellar bone. Remodeled back to normal shape (restore anatomical structure and support loads). Collagen re-orients along lines of stress. Continues for many months to a few years in adults.

154
Q

Things that form insoluble complezes with Ca2+?

A

Phytates in high fibre foods (cereal, seeds). Oxalates in spinach, rhubarb, walnuts. Tannins (tea)

155
Q

Dietary factors that may increase Ca2+ excretion

A

excess protein, excess sodium, excess sulfate and chloride, excess caffeine

156
Q

High bioavailable sources of calcium

A

Low-oxalate greens (bok choy, broccoli, Chinese cabbage, collards and kale…50-60%). Fortified fruit juice (calcium citrate malate…40-50%)

157
Q

Good calcium bioavilable foods

A

calcium-set tofu, cow’s milk, soy milk (30-35%)

158
Q

Lower bioavailable Ca2+ foods

A

sesame seeds, almonds, and dried beans (21-27%)

159
Q

KNOW THE PLAN FOR SHEENA AND HOW YOU WOULD IMPLEMENT IT!!

A

Read over notes

160
Q

What is osteoporosis according NIH definition?

A

A skeletal disorder characterized by compromised bone strength predisposing a person to an increased risk fracture. Bone strength reflects the integration of 2 main features: bone density and bone quality

161
Q

What is a fragility fracture?

A

WHO definition: a fracture caused by injury that would be insufficient to fracture normal bone: the result of reduced compressive and/or torsional strength of bone. Clinically: a fracture that is a result of minimal trauma or no identifiable trauma (bending forward, fall from standing height, hug, being turned in a bed, transfer)

162
Q

3 primary causes of steoporosis

A

1) Postomenopusal osteoporsis. Bone loss of 3-5% per year in frist five years. 1% year after 2) Age-associated osteoporsis. Slow loss of bone due to increased bone turnover, or unbalanced resorption with age 3) Idiopathic unknown cause can affect men and women of all ages

163
Q

Secondary causes of osteoporsis?

A

Medications, hereditary smkeletal/connective tissue disease, endocrine or metabolic disorders, chronic kidney, GI or lung disease, blood or bone marrow disorders, spinal cord injury, breast and other cancers, multiple sclerossis (GC use and immbobility)

164
Q

Risk factors for osteoporosis in men

A

advancing age, smoking (current or former), low weight and weight loss, physical/functional limitations, history of fracture after age 50

165
Q

Common fracture sites in osteoporosis

A

Distal radius (most common type in women <75 yrs), vertebal (usually undiagnosed unless pain or height loss), hip fracture (mortality = 20%, recover health and mobility = 50%)

166
Q

Types of vertebral fractures?

A

Wedge, biconcave, crush fracture

167
Q

Types of hip fracture

A

Femoral neck or intracapsular, intertrochanteric, subtrochanteric

168
Q

What is a T-score in osteoporosis?

A

Number of standard deviations from the mean value of a 25 year old woman

169
Q

T-score for a normal BMD

A

+2.5 to -1.0 inclusive

170
Q

T-score for an osteopenia BMD

A

Between -1.0 and -2.5

171
Q

T-score for an osteoporosis BMD

A

< -2.5

172
Q

T-score for a sever osteoporosis diagnosis

A

< -2.5 + a fragility fracture

173
Q

What are two tools that are currently available for assessing fracture risk?

A

CAROC 10 yr fracture and WHO FRAX

174
Q

In what population does FRAX underestimate fracture risk?

A

FRAX underestimates fracture risk in diabetic patients (more so in Type I than Type II)

175
Q

What are some possible mechanisms behind increased fracture risk in diabetic patients?

A

Increased fall risk/load on bone (neuropathy, visual impairment (diabetic neuropoathy), cognitive impairment, sarcopenia, orthostatic hypotension and hypoglycemia). Affects on bone structural or material properties (accumulation of advanced glycation end products, TZDs)

176
Q

What does FRAX not assess?

A

Does not include fall risk or alter the risk profile with multiple fractures or therapy

177
Q

Consequences of a hip fracture?

A

25% died within one year of hip fracture, 24% of surivors were institutionalized, 40% mortality for those living in LTCFs, 5% had another hip fracture in follow-up year, 50% survivors dependent on assistive aids

178
Q

Consequence of hip fracture in older adults

A

immobility, bed rest, pressure ulcers, infection (MRSA), cardiac and pulmonary complications, delirium (decreased awareness and confusion), impaired ADLS and IADLS, dependence on walking aids

179
Q

Physical consequences on spine fractures

A

height loss, wall0occuput distance, rib-pelvis distance

180
Q

What is hyperkyphosis? What causes it? What are the consequences?

A

An exaggerated anterior curvature of the thoracic spine. Weak extensors, discdengeneration, and fracture cause it. Consequences include impaired mobility, increased risk of vertebral fractures, increased risk of falls, more likely to die

181
Q

Clinical consequences of vertebral fractures and hyperkyphosis

A

Height loss, upright posture becomes impossible, pulmonary volume loss, 1 thoracic vertebral fracture = 9% loss of forced vital capacity –> 2-3 x more likely to die of pulmonary causes. Protruding abdomen –> distension constipation , early satiety, eructation, reflux. Acute and chronic pain

182
Q

What is the most common fracture that occurs as a result of osteoporosis?

A

Vertebral fractures (mostly at T7 and T8 and T10 - L1)

183
Q

Postural adaptations with vertebral compression fractures

A

Knees bend, pelvis tilts forward to counteract forward bending, change in balance, decrease in gait velocity, increased muscle fatigue, increased risk of fall and additional fractures

184
Q

How does posture affect spine loads?

A

Weak muscle strength or endurnace –> less able to produce extensor moment for upright posture. Flexed posture lengthens extensor muscles –> decreases force generating capacity. Lever arms of extensors are smaller in flexed –> larger forces required, therefore, higher compressive forces. Flexed posture shifts line of gravity further forward, requiring larger forces to stablize the spine.

185
Q

What is the cycle of vertebral fractures?

A

Compression fracture –> hyperkyphosis –> lines of gravity shift forward –> increased compression on vertebra

186
Q

What is RANK-L and what does it do?

A

It is a cytokine that is expressed by osteoblast precursors. RANK-L binds to RANK receptor on pre-osteoclast, resulting in osteoclast development

187
Q

What is the difference between bone modeling and remodeling?

A

Bone modeling is when osteoblasts add bone in one spot and osteoclasts remove bone in another spot. THe shape of the bone changes and it is only DURING GROWTH. Bone remodeling is when osteoclasts remove bone first, forming a cavity, then osteoblasts fill in the cavity. Allows for the replacement of old bone with new bone, and sometimes results in bone loss or gain. Happen throughout the LIFETIME

188
Q

What are the laboratory findings in osteomalacia?

A

Hypocalcemia or normal serum calcium (can’t mineralize bone), hypophosphatemia or normal. Elevated PTH (increaesed bone turnover), elevated alkaline phosphatase (marker of mineralization), low serum 25 (OH) D is due to deficiency

189
Q

What does Wolf’s law mean?

A

The form of bone reflects its function

190
Q

What are the assumptions of the mechanostat theory (Frost) that make it not 100% correct?

A

It assumes bone only responds to strain magnitude not the type of loading or the rate or that men and women respond differently and different bones respond differently. Age also affects this.

191
Q

What is the theoretical explanation for how loads can cause signal transduction in osteocytes?

A

Mechanical load deforms bone matrix, fluid around osteocytes is perturbed, causing sheer stress –> mechanotransduction. Bone deformation could perturb cell membrane (cell body or dendritic processes) –> mechanotransduction

192
Q

Steps in Wnt/Beta-catenin signaling?

A

Wnt binds to frizzled and LRP5 and controls osteoblast differentiation–required for bone formation. Beta-catenin increases OPG expression.

193
Q

What is SOST, and what cells express it?

A

It is a gene that encodes for sclerostin. Scelostin controls Wnt/B catenin signaling and increased sclerostin inhibits Wnt/B catenin signaling

194
Q

What is the relationship between mechanical loading and Wnt?

A

Mechanical loading down-regulates sclerostin expression therefore increasing Wnt/B catenin signaling. Osteocytes need loading to surve. Disuse or unloading results in reduced Wnt/Beta catenin signaling. If there is no LRP5 receptor, bones do no respond to increased mechanical loading

195
Q

Mechanical loading characteristca that are good for bone?

A

Animal studies show that the magnitude of the loading, loading frequency (cycles/sec), strain rate (rate of change of deformation), dynamic loading, short duration of loading

196
Q

What is the impact of exercise on BMD in growth?

A

Physical activity during growth increased BMD 1-6% with weight-bearing exercise before puberty, 0.3-2% in adolescence. Initiated before puberty, variable patterns, higher impact, short frequent bouts. Transition from childhood to adolescence is critical period for bone mineral accrual

197
Q

Results from the calcium vs. loading during growth

A

Calcium alone had no effect on BMC. Exercise alone increased the size of the bone, but there was no difference in content. Exercise plus calcium led to an increase in size and content. Strength advantage from greater bone circumference not apparent with DXA.

198
Q

Impact of exercise on aBMD in premenopausal women

A

High intensity progressive RT increased lumbar spine aBMD. High-impact training results in increased femoral neck aBMD. Breif, high impact exercise or jumping may increase FN aBMD, but not spine BMD.

199
Q

Effects of exercise on aBMD in postmenopausal women

A

Small, NS effect with variability. Effect may vary by activity: high force dynamic = hip aBMD +1.55%, no effect LS. Low force dynamic: LS aBMD +0.87%, no effect on hip. Progressive RT: LS aBMD +0.86%, FN aBMD +1.03%. Low weights had no effect on aBMD. Combination programs (+3.22)

200
Q

What is the impact of exercise on bone structure in postmenopausal women?

A

Site specific changes, increased cortical area and diameter, increased cortical BMD and trabecular BMD

201
Q

What interventions in the cochrane review showed to have an positive effect on rate of falls and risk of falling?

A

multiple component group or home based exercise, Tai-Chi, home safety assessment and modification interventions –> best when delivered by an OT

202
Q

When setting goals or prescribing exercise, what key things should a health care provider ask, observe, screen for, or assess?

A

1) Medical history, comorbities, exercise contraindications 2) Fracture risk FRAX or CAROC or assessment of risk factors 3) Fall risk acute falle >2 falls in past 12 months, gait/balance difficulties 4) Physical performance impairment or pain during movements 5) Standing posture look for hyperkyphosis hyperlordosis or hypolordosis 6) Barriers and facilitators to physical activity (e.g. current physical activity, self-efficacy, time, pain, access, preferences

203
Q

What therapeutic goals should be targeted in individuals with osteoporosis?

A

Prevent fractures via: 1) fall prevention: improve dynamic balance, mobility, muscle strength, posture 2) Safe movement or spine sparing strategies (attention to posture during movements to protect the spine, train back extensor muscles to improve endurance, stretch muscles restricting optimal posture 3) prevention of further bone loss (exercise may not have a certain effect on bone mineral density, muscle strengthening and weight-bearing dynamic exercise)

204
Q

GRADE recommendations for exercise in osteoporosis

A

A multicomponent exercise program that includes RT in combination with balance training. Do not engage in aerobic training to the exclusion of resistance or balance training.

205
Q

Exercise recommendations for people with history of spine fracture

A

Focus on good alignment and fall prevention rather than intensity. Choose position with least spine load: lying on back < standing < sitting. Consult a BoneFit trained instructor. If a consultation with a BoneFit trained instructor is not possbile, may want to use resistance bands or body weights as resistance

206
Q

Some examples of balance training

A

Redue BOS in static stance, shift weight or moving to limit stability, dynamic balance exercises, three dimensional movements

207
Q

KNOW HER PAPER!!

A

ALL OF IT.

Fall 2014 (3 decks)

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