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MSS > 9: Intro to Bone > Flashcards

9: Intro to Bone Flashcards

1
Q

Osteoblasts are derived from:

A

mesenchymal stem cells, which also give rise to

fibroblasts, chondrobasts/cytes, and adipocytes.

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2
Q

Function of Osteoblasts

A

Their function is to synthesize the
organic components of the bone matrix. Mineralization appears to be a passive process that does not require cellular activity once mature matrix is present.

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3
Q

Osteoblast are commited to their lineage via expression of which to TFs

A

RUNX2 (Cbfa1) and osterix (SP7).

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4
Q

In the Alizarin red/alcian blue prep… what do we expect to see if the RUNX2 is missing

A

all blue.. no formation of bone
cartilage = blue
calcified stuff = red

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5
Q

Osteoblasts have two fates:

A

osteoblasts either undergo apoptosis or are embedded within newly secreted
matrix, and undergo terminal differentiation to osteocytes.

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6
Q

Cells in bones responsible for mechanotransduction in bone.

A

Osteocytes
Important mechanotransductive
functions rely on the primary cilium, and mechanotransduction at the tissue level
depends on intercellular communications via gap junctions.

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7
Q

Helpful stains for osteocytes

A

dental matrix protein 1 (DMP1) and sclerostin

(SOST) are useful histochemical stains for osteocytes.

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8
Q

origin of Osteoclasts (what are they structually related to?)

A

Osteoclasts are of hematopoietic origin and are closely related to macrophages in
lineage, structure, and function.

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9
Q

Terminal differentiation of osteoclasts requires

combinatorial signaling of both

A

M-CSF and RANKL

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10
Q

What makes RANK ligand?

A

osteoblasts.

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11
Q

What does osteoblasts make as a soluble decoy receptor for RANKL?

A

osteoprotegerin (OPG),

RANKL that binds to OPG is not able to bind RANK, and so high OPG levels inhibit terminal osteoclast differentiation.

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12
Q

What stimulates osteoclast activity

A

PTH and 1, 25 di-OH-D

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13
Q

What inhibits osteoclast activity

A

CAlcitonin

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14
Q

multinucleated giant cells that bind tightly to the bone surface via
the sealing zone to enclose a compartment in which bone matrix can be degraded.

A

Osteoclasts

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15
Q

multinucleated giant cells that bind tightly to the bone surface via the sealing zone to enclose a compartment in which bone matrix can be degraded.

A

Mature osteoclasts

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16
Q

What two things do osteoclasts secreate to

  1. Degrade mineral
  2. Degrade bony matrix
A

Within this compartment, osteoclasts secrete HCl to dissolve the mineral and cathepsin
K to degrade the bone matrix proteins.

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17
Q

STain to see osteoclasts

A

tartrate resistant acid phosphatase (TRAP)

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18
Q

makes up ~80-85% of the total bone. Its function is primarily structural, providing protection for organs and levers used for movement.

A

Cortical bone

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19
Q

Organization of Cortical Bone

A

osteons (also called Haversian systems), cylindrical structures in which concentric layers of bone matrix form lamellae around a central canal.

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20
Q

What about cortical bone lends its resistance to fracture

A

The lamellar organization of osteons

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21
Q

_____ of cortical bone is calficied

A

80-90%

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22
Q

What part of bone is always on outside of bone and surrounds trabecular bone?

A

Cortical Bone

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23
Q

What % of trabecular bone is calcified

A

15-25

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24
Q

Function of trabecular bone

A

metabolic

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25
Q

Accounts for most of the bone surface area and most of the remodeling activity. The large surface area is necessary to allow for mineral homeostasis.

A

Trabecular bone

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26
Q

How is trabecular organization similar and different from cortical bone?

A

trabecular bone is normally organized in a lamellar fashion, but the individual trabeculae are too small to contain osteons.

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27
Q

When do osteocytes make sclerosin and why

A

Make is when bone is mechanically loaded… goes to osteoblast to inhibit maturation. When mechanical loading is gone, remove repression

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28
Q

formed by formation of osteoblasts from mesenchymal stem cells present within what will become the periosteum.

A

Intramembranous bone

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29
Q

What bones are intramembranous

A

Examples of bones that are intramembranous in origin include many bones of the skull and the ribs.

30
Q

What type of bone is formed at the bone collar of a healing frx. ?

A

Intramembranous bone

31
Q

How do long bones remodel to increase in diameter?

A

Via intramembranous bone at the periosteal surface of long bones

32
Q

bones replace previously formed cartilage models

A

Endochondral

33
Q

How do Endochondral bones grow?

A

grow in length by proliferation of chondrocytes within the growth plate, a specialized structure present within growing endochondral bones. Linear growth ceases when the growth plates fuse.

34
Q

Examples of endrochondral bones

A

the long bones of the limbs.

35
Q

highly organized tissue in which chondrocytes are arrayed in columns, with different positions within the column occupied by cells at a distinct point of maturation.

A

The growth plate

36
Q

How do chondrocytes grow during growth phase

A

is a Chondrocytes in the proliferative zone divide, replenishing the growth plate. The chondrocytes then hypertrophy, undergo apoptosis, and are mineralized. Blood vessels invade the zone of calcified cartilage, which is resorbed by chondroclasts and the space is filled by osteoblasts and bone matrix.

37
Q

Linear growth of the long bones

depends on

A

the relative speed with which cells in the hypertrophic zone undergo apoptosis and those in the proliferative zone divide.

38
Q

In humans, the growth plates close in late adolescence in response to

A

estrogen signaling.

39
Q

Which has more active remodeling: cortical or trabecular

A

At any given time, about 10%
of the skeleton is being remodeled. Trabecular bone is much more actively remodeled than cortical bone. This makes sense in light of its more prominent role in maintaining mineral homeostasis.

40
Q

2 key principles in bone remodeling

A

First, bone resorption and bone formation are coupled processes.
Second, bone resorption is relatively rapid, requiring ~2 weeks, while bone formation is slow, requiring
4-6 months for full mineralization to take place.

41
Q

Method of measuring bone remodel?

A

Tetracycline labeling

42
Q

Bone’s role in moment-moment homeostasis

A

The amount of Ca exchanged by trabecular bone each day is approximately twice the amount that is
absorbed from food or lost in urine each day. This active exchange of minerals between the bone and the circulation is essential for moment-to-moment mineral
homeostasis.

43
Q

Bones do not only grow in length, but grow in radial size and change shape as well: this is called

A 
Bone modeling
(dt mechanical loading)
44
Q

At the level of the whole bone, ________is the primary stimulus to modeling

A

strain (fractional change in length)

45
Q

At the level of the cell, ________, requiring both anchoring of osteocytes by focal adhesion complexes and fluid flow sensed by each cell’s primary
cilium appear to be the critical stimulus.

A

shear stress

46
Q

How do bones direct their growth at the appropriate site?

A

The connections among the osteocytes via
their processes allow integration of the response across cells, allowing new bone
growth to be directed to the sites experiencing the greatest strain.

47
Q

_____forms at the fracture site, which becomes organized as a consequence of
the inflammatory process.

A

hematoma

48
Q

After hematoma formation… mesenchymal stem cells are present and become chondrocytes so they can:

A

form a cartilaginous soft callus.

49
Q

How does a hard callus form

A

Blood vessels invade the soft callus and bone replaces cartilage in a process very similar to that seen in the growth plate, forming a hard callus.

50
Q

Durning hard callus formation… what goes on with the osteoblasts

A

osteoblasts on the subperiosteal surface form an intramembranous bone collar.

51
Q

The hard callus is much bigger at first then what it ends up being… how does that happen

A

callus undergoes remodeling to form lamellar bone and modeling

52
Q

How long does it take to heal a fracture

A

Time required is ~8-12 weeks, though the final remodeling and mineralization may take considerably longer.

53
Q

bone, compressive strength comes from the

A

mineral phase (about 2/3 of the bone extracellular matrix by mass),

54
Q

Bone tensile strength comes from the

A

protein and water (about 1/3 of the bone extracellular matrix by mass).

55
Q

Primary protein compoment of bone’s ECM

A

type 1 collagen. This is a large triple helical protein that self-assembles into fibrils with an offset of ~1/4 the
molecule length, leading to a regular striped appearance on electron microscopy, with a periodicity of ~6.7 nM.

56
Q

Assembly of toropcollagen into fibers provides

A

tensile strength: more x-linking = stronger

57
Q

IN type I collagen: mature aromatic cross-links have higher bond energy than the aliphatic cross-links, thus:.

A

and are therefore harder to break

58
Q

Collagen:
packs tight or loose
forms covalent bonds, non-covalent bonds
formation depends on which Vitamin

A

Tight
covalent
Vit C dependent

59
Q

______ structure of the individual collagen molecules allows them to be stretched, for tensile strength

A

Helical

60
Q

Cracks in bone have outcomes based on cement lines and toughness:
Which cracks propagate ealisly

A

ones along longitudinal lines

Transverse cracks are less able to propagate

61
Q

Most abundant minerals in bone

A

Ca and PO4 are the most abundant ions in bone mineral, but significant amounts of Mg,
Na, OH, CO3, SO4, and Cl are also present

62
Q

Disease of OsteoBlasts resulting in bones that easily frx

A

Osteogenesis Imperfecta

63
Q

What is the pathology of osteogeneis imperfecta

A

Type I col defect, either synthesis or assembly. See bent fibrils, see bowing of legs

64
Q

inadequate mineralization of the bone matrix and can be a consequence of several different conditions, including various malabsorptive disorders, vitamin D deficiency or resistance, phosphate wasting disorders, or even low Ca diet.

A

Cause Osteomalacia

65
Q

Osteomalacia causes what type of bones

A

weak, undermineralized bones

66
Q

What happens in growing individual gets osteomalacia

A

bone modeling is abnormal and the long bones assume a bowed shape. This is called rickets. –not dt abnormal cellular funx but lack of appropriate substrates

67
Q

disorders in which the skeletal mass is

abnormally high, due to mutations of the protein sclerostin.

A

Sclerosteosis and Van Buchem’s disease

68
Q

Pathology of Sclerosteosis

A

Lack of sclerostin the mechanosensory system, resulting in bones perceiving that they are being loaded even
when they are not. These can be thought of as osteocyte diseases.

69
Q

group of diseases in which osteoclast function or maturation is impaired. As a result, remodeling is deficient.

A

Osteopetrosis

70
Q

disorder characterized by focally excessive and

disorganized bone remodeling.

A

Pagets

71
Q

see presenence of woven bone and increased serum alkaline phosphatase and urinarly hydroporline increase

A

Pagets

72
Q

Pagets increases disposition to

A

osteosarcoma

MSS (26 decks)

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