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Oral Sciences > 2/27 Reading > Flashcards

2/27 Reading Flashcards

1
Q

Fxn of osteocytes:

A

mechanosensors, control remodelling

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2
Q

remodelling is controlled by:

A

local factors: growth factors, cytokines, systemic: calcitonin, strogen

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3
Q

These are coupled:

A

bone resorption and formation

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4
Q

Osteocyte apoptosis is followed by:

A

bone resorption (clasts)

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5
Q

TF? Bone cells can communicate w other organs.

A

T. and vice versa

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6
Q

4 types of cells of mineralized CT of bone:

A

blasts, clasts, cytes, and bone lining cells,

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7
Q

Fxns of bone:

A

locomotion, support, protection of soft tissue, ca and P storage, bone marrow storage, bone endocrine functions (able to effect other organs)

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8
Q

Fxn of bone lining cells:

A

resorption-formation coupling (possibly)

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9
Q

3 phases of remodeling:

A

resorption initiation, transition (reversal period) from resorption to formation, formation

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10
Q

Components of the basic multicellular unit:

A

blasts, clasts, cytes, and bone lining cells,

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11
Q

This structure is required for formation:

A

BMU

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12
Q

TF? BMU is a permanent anatomical structure.

A

F. temp

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13
Q

remodeling is needed for:

A

fracture healing, skeletal adaptation to mechanic use, calcium homeostsis

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14
Q

Excessive clast fxn leads to:

A

osteoporosis

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15
Q

Excessive blast fxn leads to:

A

osteopetrosis

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16
Q

bone homeostasis depends on:

A

local/ systemic factors, hormones, cytokines, chemokines, and biochemical stimulation

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17
Q

Shape of blasts:

A

cuboidal

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18
Q

% of bone occupied by blasts:

A

4-6%

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19
Q

Location of blasts:

A

bone surface

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20
Q

Morphological characteristics of blasts:

A

lots of RER and prominent golgi, many secretory vesicles

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21
Q

How are blasts polarized?

A

secrete osteoid toward bone matrix,

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22
Q

Blasts are derived from:

A

mesenchymal stem cells

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23
Q

What is req for mesenchymal stem cells to commit to differentiate to the osteoprogenitor lineage?

A

expression of sp genes, then timely programmed steps, synthesis of bone morphogenic protein (BMP) and members of the Wingless (Wnt) pwy

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24
Q

Expression of these is crucial for osteoblast differentiation:

A

Runt-reltated TF2, Distal-less homeobox5(Dlx5), osterix (Osx), Runx2

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25
Q

A master gene of osteoblast differentiation

A

Runx2

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26
Q

Runx2-null mice:

A

no blasts

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27
Q

Runx2 upregulates these genes:

A

ColIAI, ALP, BSP, BGLAP, OCN

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28
Q

Proliferation phase begins when:

A

a pool of blast progenitors expressing Runx2 and ColIAI has been established

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29
Q

What type of activity do blast progenitors show in proliferative phase?

A

alkaline phosphatase activity

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30
Q

blast progenitors are considered:

A

preosteoblasts

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31
Q

Transition from preosteoblasts to blasts is characterized by:

A

inc expression of Psx, secretion of bone matrix proteins like osteocalcin (OCN), bone sialoprotein (BSP) I/II and Type I collagen, cells become large, cuboidal

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32
Q

Other factors involved in blast differentiation:

A

FGF, microRNAs, connexon 43

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33
Q

FGF2-knockout mice:

A

dec bone mass coupled to inc of adipocytes in BM, indicating role in blast differentiation

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34
Q

Mechanism by which FGF-18 upregulates blast differentiation:

A

autocrine mechanism

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35
Q

Fxn of microRNAs:

A

regulate gene expression, some inc, some dec blast differentiation

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36
Q

The main connexin in bone:

A

Connexin 43

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37
Q

Mutation of gene encoding Connexin 43:

A

impaired blast differentiation, skeletal malformation

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38
Q

2 main steps to bone matrix synthesis:

A

deposition of organic matrix, mineralization

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39
Q

1st step of bone matrix synthesis:

A

blasts secrete collagen proteins, mainly type 1 collagen, non collagen proteins (OCN, osteonectin, BCP II, osteopontin) and proteoglycans including decorin and biglycan (all make organic matrix)

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40
Q

2 phases, organic matrix mineralization:

A

vesicular phase, fibrillar phase

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41
Q

When does vesicular phase occur:

A

portions of matrix vesicles released from apical membrane domain of blasts into new bone matrix

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42
Q

matrix vesicles released from apical membrane domain of blasts binds:

A

proteoglycans and other organic componenets

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43
Q

Charge of sulfated proteoglycans:

A

negative

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44
Q

Fxn of binding of matrix vesicles to sulfated proteoglycans:

A

immobilization of ca stored in matrix vesicles

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45
Q

When is ca released from proteoglycans and cross channels in matrix vesicle membrane?

A

When blasts secrete enzymes that degrade the proteoglycans

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46
Q

Ca channels in the matrix vesicle membrane are made by:

A

annexins

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47
Q

Compounds that are degraded by the ALP, secreted by osteoblasts:

A

phosphates

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48
Q

Cell that secretes ALP:

A

blasts

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49
Q

These are both required for HA formation :

A

ALP to release P, release of enzymes that degrade proteins from blasts (Ca release)

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50
Q

Where is HA formed?

A

In matrix vesicle

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51
Q

When does fibrillar phase occur:

A

when supersaturation of Ca and P inside the matrix vesicles leads to rupture, HA spreads to surrounding matrix

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52
Q

How many layers is the blast front?

A

1 layer

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53
Q

TF? Blasts have cytoplasmic process.

A

T. some, reach toward bone matrix and cyte processes

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54
Q

What happens to mature blasts in the fibrillar phase?

A

either undergo apoptosis or bc osteocyte or bone lining cell

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55
Q

These can be found inside the blast vacuoles:

A

round/ ovoid structures containing dense bodies –> blasts can phagocytose, engulf, and degrade apoptotic bodies during alveolar bone formation

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56
Q

Quiescent cells of the bone:

A

bone lining cells

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57
Q

Shape of bone lining cells:

A

flat shaped osteoblasts

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58
Q

Location of bone lining cells:

A

bone surfaces where neither resorption or formation is occurring

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59
Q

TF? Bone lining cells contain the same amt of rough RER and Golgi as blasts.

A

F. fewer

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60
Q

Processes of bone lining cells can extend to here:

A

into canaliculi

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61
Q

What hold bone lining cells and osteocytes together?

A

Gap junctions

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62
Q

What does the secretory activity of bone lining cells depend upon?

A

bone physiological status, can regain blast morphology and start secreting

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63
Q

Fxn, bone lining cells:

A

prevent direct interaction bw blasts and bone matrix, when bone resorption should not occur, participate in clast differentiation, producing osteoprotegerin (OPG) and the receptor activator of nuclear factor kappa-B ligand (RANKL)

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64
Q

% of total bone cells occupied by cytes:

A

90-95%

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65
Q

Life span of cytes:

A

up to 25y

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66
Q

Location of cytes:

A

within lacunae surrounded by mineralized bone matrix

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67
Q

Morphology of cytes:

A

dendritic

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68
Q

How does the morphology of cytes differ?

A

with the different types of bone

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69
Q

Osteocytes of trabecular bone:

A

more rounded than cytes of cortical bone (elongated)

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70
Q

Cytes are derived from:

A

MSC’s, through blast differentiation

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71
Q

Are cytes formed through blast or clast differentiation?

A

blast

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72
Q

4 stages of cyte differentiation:

A

osteoid–cyte, preosteocyte, young -cyte, and mature -cyte

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73
Q

What happens at the end of a formation cycle?

A

subpop of blasts bc cytes incorporated into bone matrix, morphological change, ultrastructural change, reduction in blast size, organelles dec, N/C ratio inc, dec in protein synthesis and secretion

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74
Q

Effect of dec protein synthesis and secretion on the N/C ratio:

A

increases

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75
Q

protein E1/gp38 is aka:

A

podoplanin

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76
Q

Fxn of protein E1/gp38 (podoplanin):

A

cyte cytoplasmic process development, highly expressed in embedding or recently embedded cytes

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77
Q

Cells w dendritic morphology:

A

cytes, podocytes, Type II alveolar lung cells, cells of choroid plexus

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78
Q

How might E11/gp38 regulate actin cytoskeleton dynamics?

A

use GTPase activity to interact w cytoskeletal components and molecules involved in cell motility

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79
Q

Inhibition of E11/gp38 expression in cytes-like MLO-Y4 cells:

A

block dendritic elongation (podoplanin might be involved in dendrite formation in cytes)

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80
Q

Mature cyte stage:

A

totally entrapped in mineralized bone matrix

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81
Q

These are downregulated once the mature cyte stage has been reached:

A

OCN, BDPII, collagen Type I, ALP

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82
Q

These are highly expressed once the mature cyte stage has been reached:

A

osteocyte markers: dentine matrix protein 1 (DMP1), sclerostin

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83
Q

Location of cyte cell body:

A

lacuna

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84
Q

Location of cytoplasmic processes of cytes

A

cross tiny tunnels, canaliculi, forming the osteocyte lacunocanalicular system

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85
Q

How are the cytoplasmic process of cytes connected to each other?

A

gap junctions

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86
Q

Cytoplasmic processes of cytes connect to what other cell types?

A

cytes, blasts, bone lining cells

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87
Q

Fxn of lacunocanalicular system:

A

intercellular transport of small signalling molecules: prostaglandins, NO, oxygen and nutrient delivery to osteocytes due to close proximity of processes to vasculature

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88
Q

How does the sa of the osteocyte compare to that of the Haversian and Volkmann system?

A

osteocyte surface 400X larger

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89
Q

How many times larger is the osteocyte sa than the trabecular bone surface?

A

100X

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90
Q

Besides Gap junctions, how is cell-cell communication achieved?

A

by interstitial fluid bw cyte processes and canaliculi

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91
Q

This allows for cytes to acts as mechanosensors:

A

lacunocanalicular system

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92
Q

lacunocanalicular system can sense:

A

mechanical pressure and loads

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93
Q

Fxn of mechanosensor ability of lacunocanalicular system

A

bone adaptation to daily forces

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94
Q

How do cytes seem to be the orchestrators of remodeling?

A

Via the lacunocanalicular system, mechanosensor function

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95
Q

This is a chemotactic signal to clastic resorption:

A

cyte apoptosis

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96
Q

What happens to apoptotic cytes during resorption?

A

engulfed by clasts

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97
Q

How is the mechanosensory function of the lacunocanalicular system achieved?

A

strategic location of cytes in bone matrix, shape and spatial arrangement in agreement w their sensing and signalling transport functions

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98
Q

Define piezoelectric effect:

A

mechanical into biochemical signals (mechanosensory fxn of lacunocanalicular system)

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99
Q

2 proposed mechs for the piezoelectric effect:

A
  1. protein complex formed by cilium and its assoc proteins PolyCysitns 1 and 2, crucial for cyte mechanosensing and blast/cytes-mediated formation 2. cyte cytoskeleton components (focal adhesion protein complex and its multiple actin-assoc proteins such as paxillin, vinculin, talin, and zyxin) stimulation –> cytes make several 2’ msgs (ATP, NO, Ca, prostaglandins (PGE2, PGI2) –> influence bone physiology
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100
Q

Mechanosensory function would not be possible wo:

A

canalicular network

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101
Q

Terminally differentiated multinucleated cells:

A

clasts

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102
Q

Clasts originate from:

A

mononuclear cells, hematopoietic stem cell line

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103
Q

Factors that lead to the differentiation of hematopoietic stem cells to clasts:

A

mac-CSF, RANK ligand

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104
Q

M-CSF is secreted by:

A

osteoprogenitor mesenchymal cells and blasts

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105
Q

RANK ligand is secreted by:

A

blasts, cytes, and stromal cells

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106
Q

mac-CSF and RANK ligand together lead to:

A

activation of TF and gene expression in clasts

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107
Q

M-CSF receptor:

A

cFMS

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108
Q

Where is the M-CSF ligand located?

A

in clast precursors

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109
Q

Fxn of M-CSF binding cFMS:

A

inc proliferation of clast precursors, inhibit clast precursor apoptosis

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110
Q

This is crucial for osteoclastogenesis:

A

RANKL

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111
Q

Cell that expresses RANKL:

A

balsts, stromal cells, cytes

112
Q

Where is the receptor for RANK?

A

clast precursors

113
Q

Function of RANKL and RANK binding:

A

induction of clast formation

114
Q

Cells that produce osteoprotegrin (OPG):

A

blasts, stromal cells, gingival and periodontal fibroblasts

115
Q

OPG binds:

A

RANKL

116
Q

Function of OPG binding RANKL:

A

inhibition of osteoclastogenesis due to blocking RANK/ RANKL interaction

117
Q

RANK/ RANKL/ OPG system is a key mediator of:

A

osteoclastogenesis

118
Q

RANK/ RANKL interactions promotes the expression of these osteogenic factors:

A

NFATc1, DC-STAMP

119
Q

Fxn of NFATc1:

A

regulate clast specific genes that are crucial for clast activity by interacting w TFs, induces expression of Dc-STAMP

120
Q

TF”s w which NFATc1 interacts to regulate clast activity:

A

PU.1, cFos, MITF

121
Q

Osteoclast specific genes regulated by interaction of NFATc1 w TFs:

A

TRAP, cathepsin K

122
Q

How does NFATc1 induce expression of Dc-STAMP?

A

under the influence of the RANKL/RANK interaction

123
Q

What is Dc-STAMP needed for?

A

fusion of clast precursors

124
Q

How might osteoclastogenic potential differ?

A

depending on bone site

125
Q

TF? Clasts from long bone marrow are formed slower than in jaw.

A

F. faster

126
Q

This may be responsible for the different dynamic of osteoclastogenic potential:

A

cellular composition of the bone-site specific marrow

127
Q

When do clasts polarize?

A

during remodeling

128
Q

How many clast membrane domains are visible during remodeling?

A

4: sealing zone, ruffled border, basolateral and functional secretory domains

129
Q

Clast membrane domains in contact with the bone matrix:

A

sealing zone, ruffled border

130
Q

Clast membrane domains not in contact with the bone matrix:

A

basolateral and functional secretory domains

131
Q

What does polarization of clasts during resorption involve?

A

rearrangement of the actin cytoskeleton

132
Q

What is formed in the cytoskeleton of clasts during remodeling for resorption?

A

F-actin ring, isolation of portion of membrane that develop into the ruffled border

133
Q

What is the F-actin ring?

A

dense continuous zone of highly dynamic podosomes

134
Q

When are the clast membrane domains formed?

A

only when clasts are in contact w extracellular mineralized matrix

135
Q

Fxn of avB3-integrin and CD44:

A

attachment of clast podosomes to bone

136
Q

This is a membrane domain formed by microvilli, isolated by surrounding clear zone

A

ruffled border

137
Q

Cleas zone is aka:

A

sealing zone

138
Q

What is the clear zone devoid of?

A

organelles

139
Q

Location of clear zone:

A

periphery of the clast, adjacent to bone matrix

140
Q

Forms the sealing zone:

A

actin ring, actin, talin, vinculin, paxillin, tensin, actin-asoc proteins such as a-actinin, fimbrin, gelsolin, dynamin

141
Q

AvB3 binds:

A

noncollagenous bone matrix containing-RGD sequence such as bone sialoprotein, osteopontin, and vitronectin, establishing a peripheric sealing that delimits the central region, here the ruffled border is located

142
Q

Location of ruffled border:

A

center

143
Q

Maintenance of this is essential for clast activity:

A

ruffled border

144
Q

Ruffled border is formed due to:

A

intense trafficking of lysosomal and endosomal components

145
Q

This help to acidify the resorption lacuna, enabling dissolution of HA crystals

A

vacuole-type H+-ATpase in teh ruffled border

146
Q

vacuole-type H+-ATpase is aka:

A

V-ATPase

147
Q

Transportation of THESE within the ruffled border to HERE lead to bone degradation:

A

protons and enzymes: tartrate-resistnat acid phosphatase (TRAP), cathepsin K, matrix metalloproteinase-9 (MMP-9) transported to Howship lacuna

148
Q

What happens to the degradation of bone in Howship’s lacuna?

A

endocytosed across ruffled border and transcytosed to functional secretory domain at plasma membrane

149
Q

This leads to osteoporosis:

A

Abnormal inc in clast formation and activity:

150
Q

Abnormal inc in clast activity can also lead to:

A

bone metastases (results in periarticular erosions) and inflammatory arthritis (results in painful lesions)

151
Q

Inflammatory cells in periodontitis produce:

A

chemical mediators: IL-6, RANKL

152
Q

IL-6 and RANKL stimulate:

A

migration of clasts –> abnormal inc in bone resorption –> progression of periodontitis

153
Q

Genetic mutation affecting formation and resorption functions of clasts:

A

osteopetrosis, dec bone resorption

154
Q

Clasts produce THIS that controls blasts during remodeling:

A

clastokines (factors), involved in both resorption and cytokine secretion that influences the activity of other cells

155
Q

Cell type that may directly regulate the hematopoietic stem cell niche:

A

clasts

156
Q

Components of extracellular bone matrix:

A

inorganic salts, organic matrix

157
Q

% of organic matrix taken up by collagenous proteins:

A

90%

158
Q

Predominant collagen type of extracellular bone matrix:

A

Tyoe 1

159
Q

These make up the organic portion of the extracellular bone matrix:

A

Type 1 collagen, non-collagenous proteins (osteocalcin, osteonectin, osteopontin fibronectin, bone sialoproteins (BPM), GF”s, small leucine-rich glycoproteins

160
Q

small leucine-rich glycoproteins found in extracellular bone matrix:

A

decorin, biglycan, lumican, osteoderin, seric proteins

161
Q

Inorganic portion of bone:

A

Ca, P, bicarbonate, sodium, potassium, sitrate, magnesium, carbonate, flourite, zinc, barium, strontium

162
Q

HA chemical formula:

A

Ca10(PO4)6(OH)2

163
Q

These form a scaffold for HA deposition:

A

collagen + noncollagenous matrix poteins

164
Q

What is responsible for the stiffness and resistance of bone?

A

HA deposition into scaffold of collagenous and noncollagenous proteins

165
Q

Functions of bone matrix:

A

mechanical support, bone homeostasis via release of several molecules that interfere in bone cell activity

166
Q

These are believed to be important in understanding and prediction of bone fracture when loss of bone mass alone is insufficient to cause fracture

A

factors, including changes in bone matrix proteins and their modifications

167
Q

Fxn of collagen:

A

structure and function of bone tissue

168
Q

Factors that can lead to variation in concentration of bone matrix proteins:

A

age, nutrition, disease, antiosteoporotic tx

169
Q

These can lead to postyield deformation and bone fracture:

A

age, nutrition, disease, antiosteoporotic tx

170
Q

There is a possible relationship bw hyaluronic acid synthesis and:

A

inc in clast activity

171
Q

What is the inc in hyaluronic acid synthesis after PTH tx related to:

A

subsequent bone resorption

172
Q

Most common molecule involved in interactions bw bone cells and bone matrix:

A

integrins

173
Q

Fxns of bone matrix:

A

support for bone cells, regulation of activity of bone cells through several adhesion molecules

174
Q

How do blasts interact w bone matrix?

A

via integrins

175
Q

integrins of blasts attach to:

A

RGD and other sequences in bone matrix proteins (osteopontin, fibronectin, collagen, osteopontin, bone sialoprotein

176
Q

Most common integrins in blast:

A

a1B1, a2B1, and a5B1

177
Q

Functions of a1B1, a2B1, and a5B1

A

cell-cell adhesion, blast organization on bone surface during osteoid synthesis

178
Q

Why are interactions bw clasts and bone matrix essential for osteoid synthesis?

A

bone resorption only occurs when clasts bind to mineralized bone

179
Q

What do clasts express during resorption?

A

avB3, a2B1 integrins to interact with extracellular matrix

180
Q

These are required for clasts to interact with extracellular matrix:

A

avB3, a2B1 integrins

181
Q

avB3 bind:

A

bone enriched, RGD-containing proteins such as bone sialoprotein and osteopontin

182
Q

B1 integrins bind:

A

collagen fibrils

183
Q

Do clasts express cadherins?

A

no, bc they are migrating cells

184
Q

Where are cadherins found in bone?

A

contact bw clasts precursors and stromal cells

185
Q

Stromal cells express:

A

GF for clast differentiation

186
Q

Interaction integrins play a role in:

A

osteocyte-bone matrix interactions

187
Q

osteocyte-bone matrix interactions are important for:

A

mechanosensitive function of cytes, whereby signals induced by tissue deformation are generated and amplified

188
Q

Integrins suggested to be involved in cyte-bone matrix interaction:

A

B3, B1 (involved in mechanosensing)

189
Q

B3 and B1 interaction occur bw:

A

cyte body and bone matrix of lacuna wall, bw cyte processes and canalicular wall

190
Q

Fluid filled narrow space bw cyte body and processes from mineralized bone matrix:

A

pericellular space, non-organized pericellular matrix

191
Q

Which is wider, space bw cyte cell body and lacunar wall or cyte processes and canalicular wall?

A

cell body and lacunar wall

192
Q

Macromolecules present in pericellular fluid and produced by cytes::

A

osteopontin, osteocalcin, dentin matrix protein, proteoglycans, hyaluronic acid

193
Q

Delicate fibrous connection in the canalicular network:

A

tethers, perlecan is a possible compound of tethers

194
Q

Cytes can attach directly via:

A

hillocks, protruding structures from canalicular wall, form close contacts, possibly via B3-integrins, w the membrane of cyte processes, role in mechanosensation?, sensing fluid movement in pericellular space

195
Q

Essential for bidirectional solute transport in pericellular space:

A

fluid flux movements

196
Q

Bidirection solute transport influences:

A

cyte signalling pwy, communication bw bone cells

197
Q

Local factors controlling formation, proliferation, differentiation and activity of remodeling:

A

autocrine and paracrine molecules: GF’s, cytokines, prostaglandins produced by bone cells, factors of bone matrix released during bone resorption

198
Q

Systemic factors important for bone homeostasis:

A

PTH, calcitonin,1,25-dihydroxyvitamin D3 (calcitrol), glucocorticoids, androgens, estrogens

199
Q

2 molecule that can bind PTH receptor:

A

PTH, PTHrP (can influence bone remodeling)

200
Q

Main cause of bone loss and osteoporosis:

A

dec in estrogen at menopause

201
Q

How does estrogen maintain bone homeostasis?

A

inhibit blast and cyte apoptosis, prevent excessive resorption, suppress clast formation/ activity, induce clast apoptosis

202
Q

How does estrogen dec clast formation?

A

by inhibiting synthesis of osteoclastogenic cytokine RNKL by blasts and cytes, by red level of other osteoclastogenic cytokines

203
Q

Estrogen stimulates blasts and cytes to produce:

A

osteoprotegrin (OPG)

204
Q

What is OPG?

A

decoy receptor of RNK in clast, inhibits osteoclastogenesis

205
Q

osteoclastogenic cytokines:

A

IL-1, 6, 11, TNF-a/ -B, M-CSF

206
Q

How does estrogen act directly on bone cells?

A

estrogen receptors a and B

207
Q

This is a direct target of estrogen:

A

clast

208
Q

This participates in control of clast life span:

A

estrogen, via estrogen receptors

209
Q

Where does remodelling take place?

A

in bone cavities needed to be remodeled

210
Q

This forms before remodeling begins:

A

BMU

211
Q

These form the cutting cone ahead during remodeling:

A

clasts

212
Q

These form the closing cone from behind during remodeling:

A

blasts

213
Q

The closing cone is assoc w:

A

BV’s and peripheral innervation

214
Q

Its’ suggested that the BMU is covered by:

A

a canopy of cells (possibly bone lining cells)

215
Q

These cells form the bone remodelling compartment:

A

bone lining cells

216
Q

What is the BRC connected to:

A

bone lining cells on bone surface, in communication w cytes in bone matrix

217
Q

Bone remodelling cycle phases:

A

initiation phase, reversal, bone formation

218
Q

Initiation phase consists of:

A

bone resorption, transition (reversal phase) phase of bone

219
Q

Completes the bone remodeling cycle:

A

coordinated action of tes and bone lining cells

220
Q

How are hematopoietic cells recruited in the initiation phase?

A

osteogenic factors: RANKL and M-CSF, then differentiate to mature clasts

221
Q

Process during remodeling w direct and indirect communications among bone cells:

A

coupling mechanism, includes coupling factors stored in bone matrix that would be released after clast resorption

222
Q

These can act as coupling factors:

A

insulin-like GF(IGF), TGF-B, BMP’s, FGF, platelet-derived GF

223
Q

Where are the coupling factors stored?

A

in bone matrix

224
Q

When are coupling factors released?

A

during resorption

225
Q

Category of molecule suggested to be involved in bone cell communication during remodeling:

A

semaphorins

226
Q

this must be inhibited in the initiation phase of remodeling

A

blast activity and differentiation, to completely remove damaged or aged bone

227
Q

Factor expressed by clasts that inhibits bone formation during resorption:

A

Sema4D

228
Q

What are semaphorins:

A

large family of glycoproteins, membrane bound or soluble, in a wide range of tissues,

229
Q

semaphorins are involved in:

A

immune response, organogenesis, CV development, tumor progression, cell-cell communication bw clasts and blasts during remodelling

230
Q

Where is Sema4D expressed?

A

clasts

231
Q

Receptor to Sema4D:

A

Plexin-B1

232
Q

where is the Sema4D receptor located?

A

blasts

233
Q

Fxn of binding Sema4D and Plexin-B1:

A

inhibits IGF-1 pwy

234
Q

Fxn of IGF-1 pwy:

A

blast differentiation

235
Q

How do clasts suppress bone formation?

A

by expressing Sema4D

236
Q

member of Sema family found in blasts:

A

Sema3A

237
Q

Fxn of Sema3A:

A

inhibitor of osteoclastogenesis

238
Q

This is expressed by clasts to initiate bone resorption:

A

Sema4D

239
Q

When is Sema3A expressed by blasts?

A

prior to bone formation

240
Q

Fxn of ephrinB2:

A

bind ephrinB4, leading to transduction of bidirectional signals, promoting blast differentiation

241
Q

Where is ephrinB2 expressed?

A

membrane of mature clasts, also in blasts

242
Q

Where is ephrinB4 expressed?

A

membrane of blasts

243
Q

***ephrinB4/ephrinB2 binding leads to:

A

inhibit formation of new clasts (this is the reversal signal)

244
Q

***ephrinB2/ephrinB4 binding leads to:

A

promotes blast differentiation

245
Q

Factors secreted by mature clasts that stimulate blast differentiation:

A

secreted signalling molecules Wnt10b, BMP6, and the signaling sphingolipid, sphingosine 1-phosphate

246
Q

complex mech during remodeling

A

of ephrins w other factors in calst/blast communication

247
Q

TF? direct communication bw mature blasts and clasts has been demonstrated.

A

F

248
Q

How does mechanical loading effect cytes?

A

stimulate cytes to produce factors that exert anabolic action on bone

249
Q

***These have anabolic actions on bone:

A

PGE, prostacyclin (PGI2), NO, and IGF-1

250
Q

Effect of unloading on cytes:

A

Downregulates anabolic factors, stimulate cyte to produce sclerostin and DKK-1, specific factors that stimulate local osteoclastogenesis

251
Q

***Fxn of sclerostin and DKK-1:

A

inhibit blast activity

252
Q

Gene that makes sclerostin:

A

SOST gene

253
Q

Fxn of sclerostin:

A

neg regulator of bone formation, by antagonizing in blasts the actions of Lrp5, a key receptor of the Wnt/B-catenin signalling pwy

254
Q

What is Lrp5?

A

receptor of Wnt/B-catenin signalling pwy

255
Q

chemotactic signal for local clast recruitment:

A

cyte apoptois

256
Q

These engulf apoptotic cytes:

A

clasts

257
Q

What can clasts remove from remodelling sites?

A

dying cytes and/or blasts

258
Q

What produce osteoclastogenic factors nearby dying cytes?

A

viable cytes

259
Q

Main source of RANKL to promote osteoclastogenesis:

A

cytes, also stromal cells, blasts, fibroblasts

260
Q

What do viable osteocytes near apoptotic ones express?

A

high RANKL/ OPG ratio, inc level of VEGF, and monocyte chemoattractant protein-1 (CCL2) promoting inc in local osteoclastogenesis

261
Q

What may induce the release of local proosteoclastogenic cytokines?

A

disruption in cell-cell communication bw osteocytes

262
Q

These may be produced by osteocytes that stimulate osteoclast recruitment during remodeling:

A

high mobility group box protein 1 (HMGB1) and M-CSF

263
Q

2 forms of osteocalcin:

A

carboxylated and undercarboxylated

264
Q

**Which form of osteocalcin has high affinity to HA crystals:

A

carboxylated, it remains in bone matrix during mineralization

265
Q

Why does the undercalcified show lower affinity to minerals:

A

due to acidification of bone matrix during resorption

266
Q

To where is undercalcified osteocalcin shuttled:

A

other organs via blood stream

267
Q

Where has undercalcified osteocalcin been shown to have effects?

A

pancreas, adipose tissue, nervous system

268
Q

Effect of undercalcified osteocalcin in pancreas:

A

positive regulator of pancreatic insulin secretion/ sensitivity, proliferation of pancreatic B-cells

269
Q

Fxn of undercalcified osteocalcin in adipoes tissue:

A

stimulates adiponectin gene expression –> enhances insulin sensitivity

270
Q

Fxn of undercalcified osteocalcin in testis:

A

binds receptors in Leydig cells, enhances testosterone syntheses, increases fertility

271
Q

Effects of undercalcified osteocalcin in brain:

A

stimulates synthesis of monoamine NTs’ in hippocampus and inhibits gamma-aminobutyric acid (GABA) synthesis, improving memory and learning

272
Q

Endocrine fxn of bone promoted by cytes:

A

regulate P metabolism via production of FGF23 –> acts on other organs inc parathyroid gland and kidneys to red circulating phosphates

273
Q

***How do cytes act on immune system?

A

by modifying microenvironments in primary lymphoid organs, influencing lymphopoeisis

274
Q

Cells that influence immune system, mainly upon bone inflammatory destruction:

A

cytes, blasts, and clasts

275
Q

study of communication interplay bw skeletal and immune system:

A

osteoimmunology

276
Q

This is responsible for bone formation and resorption:

A

bone matrix integrins-dependent bone cells interactions

Oral Sciences (16 decks)

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