3/6/17 Bone Resorption: Osteoclast Formatio and Regulation Flashcards

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1
Q

Phase turned on first in bone remodelling:

A

osteoclast resorption, reversal, osteoblast/ formation

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2
Q

About how many factors are involved in bone remodelling?

A

100s

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3
Q

Bifunctional role of Wnt-signalling pwy:

A

regulation of blast and last differentiation

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4
Q

What diverts mesenchymal stem cell down the pwy of blast differentiation?

A

Wnt signalling

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5
Q

This leads prevents blast proliferation and differentiation:

A

DKK-1 binding Wnt receptor complex on blast lineage cell surface

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6
Q

How do precursors of the mature osteoblast enhance bone resorption?

A

by boosting RANKL induced osteoclastogenesis

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7
Q

Blockade of DKK-1 leads to:

A

progression of blast differentitation

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8
Q

Upregulation of OPG leads to:

A

blocking RANKL-induced osteoclastogenesis, inhibition of bone resorption

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9
Q

What leads to upregulation of OPG?

A

Activation of Wnt signalling pwy

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10
Q

Precursors to pre osteoclasts;

A

monos, macs

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11
Q

How are multinucleated cells formed?

A

mononuclear cells fuse, make clasts

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12
Q

Portion of clast that attached to bone to be resorbed:

A

ruffled border

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13
Q

This factor downregulating WNT pwy, inhibiting differentiation of mesenchymal cells:

A

DKK-1

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14
Q

What can induce DKK-1?

A

TNF-a

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15
Q

What will form if mesenchymal stem cells go down the path of endochondral bone formation?

A

chondrocyte

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16
Q

This is a coupling agent in bone forming/ absorbing:

A

RANKL

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17
Q

OPG sf:

A

osteoprotegerin

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18
Q

Ratio of these is important in formation of osteoclasts:

A

OPG and RANKL

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19
Q

Factors that stimulate blast expression of RANK Ligand:

A

TNF-a, PTHrP, IL-1, 6, 11, Vit D, Glucocorticoids, PTH, PGE2, local factors: cytokine, inflammation

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20
Q

PTHrP is involved in:

A

bone mineralization (PTH related protein)

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21
Q

How does PTH influence blast activity:

A

receps on blasts for PTH

22
Q

Precursors for clasts:

A

CFU-macs

23
Q

TF? RANKL is made by clasts and influence blast activity.

A

F vice versa, act on prefusino clasts

24
Q

Decoy receptor that prevent RANKL-RANK binding:

A

OPG

25
Q

OPG inhibits:

A

calst formation, function, and survival

26
Q

3 general groups that induce blasts to release RANKL:

A

hormones, GF’s, cytokines

27
Q

There is cross talk bw:

A

immune cells and bone cells

28
Q

immunoregulatory cytokines influence:

A

fate of bone cells, helps explain inflammatory rxn in RA, PDD and bone loss

29
Q

All cells of the mammalian immune system are derived from:

A

HSC (hemat..)

30
Q

Cell types that can produce RANKL:

A

T cells, gingival fibroblasts/PDL cells, blasts

31
Q

TF? The release of RANKL, wo OPG, will always lead to monocyte/ preosteoblasts.

A

T

32
Q

Cells that produce the most RANK in pdd, leading to bone resorption

A

T cells

33
Q

Cytokines and inflammatory mediators that can stimulate clast formation and bone resorption, all implicated in inflammation induced bone resorption:

A

IL-1, 6, 11, 17, TNFa, LIF, OSM, Bradykinin, Kallidin, Thrombin

34
Q

Cytokines and inflammatory mediators that can inhibit blastic cells

A

IL, 4, 10, 12, 13, 18, IFN-B, IFN-y

35
Q

IL-1, 6, 11, 17, TNFa, LIF, OSM, Bradykinin, Kallidin, Thrombin all act directly on these cells:

A

blasts, stromal cells

36
Q

High RANKL/ OPG ratio will lead to:

A

clast formation, bone resorption

37
Q

IL, 4, 10, 12, 13, 18, IFN-B, IFN-y directly inhibit these cells:

A

blasts, stromal cells, osteoclast progenitors

38
Q

Where in the cycle do chemokines exert their influence?

A

on clast progenitor cells, distal to RANKL/OPG

39
Q

Concentrations of these need to be evaluated to determine whether bone will be lost or not:

A

RANKL/ OPG

40
Q

Role of IL, 4, 10, 13, IFN-y:

A

inhibit RANKL and the cytokines that stimulate it

41
Q

Factors that stimulate RANKL:

A

IL 1, 6, 7, 11, 17, TNFa, LIF, OSM

42
Q

Effect of PGE2 on RANKL:

A

upregulates

43
Q

TF? TNF acts indirectly on RANKL production.

A

T

44
Q

These upregulate preosteoblasts:

A

CXCL 10, 12, 13, CCL5, PGE2, PGI2, PGF2a, GFs: FGF, PDGF, BMP2, TGFB, IGF

45
Q

This mediator of inflammation works on both the clastic and blastic side:

A

PGE2

46
Q

Upregulate clast precursors:

A

RANKL, TNF, M-CSF

47
Q

These indirectly stimulate osteoclastogenesis by effects on RANKL, M-CSF, or TNF-a:

A

cytokines or lipid based mediator such as prostaglandins or leukotrienes

48
Q

These stimulate recruitment of clast precursors or clast activity:

A

chemokines

49
Q

During inflammatory conditions, inc production of more cytokines w IL-1,6,7,11,17, TNF-a, LIF, OSM and RANK are primarily produced by:

A

leukocytes

50
Q

These are released from bone matrix or synthesized locally by various cell types after bone resorption and stimulate proliferation of blast precursor, osteoblast differentiation, or synthesi of bone matrix

A

GFs like FGF, PDGF, BMP-2, TGF-2, IGF

51
Q

These may affect bone formation by effects on blast precursors or blasts:

A

chemokines like CXCL10, 12, 13, CCL5

52
Q

stopped at slide 11

A

ok