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Perio > Pathogenesis 3.2 > Flashcards

Pathogenesis 3.2 Flashcards

1
Q

RankL
what does it stand for?
where is it found?

A

Receptor Activated Nuclear Factor kappa B Ligand

RANK is the receptor on the proosteoclast

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2
Q

OPG

function?

A

osteoprotegerin

- An inhibitor that binds up all of the RANKL from binding to the RANKL receptor (IL-4, or IL-10)

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3
Q

Osteoclasts
# of nuclei
located where?
favor what type of environment?

A
  • Multinucleated
  • Sits on top of the bone
  • Acidic environments fosters bone resorption
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4
Q

what attaches osteoclasts to the bone?

A

osteopontin

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5
Q

TRAP

A
  • tartrate resistant acid phosphate
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6
Q

Increase RANKL/OPG ratio = ?

A

increased production of osteoclasts

o They can take the osteoclast progenitors and turn them into osteoclasts

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7
Q

Interleukins associated with disease?

A

IL-1, IL-6

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8
Q

Interleukins associated with health?

A
  • IL-4, IL-10

- antiinflammatory

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9
Q

Decreases the RANKL/OPG ratio=?

A

health

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10
Q

Bisphosphonates function?

A

drive the killing of the cells (osteoclasts) to give osteonecrosis

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11
Q

Bone resorption occurs when (in reference to RANKL and OPG)?

A

increase RANKL or decrease OPG

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12
Q

Bone Formation occurs when in reference to RANKL and OPG)?

A

increase OPG or decrease RANKL

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13
Q

what causes the release of Arachidonic Acid Metabolites from cell membranes?

A

Cell death and stimulations of phospholipase to breakdown cell membrane to release arachidonic acid

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14
Q

what COX is constitutive (there all the time)?

which COX is undetectable in normal tissues?

A

COX 1 - present in all cells

COX 2- undetectable in normal tissues

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15
Q

function of COX 1

A
  • Prostaglandin synthesis and protects the stomach from acids
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16
Q

what are Lipoxins?

functions?

A
  • Agoists that stimulate the resolution of inflammation (anti-inflammatory)
  • 15-LO and 5-LO
    o limit PMN migration
    o activate non-inflammatory macrophages that do not generate superoxide
    o stimulate the uptake of apoptotic PMN’s by macrophages
    o –the cause and resolve inflammation
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17
Q

Inflamed Periodontal tissues is theoretically attributable to______

A

PGE2 in the presence of IL-1 and TNF alpha

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18
Q

high levels of ________ are capable to inducing gingival inflammation and bone resorption

A
  • PGE2

- micromolar (um) is sufficient enough to be pharmacologically active

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19
Q

Arachidonic Acid Metabolites induce?

A

increased vasopermeabilty and vasodilation = rednesss and edema

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20
Q

Arachidonic Acid Metabolites are potential inducers of _________ by the secretion of __________?

A

potential inducer of MMPs by secretion of monocytes and fibroblasts

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21
Q

Activity of Arachidonic Acid Metabolites is a marker for disease activity. There is a
____ times increase in gingivitis and periodontitis
______ times increase during period of progression

A
  • 2-3 x increase in gingivitis and periodontitis

- 5-6 fold increase during period of progression

22
Q

what be be used as a screening test in gingival crevicular fluid to predict future attachment loss?

A

PGE2 levels

23
Q

NSAIDS can block ________ to limit the progression of periodontitiis?

A
  • block PGE2 synthase – diminishes attachment and bone loss – limits progression
24
Q

Corticotropin releasing factor (CRF) has what affect on lymphocytes and PMN’s?

A
  • CRF depresses lymphocyte function leading to inhibition of antibody secretion
  • CRF inpairs neutrophil phagocytic and killing function
25
Q

PMN’s release ______ responsible for breaking the membrane - releases arachidonic acid

A
  • 5-LO
26
Q

rankL receptor is located where?

A

on proosteoclast

27
Q

decreases CD8 causes what syndrome?

A

chronic fatigue snydrome

28
Q

increased CD8 causes what snydrome?

A

sjogren’s syndrome - nk cells destroy salivary glands

29
Q

what disease/ virus can kill CD4 cells

A

HIV

30
Q

compare type of immune cells in periodontitis before and after puberty?

A

before puberty- T-cell response

After Puberty - B- cell response

31
Q

cytokines can be pliomorphic which means what?

A

elicit different biological response in different cells

32
Q

when speaking of cytokines, what is the hallmark of periodontitis?

A

receptors can not come together and clucter

33
Q

IL-1 is _______ is health and _____ in disease

A

low health and high in disease

34
Q

IL-2 name?

A

T-cell growth factor

35
Q

IL-2 function?

A 
Name = T-cell growth factor
Function = stimulates macrophages and NK function and proliferation
36
Q

IL-4 function

A

-B-cell activation, proliferation and differentiation

37
Q

IL-8 function?

A

stimulates PMN and MMP activity

38
Q

IL-9 function

A

promotes growth of mast cells

39
Q

IL-10 function?

A

inhibits cells to present antigens

40
Q

INF function?

A
  • bone resorption

- antiviral -treat hepatitis C

41
Q

TNF

A
  • bone resorption
  • alpha- increase PMN activity
  • beta- cytotoxic to fibroblasts
  • can interfere with insulin and glycemic control
42
Q

collagenase MMP’s?

A

MMP1, MMP 8, MMP 13

43
Q

MMP-1 from what?

A

fibroblasts

44
Q

MMP-8 from?

A

PMN’s

45
Q

MMP 13 from ?

A

bacterial cells

46
Q

endo vs exoproteases?

A

endoprteases like MMP 1, 8 only break within the molecule where as MMP 13 is an exoprotease that breaks down into multiple peptide fragments

47
Q

MMP-2 type and from?

A

MMP-2 = gelatinase from ground substance

48
Q

MMP-12 from?

A

macrophage elastase

49
Q

what are two things that are good indicators of disease activity?

A

Il-1 and PGE2

50
Q

What two types of cells can induce MMP’s that are secreted from arachidonic acid metabolites?

A

monocytes and fibroblasts

Perio (5 decks)

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