Pathogenesis 3.2 Flashcards
RankL
what does it stand for?
where is it found?
Receptor Activated Nuclear Factor kappa B Ligand
RANK is the receptor on the proosteoclast
OPG
function?
osteoprotegerin
- An inhibitor that binds up all of the RANKL from binding to the RANKL receptor (IL-4, or IL-10)
Osteoclasts
# of nuclei
located where?
favor what type of environment?
- Multinucleated
- Sits on top of the bone
- Acidic environments fosters bone resorption
what attaches osteoclasts to the bone?
osteopontin
TRAP
- tartrate resistant acid phosphate
Increase RANKL/OPG ratio = ?
increased production of osteoclasts
o They can take the osteoclast progenitors and turn them into osteoclasts
Interleukins associated with disease?
IL-1, IL-6
Interleukins associated with health?
- IL-4, IL-10
- antiinflammatory
Decreases the RANKL/OPG ratio=?
health
Bisphosphonates function?
drive the killing of the cells (osteoclasts) to give osteonecrosis
Bone resorption occurs when (in reference to RANKL and OPG)?
increase RANKL or decrease OPG
Bone Formation occurs when in reference to RANKL and OPG)?
increase OPG or decrease RANKL
what causes the release of Arachidonic Acid Metabolites from cell membranes?
Cell death and stimulations of phospholipase to breakdown cell membrane to release arachidonic acid
what COX is constitutive (there all the time)?
which COX is undetectable in normal tissues?
COX 1 - present in all cells
COX 2- undetectable in normal tissues
function of COX 1
- Prostaglandin synthesis and protects the stomach from acids
what are Lipoxins?
functions?
- 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
Inflamed Periodontal tissues is theoretically attributable to______
PGE2 in the presence of IL-1 and TNF alpha
high levels of ________ are capable to inducing gingival inflammation and bone resorption
- PGE2
- micromolar (um) is sufficient enough to be pharmacologically active
Arachidonic Acid Metabolites induce?
increased vasopermeabilty and vasodilation = rednesss and edema
Arachidonic Acid Metabolites are potential inducers of _________ by the secretion of __________?
potential inducer of MMPs by secretion of monocytes and fibroblasts
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
- 2-3 x increase in gingivitis and periodontitis
- 5-6 fold increase during period of progression
what be be used as a screening test in gingival crevicular fluid to predict future attachment loss?
PGE2 levels
NSAIDS can block ________ to limit the progression of periodontitiis?
- block PGE2 synthase – diminishes attachment and bone loss – limits progression
Corticotropin releasing factor (CRF) has what affect on lymphocytes and PMN’s?
- CRF depresses lymphocyte function leading to inhibition of antibody secretion
- CRF inpairs neutrophil phagocytic and killing function
PMN’s release ______ responsible for breaking the membrane - releases arachidonic acid
- 5-LO
rankL receptor is located where?
on proosteoclast
decreases CD8 causes what syndrome?
chronic fatigue snydrome
increased CD8 causes what snydrome?
sjogren’s syndrome - nk cells destroy salivary glands
what disease/ virus can kill CD4 cells
HIV
compare type of immune cells in periodontitis before and after puberty?
before puberty- T-cell response
After Puberty - B- cell response
cytokines can be pliomorphic which means what?
elicit different biological response in different cells
when speaking of cytokines, what is the hallmark of periodontitis?
receptors can not come together and clucter
IL-1 is _______ is health and _____ in disease
low health and high in disease
IL-2 name?
T-cell growth factor
IL-2 function?
Name = T-cell growth factor Function = stimulates macrophages and NK function and proliferation
IL-4 function
-B-cell activation, proliferation and differentiation
IL-8 function?
stimulates PMN and MMP activity
IL-9 function
promotes growth of mast cells
IL-10 function?
inhibits cells to present antigens
INF function?
- bone resorption
- antiviral -treat hepatitis C
TNF
- bone resorption
- alpha- increase PMN activity
- beta- cytotoxic to fibroblasts
- can interfere with insulin and glycemic control
collagenase MMP’s?
MMP1, MMP 8, MMP 13
MMP-1 from what?
fibroblasts
MMP-8 from?
PMN’s
MMP 13 from ?
bacterial cells
endo vs exoproteases?
endoprteases like MMP 1, 8 only break within the molecule where as MMP 13 is an exoprotease that breaks down into multiple peptide fragments
MMP-2 type and from?
MMP-2 = gelatinase from ground substance
MMP-12 from?
macrophage elastase
what are two things that are good indicators of disease activity?
Il-1 and PGE2
What two types of cells can induce MMP’s that are secreted from arachidonic acid metabolites?
monocytes and fibroblasts
