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
