LPS are endotoxins that are from cell walls of gram negative bacteria. They are long lived. They are responsible for a range of inflammatory reactions due to interacting and regulating leuokocytes(PMN's). They also have a role in periodontla disease by activating macrophages. simply put LPS->macrophages->preosteoclasts-> produce a cytokine called RANK. This is involved in osteoclastogenesis. there is usually a balance between RANK and OPG(which is also involved in osteoclastogenesis and is produced by endothelial cells and osteoblasts). So i guess more LPS=more macrophages=more RANK= imbalance in RANK and OPG so more bone loss.??
Need someone else to fill in gaps and help explain. im not 100% sure of this answer but this is what i interpret from my notes.. ?? hope its correct?
Lipopolysaccharides are one component of the outer membrane of the cell wall of gram-negative bacteria. LPSs stimulate macrophages to produce cytokines, activates the alternative complement pathway, is antigenically effective and also cytotoxic.
Specifically, LPS activates macrophages which go on to produce mediators such as:
The cytokines and PGE2 stimulate T cells to produce RANKL cytokine, which binds to RANK (pre-osteoclast) to promote bone resorption. OPG inhibits RANKL
I just want to add in a little sentence that i found- microbes usually dont have the ability to directly impact on destruction of tissues however they do have the ability to initiate and regulate the hosts immune response that then causes the inflammatory response and destruction/ i just thought this was a nice and basic way to help remember the principles of pathogenesis. :D
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LPS are endotoxins that are from cell walls of gram negative bacteria. They are long lived. They are responsible for a range of inflammatory reactions due to interacting and regulating leuokocytes(PMN's).
They also have a role in periodontla disease by activating macrophages.
simply put
LPS->macrophages->preosteoclasts-> produce a cytokine called RANK. This is involved in osteoclastogenesis.
there is usually a balance between RANK and OPG(which is also involved in osteoclastogenesis and is produced by endothelial cells and osteoblasts). So i guess more LPS=more macrophages=more RANK= imbalance in RANK and OPG so more bone loss.??
Need someone else to fill in gaps and help explain. im not 100% sure of this answer but this is what i interpret from my notes.. ?? hope its correct?
Lipopolysaccharides are one component of the outer membrane of the cell wall of gram-negative bacteria. LPSs stimulate macrophages to produce cytokines, activates the alternative complement pathway, is antigenically effective and also cytotoxic.
Specifically, LPS activates macrophages which go on to produce mediators such as:
Cytokines (TNF, IL-1, IL-6, IL-8)
Oxygen radicals
Bioactive lipids (PGE2)
The cytokines and PGE2 stimulate T cells to produce RANKL cytokine, which binds to RANK (pre-osteoclast) to promote bone resorption. OPG inhibits RANKL
haha yea tim thats exactly what i said(well its whati meant).. lol.. you made it sound SMARTY though.. Good work..
I just want to add in a little sentence that i found-
microbes usually dont have the ability to directly impact on destruction of tissues however they do have the ability to initiate and regulate the hosts immune response that then causes the inflammatory response and destruction/
i just thought this was a nice and basic way to help remember the principles of pathogenesis.
:D
Well done !!
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