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Old 02-28-2012
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Default osteomalacia vs. osteoporosis

so in Osteomalacia:
Osteoid matrix (not mineralized) is normally secreted by osteoblast but cannot further develop to mineralized bone (wooven and remodelled lamellar bone?)
what is the mechanism behind it? which cell mineralize/remodell the matrix? also osteoblast using calcium?

post menopausal Osteoporosis: There is enough calcium thus normal mineralization. but does low estrogen decrease osteoblast activity or increase osteoclast activity?


never really paid deep details about bones..not the most exciting topic imo.
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Old 02-28-2012
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in response to the second question
Estrogen regulates bone resorption by limiting the release of RANKL from osteoblasts. However, in postmenopausal osteoporosis, loss of estrogen leads to significantly increased RANKL expression. Increased levels of RANKL expression result in excess formation and activity of osteoclasts, leading to bone loss
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Old 02-28-2012
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Quote:
Originally Posted by LatinGeorge View Post
in response to the second question
Estrogen regulates bone resorption by limiting the release of RANKL from osteoblasts. However, in postmenopausal osteoporosis, loss of estrogen leads to significantly increased RANKL expression. Increased levels of RANKL expression result in excess formation and activity of osteoclasts, leading to bone loss
ah ok..i remember something about NFkB pathway from RANK receptor on osteoclast..
do u know how this path way works? does it stilmulate transcription?
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