steroids induced osteoporosis

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HiddenTruth

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So, what is the precise mechanism of this? I've got a couple of thoughts.
1. Simply steroid induced break down of bone matrix
2. A bit more complex, but it makes sense. Long term therapy can result in luid retention, and hypokalemia, producing a metabolic alkalosis, which as we have discussed before can give rise to a hypocalcemia-->increased PTH secretion, and that eventually giving rise to increased osteoclast activitiy with resultant osteoporosis. Any thoughts?

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HiddenTruth said:
So, what is the precise mechanism of this? I've got a couple of thoughts.
1. Simply steroid induced break down of bone matrix
2. A bit more complex, but it makes sense. Long term therapy can result in luid retention, and hypokalemia, producing a metabolic alkalosis, which as we have discussed before can give rise to a hypocalcemia-->increased PTH secretion, and that eventually giving rise to increased osteoclast activitiy with resultant osteoporosis. Any thoughts?


if i'm not mistaken, the steroids can actually stimulate osteoclast activity; contrast this with estrogen that induces osteoclast apoptosis thereby reducing osteoporosis. Vit D, also considered to be a steroid, can stimulate osteoclast activity (along with PTH) to increase osteoclast activity.

it this light it kinda makes sense that steroid affect the activity of the osteoclast directly.

ucb
 
obviously not what you were looking for as a good explanation but i also recall steroids inducing rankl and inducing osteoclasts. i believfe this to be the main action but **** i dont remember this as well as i did when i reviewed ****.. god i hate forgetting stuff. **** step 1!!
 
Ok. So, they can activate osteoblasts directly just like Vit D, and PTH by inducing the release of the Il-1, rankl, Il-6, etc.-->OC activ. Aite, I can deal with that. Damn, I made up some crazy crap with met. alk and hypocalcemia, etc.

In terms of estrogen, I thought that it primarily controls this precise release of osteoclast activating factors from osteoblasts, i.e it dampens the release of these factors, and thereby having a check on OC activation. Is there another mechanism that I am missing?
 
hidden i am sure your other theory also occurs, i mean it makes sense, but im just guessing for how often steroids are mentioned related to bone function the cause is a more direct one, otherwise a ****load of other things would go wrong if it went to the point of fluid retention and electrolyte damage causing other factors to come into play. So i am sure that contributes but my guess atleast in the short term is the more direct effect. Who konws though, your explanation sounded good! id buy it!
 
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