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Cortisol inhibits acid-induced bone resorption in vitro
Nancy S Krieger1, Kevin K Frick, David A Bushinsky
1Department of Medicine, Nephrology Unit, University of Rochester School of Medicine, Rochester, New York 14642, USA. Nancy_Krieger@URMC.Rochester.edu
Journal of the American Society of Nephrology : JASN
|September 20, 2002
Summary
Metabolic acidosis causes bone loss by increasing calcium excretion. This study found that cortisol, contrary to expectations, inhibits acid-induced bone resorption by reducing prostaglandin E(2) production, suggesting it doesn't worsen acidosis-related osteopenia.
Area of Science:
- Bone Biology
- Endocrinology
- Acid-Base Metabolism
Background:
- Metabolic acidosis leads to bone mineral loss by increasing urine calcium excretion without enhancing intestinal absorption.
- Acidic conditions in vitro stimulate osteoblastic prostaglandin E(2) (PGE(2)) production, which promotes osteoclastic bone resorption.
- Glucocorticoids can decrease bone mineral density, and metabolic acidosis is linked to increased glucocorticoid production, raising concerns about their combined effect on bone.
Purpose of the Study:
- To investigate whether glucocorticoids exacerbate acid-induced net calcium efflux from bone.
- To determine the effect of cortisol on acid-induced changes in prostaglandin E(2) and osteoclastic activity in vitro.
Main Methods:
- Neonatal mouse calvariae were cultured in acidic or neutral medium.
- Cultures were treated with or without cortisol (1 microM).
- Net calcium efflux, medium prostaglandin E(2) (PGE(2)) levels, and osteoclastic beta-glucuronidase activity were measured.
Main Results:
- Acidic medium increased calcium efflux, PGE(2) levels, and osteoclast activity compared to neutral medium.
- Cortisol alone decreased calcium efflux, PGE(2), and osteoclast activity.
- In acidic conditions, cortisol reduced calcium efflux, PGE(2) levels, and osteoclast activity compared to acid alone.
- Significant positive correlations were found between PGE(2) and calcium efflux, osteoclast activity and calcium efflux, and PGE(2) and osteoclast activity.
Conclusions:
- In vitro, cortisol inhibits acid-induced, cell-mediated osteoclastic bone resorption.
- This inhibition occurs via a reduction in osteoblastic PGE(2) production.
- The findings suggest that increased endogenous cortisol production is not the cause of osteopenia observed in metabolic acidosis.