Part of this work was presented at the 1996 meeting of the ASBMR, Seattle, Washington, U.S.A. (Bell et al., J Bone Miner Res 11:S334).
Cortical Remodeling Following Suppression of Endogenous Estrogen with Analogs of Gonadotrophin Releasing Hormone†
Article first published online: 1 AUG 1997
Copyright © 1997 ASBMR
Journal of Bone and Mineral Research
Volume 12, Issue 8, pages 1231–1240, August 1997
How to Cite
Bell, K. L., Loveridge, N., Lindsay, P. C., Lunt, M., Garrahan, N., Compston, J. E. and Reeve, J. (1997), Cortical Remodeling Following Suppression of Endogenous Estrogen with Analogs of Gonadotrophin Releasing Hormone. J Bone Miner Res, 12: 1231–1240. doi: 10.1359/jbmr.19188.8.131.521
- Issue published online: 4 DEC 2009
- Article first published online: 1 AUG 1997
- Manuscript Accepted: 8 APR 1997
- Manuscript Revised: 20 MAR 1997
- Manuscript Received: 7 OCT 1996
The effects of estrogen suppression on osteonal remodeling in young women was investigated using transiliac biopsies (eight paired biopsies + four single pre; three single post biopsies) taken before and after treatment for endometriosis (6 months) with analogs of gonadotrophin releasing hormone (GnRH). Estrogen withdrawal increased the proportion of Haversian canals with an eroded surface (106%, p = 0.047), a double label (238%, p = 0.004), osteoid (71%, p = 0.002), and alkaline phosphatase (ALP) (116%, p = 0.043) but not those showing tartrate-resistant acid phosphatase (TRAP) activity (p = 0.25) or a single label (p = 0.30). Estrogen withdrawal increased TRAP activity in individual osteoclasts in canals with diameters greater than 50 μm (p = 0.0089) and also the number of osteons with diameters over 250 μm (p = 0.049). ALP activity in individual osteoblasts was increased but not significantly following treatment (p = 0.051). Wall thickness was significantly correlated with osteon diameter (p < 0.001). In a separate group of patients (four pairs + one post biopsy) on concurrent treatment with tibolone, there was no significant increase in the osteon density, cortical porosity, median canal diameter, or the markers of bone formation and resorption. Enzyme activities and numbers of active canals were also not increased with the concurrent treatment, but there was still an increase in the osteon diameter. As previously shown for cancellous bone, estrogen withdrawal increased cortical bone turnover. We have now shown that resorption depth within Haversian systems was also increased with treatment. The enhanced TRAP activity in individual osteoclasts supports the concept that osteoclasts are more active following estrogen withdrawal in agreement with theoretical arguments advanced previously. Understanding the cellular and biochemical mechanisms responsible for increased depth of osteoclast resorption when estrogen is withdrawn may allow the development of new strategies for preventing postmenopausal bone loss.