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Licensed Unlicensed Requires Authentication Published by De Gruyter May 23, 2012

Bone mass density selectively correlates with serum markers of oxidative damage in post-menopausal women

  • Carlo Cervellati EMAIL logo , Gloria Bonaccorsi , Eleonora Cremonini , Carlo M. Bergamini , Alfredo Patella , Cristina Castaldini , Stefania Ferrazzini , Alessandra Capatti , Venelia Picarelli , Francesco S. Pansini and Leo Massari

Abstract

Background: Post-menopausal osteoporosis (PO) affecting a large fraction of elderly women, is triggered by the decline in 17β-estradiol (E2) level. Experimental studies in animal models and cell cultures have suggested that the fall in E2 might contribute to developing oxidative stress (OS) which in turn is believed to play an important role in PO pathogenesis. The scarcity of human studies focusing on this issue prompted us to investigate the effects of the reproductive and post-reproductive phase of women’s life on OS and bone health.

Methods: Serum parameters of oxidative challenge (lipid hydroperoxides and protein advanced oxidation products) and antioxidant defence (total serum antioxidants levels) along with bone mineral density (BMD) at femoral neck and lumbar spine were assessed in a sample of 191 women (98 pre- and 93 post-menopausal, of whom 30 osteoporotic).

Results: Pearson’s correlation analysis unveiled that spinal BMD was negatively correlated with lipid hydroperoxides in overall postmenopausal subsample (r=–0.251, p=0.012), while no significant link between these two variables was detected in women in reproductive age (r=–0.022, p=0.833). Noteworthy, stepwise multiple regression analysis showed that the association found in post-menopausal women retained significance after adjusting for potential confounding factors (p=0.001).

Conclusions: Our data showed that markers of oxidative challenge are associated with bone loss in women in post-menopausal status. We suggest that menopause-related estrogen withdrawal might contribute to make bone more vulnerable to oxidative injury thereby increasing the risk of PO development.


Corresponding author: Carlo Cervellati, PhD, Department of Biochemistry and Molecular Biology, University of Ferrara, Via Luigi Borsari, 46, 44100, Ferrara, Italy Phone: +39 3480399087, Fax: +39 0532454442

The authors thank Dr. Elizabeth Jenkins for proofreading the text.

Conflict of interest statement

Authors’ conflict of interest disclosure: The authors stated that there are no conflicts of interest regarding the publication of this article.

Research funding: None declared.

Employment or leadership: None declared.

Honorarium: None declared.

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Received: 2012-02-14
Accepted: 2012-04-23
Published Online: 2012-05-23
Published in Print: 2013-02-01

©2013 by Walter de Gruyter Berlin Boston

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