First published July 1, 2013 - More info
Advances made during the last 35 years have improved our understanding of the mechanisms of steroid hormone action on bone and how physiologic, pathologic, or iatrogenic changes in hormone levels can lead to increased fracture risk. Estrogens, androgens, and glucocorticoids alter the cellular composition of bone by regulating the supply and lifespan of osteoclasts and osteoblasts. Additionally, they influence the survival of osteocytes, long-lived cells that are entombed within the mineralized matrix and mediate the homeostatic adaptation of bone to mechanical forces. Altered redox balance is a proximal underlying mechanism of some of these effects, and sex steroid deficiency or glucocorticoid excess contributes to the aging of the skeleton.
Stavros C. Manolagas
Original citation: J. Clin. Invest. 2013;123(5):1919–1921. doi:10.1172/JCI68062.
Citation for this corrigendum: J. Clin. Invest. 2013;123(7):3182. doi:10.1172/JCI70777.
Funding sources were inadvertently omitted from the Acknowledgments section. The correct funding source information is below.
The research of the author is supported by the NIH (P01 AG13918, R01 AR56679); the Department of Veterans Affairs, Biomedical Laboratory Research and Development Service of the VA Office of Research and Development (I01 BX001405); and the University of Arkansas for Medical Sciences (UAMS) Translational Research Institute and Tobacco Settlement funds.
The author regrets the error.