The authors have no conflict of interest.
Estrogen and Bone—a Reproductive and Locomotive Perspective†
Article first published online: 1 NOV 2003
Copyright © 2003 ASBMR
Journal of Bone and Mineral Research
Volume 18, Issue 11, pages 1921–1931, November 2003
How to Cite
Järvinen, T. L., Kannus, P. and Sievänen, H. (2003), Estrogen and Bone—a Reproductive and Locomotive Perspective. J Bone Miner Res, 18: 1921–1931. doi: 10.1359/jbmr.2003.18.11.1921
- Issue published online: 2 DEC 2009
- Article first published online: 1 NOV 2003
- Manuscript Accepted: 23 JUL 2003
- Manuscript Revised: 11 JUL 2003
- Manuscript Received: 22 APR 2003
- mechanical loading;
- growth and development;
The primary function of the skeleton is locomotion, and the primary function of estrogen is reproduction. When the skeleton is considered within this locomotive context, the onset of estrogen secretion at puberty leads to packing of mechanically excess mineral into female bones for reproductive needs. Accordingly, the unpacking of this reproductive safety deposit at menopause denotes the origin of type I osteoporosis.
Introduction: According to the prevailing unitary model of involutional osteoporosis, female postmenopausal bone loss can be described as having an initial accelerated, transient phase (type I), followed by a gradual continuous phase (type II). Estrogen withdrawal is generally accepted as the primary cause of the type I osteoporosis. Thus, the quest to uncover the origin of type I osteoporosis has focused on the estrogen withdrawal-related skeletal changes at and around the menopause. However, considering that the cyclical secretion of estrogen normally begins in early adolescence and continues over the entire fertile period, one could argue that focusing on perimenopause alone may be too narrow.
Materials and Methods: This is not a systematic review of the literature on the skeletal function of estrogen(s), but rather, an introduction of a novel structure- and locomotion-oriented perspective to this particular issue through pertinent experimental and clinical studies.
Results and Conclusions: When considering locomotion as the primary function of the skeleton and integrating the classic findings of the pubertal effects of estrogen on female bones and the more recent hypothesis-driven experimental and clinical studies on estrogen and mechanical loading on bone within this context, a novel evolution-based explanation for the role of estrogen in controlling female bone mass can be outlined: the onset of estrogen secretion at puberty induces packing of mechanically excess bone into female skeleton for needs of reproduction (pregnancy and lactation). Accordingly, the unpacking of this reproductive safety deposit of calcium at menopause denotes the accelerated phase of bone loss and thus the origin of type I osteoporosis.