Advertisement

Skeletal Tissue and Ovarian Function: Puberty and Menopause

  • Annamaria Colao
  • Carolina Di Somma
  • Volha V. Zhukouskaya
Chapter

Abstract

The main sources of estrogens (E) are ovarian secretion (the major source) and peripheral conversion from androgens (the minor source) in premenopausal women, whereas in postmenopausal women, E derive only from peripheral conversion. E play a central role not only in female reproduction but also in the skeletal homeostasis, in the regulation of bone mass during puberty, adult life, and menopause. E have multiple functions on the bone and other cells related to the bone such as chondrocytes and cells of the immune system. Normally, E suppress osteoclastogenesis in the trabecular bone, increase osteoblastogenesis on endocortical surface and reduce osteoblastogenesis on periosteum of cortical bone, reduce apoptosis of osteocytes, and decrease T- and B-cell activation with consequent inhibition of osteoclastogenesis. Additionally, they possess antioxidant properties, protecting bone cells from oxidative stress, and participate in intestinal calcium absorption and renal conservation. During puberty, E enhance bone formation through direct and indirect mechanism. After reaching the peak of bone mass, E cease growth, maintaining balance between bone formation and resorption. After menopause, E decline leads to rapid bone loss due to increased bone resorption that is followed by slow bone loss associated predominantly with aging processes. In this latter phase, E worsen age-related changes.

Keywords

Bone Osteoblast Osteoclasts Osteocyte Sex steroids Estrogens Puberty Menopause 

References

  1. 1.
    Riggs BL, Khosla S, Melton LJ III. Sex steroids and the construction and conservation of the adult skeleton. Endocr Rev. 2002;23:279–302.CrossRefPubMedGoogle Scholar
  2. 2.
    Melmed S, Polonsky KS, Larsen PR, Kronenberg HM. Williams textbook of endocrinology. In: Bulun SE, editor. Physiology and pathology of female reproductive axis. 12th ed. Philadelphia: Elsevier; 2011. p. 581–644.Google Scholar
  3. 3.
    Manolagas SС, O’Brien CA, Almeida M. The role of estrogen and androgen receptors in bone health and disease. Nat Rev Endocrinol. 2013;9:699–712.CrossRefPubMedPubMedCentralGoogle Scholar
  4. 4.
    Martin-Millan M, Almeida M, Ambrogini E, Han L, Zhao H, Weinstein RS, Jilka RL, O’Brien CA, Manolagas SC. The estrogen receptor α in osteoclasts mediates the protective effects of estrogens on cancellous but not cortical bone. Mol Endocrinol. 2010;24:323–34.CrossRefPubMedPubMedCentralGoogle Scholar
  5. 5.
    Mori G, D’Amelio P, Faccio R, Brunetti G. Bone-immune cell crosstalk: bone diseases. J Immunol Res. 2015;2015:108451.  https://doi.org/10.1155/2015108451.CrossRefPubMedPubMedCentralGoogle Scholar
  6. 6.
    Nicks KM, Fowler TW, Gaddy D. Reproductive hormones and bone. Curr Osteoporos Rep. 2010;8:60–7.CrossRefPubMedGoogle Scholar
  7. 7.
    Chappell PE, Lydon JP, Conneely OM, O’Malley BW, Levine JE. Endocrine defects in mice carrying a null mutation for the progesterone receptor gene. Endocrinology. 1997;138:4147–52.CrossRefPubMedGoogle Scholar
  8. 8.
    Nicks KM, Perrien DS, Akel NS, Suva LJ, Gaddy D. Regulation of osteoblastogenesis and osteoclastogenesis by the other reproductive hormones, activinand inhibin. Mol Cell Endocrino. 2009;310:11–20.CrossRefGoogle Scholar
  9. 9.
    Perrien DS, Akel NS, Edwards PK, Carver AA, Bendre MS, Swain FL, Skinner RA, Hogue WR, Nicks KM, Pierson TM, Suva LJ, Gaddy D. Inhibin A is an endocrine stimulator of bone mass and strength. Endocrinology. 2007;148:1654–65.CrossRefPubMedGoogle Scholar
  10. 10.
    Melmed S, Polonsky KS, Larsen PR, Kronenberg HM. Williams textbook of endocrinology. In: Styne DM, Grumbach MM, editors. Puberty: ontogeny, neuroendocrinology, physiology, and disorders. 12th ed. Philadelphia: Elsevier; 2011. p. 1055–108.Google Scholar
  11. 11.
    Weaver CM, Gordon CM, Janz KF, et al. The National Osteoporosis Foundation’s position statement on peak bone mass development and lifestyle factors: a systematic review and implementation recommendations. Osteoporos Int. 2016;27:1281–386.CrossRefPubMedPubMedCentralGoogle Scholar
  12. 12.
    Berger C, Goltzman D, Langsetmo L, Joseph L, Jackson S, Kreiger N, Tenenhouse A, Davison KS, Josse RG, Prior JC, Hanley DA. Peakbonemassfromlongitudinal data: implications for the prevalence, pathophysiology, and diagnosis of osteoporosis. J Bone Miner Res. 2010;25:1948–57.CrossRefPubMedPubMedCentralGoogle Scholar
  13. 13.
    Manolagas SC. Fromestrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. Endocr Rev. 2010;31(3):266–300.CrossRefPubMedPubMedCentralGoogle Scholar
  14. 14.
    Lean JM, Davies JT, Fuller K, Jagger CJ, Kirstein B, Partington GA, Urry ZL, Chambers TJ. A crucial role forthiolantioxidantsinestrogen-deficiencyboneloss. J Clin Invest. 2003;112:915–23.CrossRefPubMedPubMedCentralGoogle Scholar
  15. 15.
    Muthusami S, Ramachandran I, Muthusamy B, Vasudevan G, Prabhu V, Subramaniam V, Jagadeesan A, Narasimhan S. Ovariectomyinducesoxidativestressandimpairsbone antioxidantsysteminadultrats. Clin Chim Acta. 2005;360:81–6.CrossRefPubMedGoogle Scholar
  16. 16.
    Almeida M, Han L, Martin-Millan M, Plotkin LI, Stewart SA, Roberson PK, Kousteni S, O’Brien CA, Bellido T, Parfitt AM, Weinstein RS, Jilka RL, Manolagas SC. Skeletal involution by age-associated oxidative stress and its acceleration by loss of sex steroids. J Biol Chem. 2007;282:27285–97.CrossRefPubMedPubMedCentralGoogle Scholar
  17. 17.
    Rizzoli R, Adachi JD, Cooper C, et al. Management of glucocorticoid-induced osteoporosis. Calcif Tissue Int. 2012;91:225–43.CrossRefPubMedGoogle Scholar
  18. 18.
    Gathercole LL, Lavery GG, Morgan SA, et al. 11β-hydroxysteroid dehydrogenase 1: translational and therapeutic aspects. Endocr Rev. 2013;34(4):525–55.CrossRefPubMedGoogle Scholar
  19. 19.
    Diaz de Barboza G, Guizzardi S, Tolosa de Talamoni N. Molecular aspects of intestinal calcium absorption. World J Gastroenterol. 2015;21(23):7142–54.CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  • Annamaria Colao
    • 1
  • Carolina Di Somma
    • 2
  • Volha V. Zhukouskaya
    • 1
  1. 1.Department of Clinical Medicine and Surgery, Division of EndocrinologyUniversity of Naples Federico IINaplesItaly
  2. 2.IRCCS SDNNaplesItaly

Personalised recommendations