Citation

Avioli LV. Exp. Gerontol. 1994; 29(3-4): 391-415.

Affiliation

Division of Endocrinology, Jewish Hospital of St. Louis, Missouri.

Copyright

(Copyright © 1994, Elsevier Publishing)

DOI

unavailable

PMID

7925758

Abstract

Evidence is rapidly accumulating that implicates calcium intake and genetic factors as important determinants of the variations in bone mass in many geographical areas as well as the loss of bone following the accumulation of peak bone mass. However, it has also been well established that the postmenopausal component of bone loss is one of the predominant factors contributing to increases in the ratio of the female/male risk of skeletal fractures after the sixth decade of life, and that vertebral bone loss can result from relatively mild changes in estrogen production and metabolism before the clinical menopause begins. Although estrogen use during early menopause prevents bone loss in the axial and appendicular skeleton in the majority of females, those estrogen-dependent mechanism(s) that initiate and perpetuate alterations in osteoclast-osteoblast interactions and bone remodeling are still ill-defined. Until the specific pathophysiological mechanisms have been defined, the informed physician should attempt to identify those peri- and postmenopausal patients at risk for more active bone turnover and rapid bone loss syndromes utilizing well-established and FDA-approved therapeutic interventional procedures to prevent the loss of skeletal tissue.

Language: en