ABSTRACT

Ever since the early reports by Fuller Albright in the 1940s1, major efforts have been dedicated to research aiming towards a better understanding of the role of estrogens in the regulation of bone turnover. The sudden and pronounced drop in circulating estrogens of ovarian origin after the menopause is by now unequivocally recognized as a major risk factor for osteoporosis. By using specific biomarkers of bone cell function, numerous follow-up studies have demonstrated the rapid and marked acceleration of osteoclastmediated bone resorption unmatched by simultaneous bone formation as the major cause underlying the negative calcium balance characteristic of osteoporotic postmenopausal women (e.g. references 2-4).