2002
DOI: 10.1210/er.23.3.279
|View full text |Cite
|
Sign up to set email alerts
|

Sex Steroids and the Construction and Conservation of the Adult Skeleton

Abstract: Here we review and extend a new unitary model for the pathophysiology of involutional osteoporosis that identifies estrogen (E) as the key hormone for maintaining bone mass and E deficiency as the major cause of age-related bone loss in both sexes. Also, both E and testosterone (T) are key regulators of skeletal growth and maturation, and E, together with GH and IGF-I, initiate a 3- to 4-yr pubertal growth spurt that doubles skeletal mass. Although E is required for the attainment of maximal peak bone mass in … Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

29
568
2
28

Year Published

2006
2006
2022
2022

Publication Types

Select...
5
4

Relationship

0
9

Authors

Journals

citations
Cited by 688 publications
(627 citation statements)
references
References 0 publications
29
568
2
28
Order By: Relevance
“…Since estrogens enhance the osteoclastpromoting activity of PTH and all the women in our study population were postmenopausal, we speculated that the inverse association between PTH and vBMDc might be also mediated by estrogen deficiency. This is also in accordance with findings reported by Riggs et al, indicating that estrogen deficiency is indirectly responsible for the secondary hyperparathyroidism observed in late postmenopausal women [35]. Our data are also in agreement with Neer et al who suggested that PTH prevent a proximal femur and total body bone loss in young women with induced estrogen deficiency [36].…”
Section: Discussionsupporting
confidence: 94%
“…Since estrogens enhance the osteoclastpromoting activity of PTH and all the women in our study population were postmenopausal, we speculated that the inverse association between PTH and vBMDc might be also mediated by estrogen deficiency. This is also in accordance with findings reported by Riggs et al, indicating that estrogen deficiency is indirectly responsible for the secondary hyperparathyroidism observed in late postmenopausal women [35]. Our data are also in agreement with Neer et al who suggested that PTH prevent a proximal femur and total body bone loss in young women with induced estrogen deficiency [36].…”
Section: Discussionsupporting
confidence: 94%
“…The ability of estrogen to decrease the expression of these cytokines in osteoblastic cells has previously been shown by several researchers (Spelsberg et al, 1999;Brady et al, 2002Khosla et al, 2002. Transfected U2OS cells were incubated overnight with 0,1nM or 1 nM E 2, after which cells were either treated for one hour with 5ng/ml TNFα or left untreated.…”
Section: Estrogen Inhibits Tnfα-induction Of Il-6 and Tnfα In U2os/ermentioning
confidence: 94%
“…It is believed that the major action of estrogen on the skeleton in vivo is through the inhibition of bone resorption (Riggs et al, 2002). Although some of the anti-resorptive effects of estrogen are via direct actions on bone-resorbing osteoclasts, estrogen has also been shown to have indirect effects by regulating bone-forming osteoblasts and bone marrow stromal cells (Zallone 2006).…”
Section: Introductionmentioning
confidence: 99%
“…Studies in animals suggest that estrogen acts by altering either the production or activity of local factors that regulate osteoblast and osteoclast precursors (Trivedi et al, 2010). A number of cytokines and growth factors are released in response to estrogenic stimulation; M-CSF, IL-1 and -6, TNF, prostaglandins, and IGF-1, all of which have effects on bone cells in vitro and in vivo (Riggs et al, 2002). Most, but not all of these cytokines can be produced by the bone cells, so some are produced by other cells in the bone microenvironment, inducing both paracrine and autocrine effects on remodeling.…”
Section: Systemic and Local Factors Affecting Bone Remodelingmentioning
confidence: 99%