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1 that inhibit further bone resorption due to estrogen deficiency.
2 ytes is required for the bone loss caused by estrogen deficiency.
3 nts that lead to cancellous bone loss during estrogen deficiency.
4 loss and fractures in preclinical models of estrogen deficiency.
5 l as the increase in B cell number caused by estrogen deficiency.
6 is also required for the bone loss caused by estrogen deficiency.
7 atment option for osteoporosis to ameliorate estrogen deficiency.
8 tions of aldosterone as a consequence of the estrogen deficiency.
9 se of infection that are most susceptible to estrogen deficiency.
10 e acquisition was achieved or as a result of estrogen deficiency.
11 k for cardiovascular diseases because of the estrogen deficiency.
12 s and strength in mice with bone loss due to estrogen deficiency.
13 as RA or periodontitis and in conditions of estrogen deficiency.
14 loss caused by inflammation, infection, and estrogen deficiency.
15 are protected from bone loss despite severe estrogen deficiency.
16 otected from the bone loss characteristic of estrogen deficiency.
17 nant of increased bone resorption induced by estrogen deficiency.
18 n are critical to the bone wasting effect of estrogen deficiency.
19 the altered bone turnover characteristic of estrogen deficiency.
20 e in osteoclastic bone resorption induced by estrogen deficiency.
21 , trochanter, and total body, despite severe estrogen deficiency.
22 the pathophysiologic changes that occur with estrogen deficiency.
23 BMD in young women with GnRH analog-induced estrogen deficiency.
24 ssion of periodontal disease associated with estrogen deficiency.
25 e in the developed world, is associated with estrogen deficiency.
26 ng behaviors, and osteopenia associated with estrogen deficiency.
28 healthy bone cells after short durations of estrogen deficiency (5 weeks), and exceeded the osteogen
29 event the development of glomerulosclerosis, estrogen deficiency accelerated the progression of glome
30 a is a potential target for the treatment of estrogen deficiency-aggravated periodontal bone loss, an
31 city to adapt to dyslipidemia, hypertension, estrogen deficiency and diabetes mellitus that appear to
37 ouse models of high bone turnover, including estrogen deficiency and sustained exposure to parathyroi
38 Ca absorption and vitamin D action in aging, estrogen deficiency, and adaptation to a low Ca diet.
39 serum cholesterol, and adipose tissues after estrogen deficiency, and show that the benzothiophene ra
40 asts resorb could also be enhanced following estrogen deficiency, and since sex steroids regulate apo
42 kappaB and a cytokine strongly implicated in estrogen-deficiency bone loss, was suppressed in osteocl
43 ators of increased osteoclastogenesis during estrogen deficiency, but increases in RANKL, the final e
44 tion contributes to the bone loss induced by estrogen deficiency, but it is presently unknown whether
45 is instrumental for the bone loss induced by estrogen deficiency, but the responsible mechanism is un
48 These observations strongly suggest that estrogen deficiency causes bone loss by lowering thiol a
49 ss has been made in our understanding of how estrogen deficiency causes bone loss, the mechanisms inv
53 model in female Wistar rats that integrates estrogen deficiency, dietary excess, and diabetic stress
56 f their study support previous findings that estrogen deficiency has a dramatic effect on bone homeos
57 r 1 y potently attenuated BMD loss caused by estrogen deficiency, improved bone turnover, promoted a
60 however, the specific roles of androgen and estrogen deficiency in hypogonadal bone loss are unclear
62 ase in bone resorption observed in states of estrogen deficiency in mice is mainly caused by lack of
67 the assay is presented in which the role of estrogen deficiency in the development and progression o
71 unity to examine the influence of endogenous estrogen deficiency, indicated by age at menopause, on r
74 e formation and bone resorption in mediating estrogen deficiency-induced cancellous bone loss was inv
77 ells to be central to the mechanism by which estrogen deficiency induces bone loss, but the mechanism
79 re disproportionally susceptible, suggesting estrogen deficiency is a significant risk factor for chr
84 rly menopause appear at risk for worse ARMD, estrogen deficiency may also contribute to the onset or
87 Elevated iron stores, oxidative stress, and estrogen deficiency may place postmenopausal women at gr
88 sed in postmenopausal women, suggesting that estrogen deficiency may play a role in the accumulation
90 our current understanding of the process of estrogen deficiency-mediated bone destruction and explor
91 the underlying cause of glucocorticoid- and estrogen deficiency-mediated osteoporosis, and at least
92 been demonstrated to reduce bone loss in an estrogen deficiency mice model and older women, although
94 important mediators of the adverse effect of estrogen deficiency on cortical, but not trabecular, bon
95 s to evaluate the effects of caffeine and/or estrogen deficiency on ligature-induced bone loss (BL),
96 logical function in RPE through ERs and that estrogen deficiency or excess may cause dysregulation of
99 ses in lean mass, muscle size, and strength; estrogen deficiency primarily accounted for increases in
101 ion-unfavorable condition created by gonadal estrogen deficiency reduced the level of differential ex
103 a novel Egr-1/Sp-1 complex in stromal cells, estrogen deficiency results in enhanced levels of free S
108 ss around the time of menopause is driven by estrogen deficiency, the roles of estrogens and androgen
109 thogenesis of osteoporosis is the ability of estrogen deficiency to increase osteoclast formation by
110 bone matrix during osteoclastic resorption, estrogen deficiency unleashes signals that can stimulate
111 to simulate metabolic bone diseases such as estrogen deficiency, vitamin D deficiency, senescence an