Inhibition of osteoblastic metalloproteinases in mice prevents bone loss induced by oestrogen deficiency

2008 ◽  
Vol 104 (5) ◽  
pp. 1803-1817 ◽  
Author(s):  
Corinne Schiltz ◽  
Caroline Marty ◽  
Marie-Christine de Vernejoul ◽  
Valerie Geoffroy
Keyword(s):  
Bone Loss ◽  
Oestrogen Deficiency

scholarly journals Factors influencing bone loss in anorexia nervosa: assessment and therapeutic options

RMD Open ◽  
2019 ◽  
Vol 5 (2) ◽  
pp. e001009 ◽  
Author(s):  
Isabelle Legroux ◽  
Bernard Cortet
Keyword(s):  
Anorexia Nervosa ◽  
Bone Loss ◽  
Mineral Density ◽  
Related Factors ◽  
Oestrogen Treatment ◽  
Oestrogen Deficiency ◽  
Resumption Of Menses ◽  
Main Factor

Decreased mineral density is one of the major complications of anorexia nervosa. The phenomenon is even more pronounced when the disease occurs during adolescence and when the duration of amenorrhoea is long. The mechanisms underlying bone loss in anorexia are complex. Oestrogen deficiency has long been considered as the main factor, but cannot explain the phenomenon on its own. The essential role of nutrition-related factors—especially leptin and adiponectin—has been reported in recent studies. Therapeutic strategies to mitigate bone involvement in anorexia are still a matter for debate. Although resumption of menses and weight recovery appear to be essential, they are not always accompanied by a total reversal of bone loss. There are no studies in the literature demonstrating that oestrogen treatment is effective, and the best results seem to have been obtained with agents that induce bone formation—such as IGF-1—especially when associated with oestrogen. As such, bone management in anorexia remains difficult, hence, the importance of early detection and multidisciplinary follow-up.

scholarly journals Corilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways

2020 ◽  
Vol 24 (18) ◽  
pp. 10444-10457
Author(s):  
Jinwei Lu ◽  
Chenyi Ye ◽  
Yanyong Huang ◽  
Donghui Huang ◽  
Lan Tang ◽  
...  
Keyword(s):  
Bone Loss ◽  
Signalling Pathways ◽  
Oestrogen Deficiency

scholarly journals Icariin protects against bone loss induced by oestrogen deficiency and activates oestrogen receptor-dependent osteoblastic functions in UMR 106 cells

2010 ◽  
Vol 159 (4) ◽  
pp. 939-949 ◽  
Author(s):  
Sao-Keng Mok ◽  
Wen-Fang Chen ◽  
Wan-Ping Lai ◽  
Ping-Chung Leung ◽  
Xin-Luan Wang ◽  
...  
Keyword(s):  
Bone Loss ◽  
Oestrogen Receptor ◽  
Oestrogen Deficiency ◽  
Umr 106

scholarly journals IGFBP7 acts as a negative regulator of RANKL‐induced osteoclastogenesis and oestrogen deficiency‐induced bone loss

2019 ◽  
Vol 53 (2) ◽  
Author(s):  
Chenyi Ye ◽  
Weiduo Hou ◽  
Mo Chen ◽  
Jinwei Lu ◽  
Erman Chen ◽  
...  
Keyword(s):  
Bone Loss ◽  
Negative Regulator ◽  
Oestrogen Deficiency

RANK deletion in neuropeptide Y neurones attenuates oestrogen deficiency‐related bone loss

2019 ◽  
Vol 31 (2) ◽  
pp. e12687 ◽  
Author(s):  
Nicola J. Lee ◽  
Ireni M. Clarke ◽  
Ayse Zengin ◽  
Ronaldo F. Enriquez ◽  
Vanj Nagy ◽  
...  
Keyword(s):  
Bone Loss ◽  
Neuropeptide Y ◽  
Oestrogen Deficiency

scholarly journals Icariin prevents oestrogen deficiency–induced alveolar bone loss through promoting osteogenesis via STAT3

2020 ◽  
Vol 53 (2) ◽  
Author(s):  
Hongyuan Xu ◽  
Siru Zhou ◽  
Ranyi Qu ◽  
Yiling Yang ◽  
Xinyi Gong ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Oestrogen Deficiency

scholarly journals Oestrogen-deficiency induces bone loss by modulating CD14+ monocyte and CD4+ T cell DR3 expression and serum TL1A levels

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Fraser L. Collins ◽  
Michael D. Stone ◽  
Jane Turton ◽  
Laura R. McCabe ◽  
Eddie C. Y. Wang ◽  
...  
Keyword(s):  
T Cell ◽  
Bone Loss ◽  
Cd4 T Cell ◽  
Oestrogen Deficiency

Norethindrone acetate only partially protects the skeleton of rats treated with the LHRH agonist buserelin from oestrogen-deficiency osteopaenia

1993 ◽  
Vol 137 (1) ◽  
pp. 27-33
Author(s):  
A. Goulding ◽  
E. Gold
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Treated Group ◽  
Prolonged Treatment ◽  
Lhrh Agonist ◽  
Total Body Calcium ◽  
Oestrogen Deficiency ◽  
Total Body ◽  
Lh Releasing Hormone ◽  
Norethindrone Acetate

ABSTRACT In women with endometriosis there is concern that therapeutic use of LH-releasing hormone (LHRH) analogues, to lower ovarian oestrogen production and control endometrial hyperplasia, leads to unwanted oestrogen-deficiency bone loss. We have developed an animal model of this LHRH-mediated oestrogen-deficiency bone loss in the rat, using buserelin. The aim was to use this model to determine whether the progestogen, norethindrone acetate, could counter oestrogen-deficiency bone loss associated with prolonged treatment with the LHRH agonist buserelin. Four groups of animals which had their bones labelled with 45Ca were studied for 4 weeks: group A, control; group B, buserelin treated; group C, norethindrone acetate treated; group D, norethindrone acetate + buserelin treated. Buserelin was given daily (19·2 pmol/kg body wt); norethindrone was given orally three times / week (1·47 μmol/kg body wt). Bone resorption was monitored by measuring the urinary excretion of hydroxyproline and 45Ca and bone 45Ca content. Buserelin-treated rats developed similarly depressed plasma oestradiol-17β values in the presence and absence of progestogen, and both groups given buserelin had significantly smaller uteri than controls or rats given norethindrone without buserelin. However, norethindrone did not prevent buserelin-mediated increases in bone resorption. At the end of the study total body calcium values (mean ± s.d.) in the four groups were (mg) respectively; 2594 ± 123; 2260 ± 92 (P < 0·001 compared with controls); 2616 ± 221; 2415 ± 130 (P < 0·02 compared with controls). Rats given norethindrone and buserelin in combination had higher values (P < 0·02) than animals given buserelin alone, but significantly less total body calcium than controls (P < 0·02). We conclude that progestogen confers partial, but not complete, protection of the skeleton of buserelin-treated rats from oestrogen-deficiency bone loss. Journal of Endocrinology (1993) 137, 27–33

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