scholarly journals Commentary-FSH and bone 2010: evolving evidence

2010 ◽  
Vol 163 (1) ◽  
pp. 173-176 ◽  
Author(s):  
Jameel Iqbal ◽  
Li Sun ◽  
Mone Zaidi
Keyword(s):  
Bone Loss ◽  
Bone Mass ◽  
Current Issue ◽  
Scientific Evidence ◽  
Primary Role ◽  
Low Bone Mass ◽  
Genetic Studies ◽  
High Bone ◽  
Estrogen Effect

Bone loss due to menopause, natural or artificial, has been attributed solely to low estrogen. However, in a woman's life, the most precipitous bone loss begins 2 years prior to the last menstrual period, during which time estrogen levels are unperturbed whereas FSH is elevated. Our cell-based and mouse genetic studies have shown that FSH stimulates bone resorption by osteoclasts directly in a pituitary–bone axis, independently of the estrogen effect. On the basis of this and evolving clinical and scientific evidence, we propose that elevated FSH contributes to bone loss across the menopausal transition, particularly during late perimenopause. In the current issue of theEuropean Journal of Endocrinology, Rendinaet al.strengthen the view for a primary role of FSH signaling in the regulation of bone mass and bone remodeling in humans by demonstrating that an ‘activating’ polymorphism AA rs6166 causes low bone mass and high bone turnover.

Intrauterine stress induces bone loss in adult offspring of C3H/HeJ mice having high bone mass phenotype but not C57BL/6J mice with low bone mass phenotype

Bone ◽  
2016 ◽  
Vol 87 ◽  
pp. 114-119 ◽  
Author(s):  
M. Raygorodskaya ◽  
Y. Gabet ◽  
C. Shochat ◽  
E. Kobyliansky ◽  
A. Torchinsky ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Mass ◽  
Adult Offspring ◽  
Low Bone Mass ◽  
High Bone Mass ◽  
High Bone ◽  
High Bone Mass Phenotype

scholarly journals Mice lacking DKK1 in T cells exhibit high bone mass and are protected from estrogen deficiency-induced bone loss

iScience ◽  
2021 ◽  
pp. 102224
Author(s):  
Juliane Lehmann ◽  
Sylvia Thiele ◽  
Ulrike Baschant ◽  
Tilman D. Rachner ◽  
Christof Niehrs ◽  
...  
Keyword(s):  
T Cells ◽  
Bone Loss ◽  
Bone Mass ◽  
Estrogen Deficiency ◽  
High Bone Mass ◽  
High Bone

scholarly journals Osteoarthritis: Insights Offered by the Study of Bone Mass Genetics

2021 ◽  
Vol 19 (2) ◽  
pp. 115-122
Author(s):  
A. Hartley ◽  
C. L. Gregson ◽  
L. Paternoster ◽  
J. H. Tobias
Keyword(s):  
Bone Mass ◽  
Causal Effect ◽  
Mendelian Randomisation ◽  
Mineral Density ◽  
High Bone Mass ◽  
Increased Risk ◽  
High Bone ◽  
Genetic Mechanisms ◽  
Additional Support

Abstract Purpose of Review This paper reviews how bone genetics has contributed to our understanding of the pathogenesis of osteoarthritis. As well as identifying specific genetic mechanisms involved in osteoporosis which also contribute to osteoarthritis, we review whether bone mineral density (BMD) plays a causal role in OA development. Recent Findings We examined whether those genetically predisposed to elevated BMD are at increased risk of developing OA, using our high bone mass (HBM) cohort. HBM individuals were found to have a greater prevalence of OA compared with family controls and greater development of radiographic features of OA over 8 years, with predominantly osteophytic OA. Initial Mendelian randomisation analysis provided additional support for a causal effect of increased BMD on increased OA risk. In contrast, more recent investigation estimates this relationship to be bi-directional. However, both these findings could be explained instead by shared biological pathways. Summary Pathways which contribute to BMD appear to play an important role in OA development, likely reflecting shared common mechanisms as opposed to a causal effect of raised BMD on OA. Studies in HBM individuals suggest this reflects an important role of mechanisms involved in bone formation in OA development; however further work is required to establish whether the same applies to more common forms of OA within the general population.

Loss of milk fat globule-epidermal growth factor 8 (MFG-E8) in mice leads to low bone mass and accelerates ovariectomy-associated bone loss by increasing osteoclastogenesis

Bone ◽  
2015 ◽  
Vol 76 ◽  
pp. 107-114 ◽  
Author(s):  
Kathrin Sinningen ◽  
Elise Albus ◽  
Sylvia Thiele ◽  
Sylvia Grossklaus ◽  
Thomas Kurth ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Bone Loss ◽  
Bone Mass ◽  
Milk Fat ◽  
Low Bone Mass ◽  
Milk Fat Globule ◽  
Epidermal Growth ◽  
Fat Globule

scholarly journals Sclareol prevents ovariectomy-induced bone loss in vivo and inhibits osteoclastogenesis in vitro via suppressing NF-κB and MAPK/ERK signaling pathways

2019 ◽  
Vol 10 (10) ◽  
pp. 6556-6567 ◽  
Author(s):  
Haiming Jin ◽  
Zhenxuan Shao ◽  
Qingqing Wang ◽  
Jiansen Miao ◽  
Xueqin Bai ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Mass ◽  
Postmenopausal Women ◽  
Postmenopausal Osteoporosis ◽  
Bone Quality ◽  
Progressive Disease ◽  
Erk Signaling ◽  
Low Bone Mass

Postmenopausal osteoporosis (PMO) is a progressive disease occurring in elderly postmenopausal women that is characterized by low bone mass and impaired bone quality.

scholarly journals Cocaine and Amphetamine-Regulated Transcript May Regulate Bone Remodeling as a Circulating Molecule

Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 3933-3941 ◽  
Author(s):  
Manvendra K. Singh ◽  
Florent Elefteriou ◽  
Gerard Karsenty
Keyword(s):  
Bone Mass ◽  
Bone Remodeling ◽  
Third Ventricle ◽  
Fold Increase ◽  
Low Bone Mass ◽  
High Bone Mass ◽  
Peripheral Tissues ◽  
Osteoclast Number ◽  
High Bone ◽  
The Brain

Cocaine- and amphetamine-regulated transcript (CART) is one of the two known mediators of the leptin regulation of bone mass. Cart is expressed in both the brain and peripheral tissues such as the pituitary gland and the pancreatic islets. Cart−/− mice present a low bone mass phenotype due to an isolated increase in osteoclast number. In an effort to rescue their bone phenotype, we delivered recombinant CART in the third ventricle of the mutant mice but never recorded any improvement of the low bone mass, although this procedure could affect fat pad mass. In contrast, transgenic mice harboring a 2-fold increase in CART circulating level display a high bone mass due to an isolated decrease in osteoclast number and could rescue the low bone mass phenotype of the Cart−/− mice. Thus, our results suggest that in its capacity of a regulator of bone remodeling, CART may act more as a circulating molecule than a neuropeptide.

The role of cytokines and adipocytokines in zoledronate-induced acute phase reaction in postmenopausal women with low bone mass

2012 ◽  
Vol 77 (6) ◽  
pp. 816-822 ◽  
Author(s):  
Athanasios D. Anastasilakis ◽  
Stergios A. Polyzos ◽  
Sideris Delaroudis ◽  
Ilias Bisbinas ◽  
Grigorios T. Sakellariou ◽  
...  
Keyword(s):  
Bone Mass ◽  
Postmenopausal Women ◽  
Acute Phase ◽  
Acute Phase Reaction ◽  
Phase Reaction ◽  
Low Bone Mass

91313094 Role of peak bone mass and bone loss in postmenopausal osteoporosis: 12 year study

Maturitas ◽  
1992 ◽  
Vol 15 (1) ◽  
pp. 83-84
Author(s):  
M.A Hansen ◽  
K Overgaard ◽  
B.J Riis ◽  
C Christiansen
Keyword(s):  
Bone Loss ◽  
Bone Mass ◽  
Postmenopausal Osteoporosis ◽  
Peak Bone Mass

Low bone mass and fast rate of bone loss at menopause: equal risk factors for future fracture. A 15-year follow-up study

Maturitas ◽  
1997 ◽  
Vol 26 (2) ◽  
pp. 154-155
Author(s):  
B.J. Riis ◽  
M.A. Hansen ◽  
A.M. Jensen ◽  
K. Overgaard ◽  
C. Christiansen
Keyword(s):  
Risk Factors ◽  
Bone Loss ◽  
Bone Mass ◽  
Fast Rate ◽  
Low Bone Mass ◽  
Follow Up Study ◽  
Future Fracture ◽  
Rate Of Bone Loss
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