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The Relationship Between Bone and Reproductive Hormones Beyond Estrogens and Androgens.

TLDR
A contemporary summary of the literature examining the relationship between bone biology and reproductive signals that extend beyond estrogens and androgens is provided, and include kisspeptin, gonadotropin releasing hormone, follicle stimulating hormone, luteinizing hormone, prolactin, progesterone, inhibin, activin and relaxin.
Abstract
Reproductive hormones play a crucial role in the growth and maintenance of the mammalian skeleton. Indeed, the biological significance for this hormonal regulation of skeletal homeostasis is best illustrated by common clinical reproductive disorders, such as primary ovarian insufficiency, hypothalamic amenorrhea, congenital hypogonadotropic hypogonadism, and early menopause, which contribute to the clinical burden of low bone mineral density and increased risk for fragility fracture. Emerging evidence relating to traditional reproductive hormones and the recent discovery of newer reproductive neuropeptides and hormones has deepened our understanding of the interaction between bone and the reproductive system. In this review, we provide a contemporary summary of the literature examining the relationship between bone biology and reproductive signals that extend beyond estrogens and androgens, and include kisspeptin, gonadotropin-releasing hormone, follicle-stimulating hormone, luteinizing hormone, prolactin, progesterone, inhibin, activin, and relaxin. A comprehensive and up-to-date review of the recent basic and clinical research advances is essential given the prevalence of clinical reproductive disorders, the emerging roles of upstream reproductive hormones in bone physiology, as well as the urgent need to develop novel safe and effective therapies for bone fragility in a rapidly aging population.

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Osteocyte-Driven Bone Remodeling

TL;DR: Osteocytes, the most abundant cells in bone, have been long postulated to detect and respond to mechanical and hormonal stimuli and to coordinate the function of osteoblasts and osteoclasts as mentioned in this paper.

Profiling insulin like factor 3 (INSL3) signaling in human osteoblasts

TL;DR: In this article, the INSL3/RXFP2 signaling pathways and targets in human osteoblasts were elucidated, and it was shown that the INsl3 receptor is involved in bone metabolism by acting on the MAPK cascade and stimulating transcription of important genes of osteoblast maturation/differentiation.
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Micro-computed tomography assessment of bone structure in aging mice

TL;DR: In this paper , the authors conducted a morphometric assessment of craniofacial bones in comparison with long bones, in aging mice and found that age-related changes were observed in the microarchitecture of the femur, tibia, vertebra, and basisphenoid bone, and were more pronounced in females than in males.
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The Distribution, Expression Patterns and Functional Analysis of NR1D1 and NR4A2 in the Reproductive Axis Tissues of the Male Tianzhu White Yak.

TL;DR: In this article, the expression patterns, distribution and functions of NR1D1 and NR4A2 receptors in HPG tissues in male Tianzhu white yaks were investigated.
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Acute Effects of Kisspeptin Administration on Bone Metabolism in Healthy Men

TL;DR: Data provide the first human evidence that kisspeptin promotes osteogenic differentiation of osteoblast progenitors and inhibits bone resorption in vitro and could have clinical therapeutic application in the treatment of osteoporosis.
References
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Bone Resorption by Osteoclasts

TL;DR: Osteopetrotic mutants have provided a wealth of information about the genes that regulate the differentiation of osteoclasts and their capacity to resorb bone.
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The diagnosis of osteoporosis

TL;DR: This paper summarizes issues and proposes diagnostic criteria for osteoporosis for practical use and addresses a number of problems which need to be addressed in adapting a conceptual definition for clinical use.
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The GPR54 gene as a regulator of puberty

TL;DR: Puberty is initiated when gonadotropin-releasing hormone begins to be secreted by the hypothalamus, and complementary genetic approaches in humans and mice identified genetic factors that determine the onset of puberty.
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Hypogonadotropic hypogonadism due to loss of function of the KiSS1-derived peptide receptor GPR54

TL;DR: The present study shows that loss of function of GPR54 is a cause of IHH, and it identifies GPR 54 and possibly KiSS1 protein-derived peptide as playing a major and previously unsuspected role in the physiology of the gonadotropic axis.
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The Amazing Osteocyte

TL;DR: Osteocytes compose 90% to 95% of all bone cells in adult bone and are the longest lived bone cell, up to decades within their mineralized environment.
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