The Role of FSH and TSH in Bone Loss and Its Clinical Relevance

Agrawal, Manasi; Zhu, Guangyu; Sun, Li; Zaidi, Mone; Iqbal, Jameel

doi:10.1007/s11914-010-0028-x

Cited by 22 publications

(11 citation statements)

References 61 publications

(81 reference statements)

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“…Iqbal et al reported that FSH increases TNF-α production in immune cells, stimulates the formation of osteoclasts and bone absorption and modifies bone mass independently of serum estrogen levels [ 29 , 30 , 31 ]. Short-term treatment with FSH and hCG altered signaling pathways involved in mesenchymal stem cell (MSC) proliferation, including Erk1/2 phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

Follicle-Stimulating Hormone Increases the Risk of Postmenopausal Osteoporosis by Stimulating Osteoclast Differentiation

Wang

Zhang

et al. 2015

PLoS ONE

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ObjectiveThe objectives of this study were to observe the changes in follicle-stimulating hormone (FSH) and bone mineral density (BMD) in postmenopausal women, to research the relationship between FSH and postmenopausal osteoporosis, and to observe the effects of FSH on osteoclast differentiation in RAW264.7 cells.MethodsWe analyzed 248 postmenopausal women with normal bone metabolism. A radioimmunoassay (RIA) was used to detect serum FSH, luteinizing hormone (LH), and estradiol (E2). Dual-energy X-ray absorptiometry was used to measure forearm BMD. Then, we analyzed the age-related changes in serum FSH, LH and E2. Additionally, FSH serum concentrations were compared between a group of postmenopausal women with osteoporosis and a control group. Osteoclasts were induced from RAW264.7 cells in vitro by receptor activator of nuclear factor kappa B ligand (RANKL), and these cells were treated with 0, 5, 10, and 20 ng/ml FSH. After the osteoclasts matured, tartrate-resistant acid phosphatase (TRAP) staining was used to identify osteoclasts, and the mRNA expression levels of genes involved in osteoclastic phenotypes and function, such as receptor activator of NF-κB (Rank), Trap, matrix metalloproteinase-9 (Mmp-9) and Cathepsin K, were detected in different groups using real-time PCR (polymerase chain reaction).Results1. FSH serum concentrations in postmenopausal women with osteoporosis increased notably compared with the control group. 2. RANKL induced RAW264.7 cell differentiation into mature osteoclasts in vitro. 3. FSH increased mRNA expression of genes involved in osteoclastic phenotypes and function, such as Rank, Trap, Mmp-9 and Cathepsin K, in a dose-dependent manner.ConclusionsThe circulating concentration of FSH may play an important role in the acceleration of bone loss in postmenopausal women. FSH increases osteoclastogenesis in vitro.

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Section: Discussionmentioning

confidence: 99%

Follicle-Stimulating Hormone Increases the Risk of Postmenopausal Osteoporosis by Stimulating Osteoclast Differentiation

Wang

Zhang

et al. 2015

PLoS ONE

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“…The activity of the growth hormone is associated with that of the thyroid hormones, which increase the energy production in all cells of the body and influence positively the growth of the skeleton [10]. It is also associated with the pituitary hormone thyrotropin, which stimulates the thyroid hormones, which may have direct effects on bone [11].…”

Section: Bone Modelingmentioning

confidence: 99%

Bone Development: Overview of Bone Cells and Signaling

Teti

2011

Curr Osteoporos Rep

110

115

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Vertebrates evolved elaborating a structure made up of more than 200 bones and cartilages articulated with one another to form the skeleton, through which locomotion, organ protection, lodging of hematopoiesis, and mineral homeostasis are allowed. Skeletogenesis starts at the fetal stage, along with marrow hematopoiesis, and evolves postnatally through modeling and remodeling processes that permit skeletal mass buildup. Preservation of skeletal mass is then implemented by balanced remodeling, which ensures continuous renovation of the tissue to allow its mechanical, structural, and metabolic properties to remain unaltered until ageing or diseases disrupt this equilibrium. Skeletal homeostasis is fulfilled by specialized bone cells in association with systemic and local regulators. Herein I review landmark discoveries that shed light on the intricate mesh connecting bone cells among themselves and with other systems, thus representing the cellular basis of normal and abnormal bone development and homeostasis.

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“…The occurrence of bone loss in late perimenopause, before estrogen levels decline, prompted an investigation of whether FSH may impact bone metabolism [71]. The effects of FSH on BMD are not fully known.…”

Section: Possible Role Of Other Hormonesmentioning

confidence: 99%

Osteoporosis in pituitary diseases: lessons for the clinic

Bolanowski¹,

Jawiarczyk-Przybyłowska

Halupczok-Żyła

2014

Expert Review of Endocrinology & Metabolism

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Osteoporosis is a systemic disease characterized by bone mass and density loss leading to fragility fractures. Osteoporosis due to endocrine disorders is an example of secondary osteoporosis. The harmful effects on bones are common in patients harboring pituitary tumors (acromegaly, prolactinoma, Cushing's disease) and suffering from hypopituitarism. Increased fracture risk and high healthcare costs of fractured patients are their consequences. The coexistence of some of these disorders and hypogonadism results in severe osteoporosis. The influence of the certain diseases, their activity and therapy and accompanying hypogonadism on bone turnover, bone mineral density and fracture incidence is presented. KEYWORDS: acromegaly • bone density • bone turnover • Cushing's syndrome • fractures • hypopituitarism • prolactinoma • secondary osteoporosisOsteoporosis in pituitary diseases: lessons for the clinic Osteoporosis is a generalized disease defined as a loss of bone mass and strength that leads to fragility fractures [1]. Bone strength is a component of bone mineral density (BMD) and bone quality. In general, certain factors can influence bone metabolism and evoke osteoporosis. These factors include aging, lifestyle, exercise, diet, calcium intake and adverse effect of medications. Furthermore, secondary osteoporosis is caused by numerous diseases such as endocrine system diseases, disorders of the gastrointestinal or biliary tract, renal diseases and neoplasms. It is also known that pituitary adenoma can affect bone metabolism through the hypersecretion of certain hormones or secondary hypopituitarism [2]. In this study, we would like to present the association between the loss of bone mass and pituitary diseases such as acromegaly, hyperprolactinemia, Cushing's syndrome (CS) and hypopituitarism. It is important to know that these disorders not always have the same effects in individual patients, because of different age, sex and associated conditions. Coexistence of several of these diseases might result in severe osteoporosis. AcromegalyAcromegaly is a rare disease caused by hypersecretion of growth hormone (GH), mainly from a pituitary tumor. It is known that patients with acromegaly have increased bone turnover as determined by changes in biochemical markers, calcium kinetics and histomorphometry [3]. Increased bone turnover suggests that acromegaly leads to the activation of both osteoblasts and osteoclasts [4]. Moreover, increased bone turnover was correlated with disease activity but was independent of gonadal status. In some in vitro experiments on human bone cells, it was shown that GH and IGF-1 may stimulate bone resorption by direct and indirect influence on formation, differentiation and activity of osteoclasts. On the other hand, it was shown that both GH and IGF-1 influence proliferation of osteoblasts but their differentiation is regulated only by IGF-1 and a lot of effects are the consequence of local secretion of IGFs [5]. In pre-pubertal period, GH is responsible for longitudinal bone growth. Duri...

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The Role of FSH and TSH in Bone Loss and Its Clinical Relevance

Cited by 22 publications

References 61 publications

Follicle-Stimulating Hormone Increases the Risk of Postmenopausal Osteoporosis by Stimulating Osteoclast Differentiation

Follicle-Stimulating Hormone Increases the Risk of Postmenopausal Osteoporosis by Stimulating Osteoclast Differentiation

Bone Development: Overview of Bone Cells and Signaling

Osteoporosis in pituitary diseases: lessons for the clinic

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