Osteoblasts mediate thyroid hormone stimulation of osteoclastic bone resorption

Britto, Joanne M.

doi:10.1210/en.134.1.169

Cited by 78 publications

(50 citation statements)

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“…This was true of PTH, 1,25-dihydroxyvitamin D, TNFα and β, IL-1, and thyroid hormone [46][47][48][49][50] . The question whether cell contact was essential was a crucial one.…”

Section: Osteoclasts?mentioning

confidence: 86%

Historically significant events in the discovery of RANK/RANKL/OPG

Martın¹

2013

WJO

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After it was suggested 30 years ago that the osteoblast lineage controlled the formation of osteoclasts, methods were developed that established this to be the case, but the molecular controls were elusive. Over more than a decade much evidence was obtained for signaling mechanisms that regulated the production of a membrane -bound regulator of osteoclastogenesis, in the course of which intercellular communication in bone was revealed in its complexity. The discovery of regulation by tumor necrosis factor ligand and receptor families was made in the last few years of the twentieth century, leading since then to a new physiology of bone, and to exciting drug development. Key words: Receptor activator of nuclear factor κB ligand; Osteoprotegerin; Receptor activator of nuclear factor κB; Osteoclasts; Bone biology Core tip: The history of discovery of receptor activator of nuclear factor κB ligand began with the hypothesis that the osteoblast lineage controls osteoclast formation. The hypothesis was confirmed by experiments showing first, that osteoblastic cells were necessary for osteoclast activation, then some years later that osteoblasts were necessary for osteoclast formation in a contact-dependent process. Ultimate confirmation came from mouse genetics, discovering inhibition of osteoblast formation by a secreted tumor necrosis factor (TNF) ligand, followed by discovery of promotion of osteoclast formation by a membrane-bound member of the TNF ligand family that signalled through its receptor in hemopoietic cells to promote osteoclast formation.Martin TJ. Historically significant events in the discovery of RANK/RANKL/OPG. World

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“…This was true of PTH, 1,25-dihydroxyvitamin D, TNFα and β, IL-1, and thyroid hormone [46][47][48][49][50] . The question whether cell contact was essential was a crucial one.…”

Section: Osteoclasts?mentioning

confidence: 86%

Historically significant events in the discovery of RANK/RANKL/OPG

Martın¹

2013

WJO

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“…At molecular level, in vitro and in vivo studies have demonstrated that deficient T 3 signaling through the TRa1 receptor in bone cells is the principal mediator of skeletal consequences of hypothyroidism independently of TSH levels (11)(12)(13).…”

Section: Discussionmentioning

confidence: 99%

“…At the cellular level, both the thyroid hormones and the TSH have been shown to play a direct role in bone metabolism, acting via specific receptors in bone cells (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Response of biochemical markers of bone turnover to oral glucose load in diseases that affect bone metabolism

Yavropoulou¹,

Tomos²,

Tsekmekidou³

et al. 2011

European Journal of Endocrinology

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Objective: Postprandial suppression of bone resorption is considered one of the main contributors in the circadian rhythm of bone turnover markers. The aim of this study was to investigate this physiological response of bone tissue in diseases that affect bone metabolism. Patients and methods: In this study, 118 patients (45 hypothyroid, 40 hyperthyroid, and 33 b-thalassemic patients) and 78 healthy individuals matched for age and body mass index were included. An oral glucose test (75 g glucose) was performed after overnight fasting. Serum levels of procollagen type-I N-terminal propeptide (P1NP), b-C-terminal telopeptide of type I collagen (b-CTX), and osteocalcin were assayed at 0, 60, and 120 min. Results: Baseline values of bone turnover markers were significantly elevated in hyperthyroid and b-thalassemic patients but not in hypothyroid patients compared with the control group. After oral glucose, the levels of b-CTX but not P1NP or osteocalcin were significantly suppressed in all groups (mean change from baseline is 46.9% for b-CTX, 7.9% for P1NP, and 8% for osteocalcin). The percentage change from baseline for b-CTX was significantly augmented in hypothyroidism (52 vs 42%, PZ0.009). Conclusion: The preservation or even augmentation of postprandial suppression of bone resorption in diseases that affect bone metabolism through distinct pathogenetic mechanisms suggests the importance of this physiological response to nutrients for the general homeostasis and functional integrity of the skeleton.

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“…Despite these observations, understanding of the molecular mechanisms by which thyroid hormones regulate the bone remodelling cycle remains incomplete. Indeed, although osteoclastic bone resorption is increased in individuals with thyrotoxicosis (Mosekilde et al 1990), in vitro studies of osteoclast and osteoblast/osteoclast co-culture have failed to resolve whether T 3 acts directly in osteoclasts or whether its actions are indirect and mediated by the effects in osteoblasts (Mundy et al 1976, Allain et al 1992, Britto et al 1994, Kanatani et al 2004. Nevertheless, T 3 has been shown to accelerate osteoblast differentiation directly, resulting in increased osteoid matrix synthesis and mineralisation, thus regulating bone mineralisation and strength (Huang et al 2000, Stevens et al 2003, Bassett et al 2010.…”

Section: Thyrotoxicosis In Adultsmentioning

confidence: 99%

The skeletal consequences of thyrotoxicosis

Nicholls¹,

Brassill²,

Williams³

et al. 2012

Journal of Endocrinology

102

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Euthyroid status is essential for normal skeletal development and the maintenance of adult bone structure and strength. Established thyrotoxicosis has long been recognised as a cause of high bone turnover osteoporosis and fracture but more recent studies have suggested that subclinical hyperthyroidism and long-term suppressive doses of thyroxine (T 4 ) may also result in decreased bone mineral density (BMD) and an increased risk of fragility fracture, particularly in postmenopausal women. Furthermore, large population studies of euthyroid individuals have demonstrated that a hypothalamicpituitary-thyroid axis set point at the upper end of the normal reference range is associated with reduced BMD and increased fracture susceptibility. Despite these findings, the cellular and molecular mechanisms of thyroid hormone action in bone remain controversial and incompletely understood. In this review, we discuss the role of thyroid hormones in bone and the skeletal consequences of hyperthyroidism.

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Osteoblasts mediate thyroid hormone stimulation of osteoclastic bone resorption

Cited by 78 publications

References 0 publications

Historically significant events in the discovery of RANK/RANKL/OPG

Historically significant events in the discovery of RANK/RANKL/OPG

Response of biochemical markers of bone turnover to oral glucose load in diseases that affect bone metabolism

The skeletal consequences of thyrotoxicosis

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