The thyroid and the skeleton

Murphy, Elaine; Williams, Graham R.

doi:10.1111/j.1365-2265.2004.02053.x

Cited by 142 publications

(110 citation statements)

References 119 publications

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“…Untreated subclinical hyperthyroidism in postmenopausal women has also been associated with decreased aBMD and a higher fracture risk compared with women who received treatment, although findings have not been unequivocal (21)(22)(23)(24). Little data exists on the influence of subclinical hyperthyroidism on the skeleton in men (5).…”

Section: Discussionmentioning

confidence: 97%

“…Thyroid hormone deficiency results in delayed skeletal development, delayed bone age, and growth arrest accompanied by epiphyseal dysgenesis (5). Hyperthyroidism in childhood, in contrast, induces not only accelerated skeletal development and growth with advanced bone age but also early premature fusion of the epiphyseal growth plates and cessation of growth (6).…”

Section: Introductionmentioning

confidence: 99%

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Thyroid hormone status within the physiological range affects bone mass and density in healthy men at the age of peak bone mass

Roef

Lapauw

Goemaere

et al. 2011

European Journal of Endocrinology

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Context: The hormonal factors involved in the regulation of peak bone mass (PBM) in men have not been fully investigated. Apart from gonadal steroids and somatotropic hormones, thyroid hormones are known to affect bone maturation and homeostasis and are additional candidate determinants of adult bone mass. Objective: We aimed to investigate between-subject physiological variation in free and total thyroid hormone concentrations, TSH, and thyroid binding globulin (TBG) in relation to parameters of bone mass, geometry, and mineral density in healthy men at the age of PBM. Design and setting: We recruited 677 healthy male siblings aged 25-45 years in a cross-sectional, population-based study. Areal and volumetric bone parameters were determined using dual-energy x-ray absorptiometry (DXA) and peripheral quantitative computed tomography (pQCT). Total and free thyroid hormones, TBG, and TSH were determined using immunoassays. Results: Free and total thyroid hormone concentrations were inversely associated with bone mineral density (BMD) and bone mineral content (BMC) at the hip and total body (free triiodothyronine (FT 3 ), total T 3 (TT 3 ), and total T 4 (TT 4 )) and at the spine (FT 3 ). TBG was negatively associated with BMC and areal BMD at all sites. At the radius, cortical bone area was inversely associated with TT 3 , TT 4 , and TBG, and trabecular bone density was inversely associated with free thyroxine, TT 4 , and TBG. We observed inverse associations between cortical bone area at the mid-tibia and FT 3 , TT 3 , TT 4 , and TBG. No associations between TSH and DXA or pQCT measurements were found. Conclusion: In healthy men at the age of PBM, between-subject variation in thyroid hormone concentrations affects bone density, with higher levels of FT 3 , TT 3 , TT 4 , and TBG being associated with less favorable bone density and content.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Thyroid hormone status within the physiological range affects bone mass and density in healthy men at the age of peak bone mass

Roef

Lapauw

Goemaere

et al. 2011

European Journal of Endocrinology

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“…This is supported by studies on mice with deletion of the TSHR gene, which show high TSH and low serum levels of TH. TH therapy in these mice affect body weight but not bone mass (7,27,28). Another study has suggested that TSH binding to its receptor in bone cells has beneficial effects on the skeleton through inhibition of osteoclastogenesis (29).…”

Section: Discussionmentioning

confidence: 99%

TSH-receptor antibodies may prevent bone loss in pre- and postmenopausal women with Graves' disease and Graves' orbitopathy

Siderova¹,

Hristozov²,

Tsukeva³

2018

Archives of Endocrinology and Metabolism

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Objective: Thyrotoxicosis is established risk factor for osteoporosis due to increased bone turnover. Glucocorticoids often administered for Graves' orbitopathy (GO) have additional negative effect on bone mineral density (BMD). Our aim was to examine the influence of thyroid hormones, TSH, TSH-receptor antibodies (TRAb) and glucocorticoid treatment on bone in women with Graves' thyrotoxicosis and Graves' orbitopathy (GO). Subjects and methods: Forty seven women with Graves' disease, mean age 55.6 ± 12.8 (23 women with thyrotoxicosis and 24 hyperthyroid with concomitant GO and glucocorticoid therapy) and 40 age-matched healthy female controls were enrolled in the study. We analyzed clinical features, TSH, FT4, FT3, TRAb, TPO antibodies. BMD of lumbar spine and hip was measured by DEXA and 10-year fracture risk was calculated with FRAX tool. Results: The study showed significantly lower spine and femoral BMD (g/cm 2 ) in patients with and without GO compared to controls, as well as significantly higher fracture risk. Comparison between hyperthyroid patients without and with orbitopathy found out significantly lower spine BMD in the first group (p = 0.0049). Negative correlations between FT3 and femoral neck BMD (p = 0.0001), between FT4 and BMD (p = 0.049) and positive between TSH and BMD (p = 0.0001), TRAb and BMD (p = 0.026) were observed. Fracture risk for major fractures and TRAb were negatively associated (p = 0.05). We found negative correlation of BMD to duration of thyrotoxicosis and cumulative steroid dose. Conclusions: Our results confirm the negative effect of hyperthyroid status on BMD. TRAb, often in high titers in patients with GO, may have protective role for the bone, but further research is needed. Arch Endocrinol Metab. 2018;62(2):221-6

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“…In the resorption phase, mature, differentiated osteoclasts adhere to the bone surface and remove mineral and bone matrix through secretion of digestive lysosomal enzymes. 6 Once resorption is complete there is a reversal phase in which osteoclasts undergo programmed cell death and mononuclear cells are seen on the bone surface. These cells may play a role in preparing the surface for osteoblasts to lay down new matrix and begin bone mineralization, which occurs in the final formation phase.…”

mentioning

confidence: 99%

“…This conclusion correlated with the findings of previous reviews. 6,42 It is recommended that post-menopausal women with thyroid cancer at high risk for recurrence, who require long-term TSH suppression with thyroxine, be monitored closely for osteoporosis. There are insufficient data to confirm an increased risk in pre-menopausal women, or men, with these conditions at present.…”

mentioning

confidence: 99%

Advances in Our Understanding of Hyperthyroidism-associated Bone Loss

Brassill¹,

Williams²

2008

US Endocrinology

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Advances in Our Understanding of Hyperthyroidism-associated Bone LossOsteoporosis is characterized by low bone mass and deterioration of bone micro-architecture associated with increased bone fragility and susceptibility to fracture. In 2005 the incidence of osteoporotic fracture in the US was over two million, at a cost of nearly $17 billion. By 2025, annual fractures and costs are projected to rise by almost 50%, making this a major healthcare priority.1 Hyperthyroidism is an important cause of secondary osteoporosis 2 and the relationship between the hypothalamicpituitary-thyroid (HPT) axis and bone is an important factor to consider in the management of sub-clinical hyperthyroidism and differentiated thyroid cancer. This article discusses animal models that provide insight into the underlying mechanisms that result in hyperthyroidism-associated bone loss. It will then review the clinical data investigating effects of hyperthyroidism on the skeleton. alternatively, T3 and T4 may be inactivated irreversibly by a third deiodinase enzyme, D3, which catalyzes removal of the 5-iodine atom. Release of thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates anterior pituitary thyrotrophs to secrete thyrotropin (TSH).The balance between activities of D2 and D3 enzymes within the target cell determines the amount of T3 available to the nuclear thyroid hormone receptors (TRs), which function as hormone-inducible transcription factors. 4 Several TR isoforms have been described. TRβ2 is expressed primarily in the hypothalamus and pituitary gland, where it mediates negative feedback inhibition of TRH and TSH synthesis. TRα1and TRβ1 are widely distributed in most tissues, but their relative levels of expression vary in temporo-spatial-specific patterns. Data from mutant mice suggest that TRα1 is the functionally predominant isoform expressed in the skeleton. 4Adult bone is a dynamic tissue that undergoes continuous re-modeling, a process mediated by the coupled activities of bone-resorbing osteoclasts and bone-forming osteoblasts. 5Precursors from the monocyte/macrophage cell lineage are activated and differentiate to mature bone-resorbing osteoclasts under the influence of macrophage colony-stimulating factor (MCS-F) and receptor activator of nuclear factor κB ligand (RANKL). RANKL and osteoprotegerin (OPG), a decoy receptor for RANKL, are secreted by osteoblasts and function as critical regulators of osteoclast differentiation, acting via a local paracrine pathway that facilitates communication between the two cell lineages.The bone re-modeling cycle consists of three consecutive phases. In the resorption phase, mature, differentiated osteoclasts adhere to the bone surface and remove mineral and bone matrix through secretion of digestive lysosomal enzymes. 6 Once resorption is complete there is a reversal phase in which osteoclasts undergo programmed cell death and mononuclear cells are seen on the bone surface. These cells may play a role in preparing the surface for osteoblasts to lay down new matrix and b...

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The thyroid and the skeleton

Cited by 142 publications

References 119 publications

Thyroid hormone status within the physiological range affects bone mass and density in healthy men at the age of peak bone mass

Thyroid hormone status within the physiological range affects bone mass and density in healthy men at the age of peak bone mass

TSH-receptor antibodies may prevent bone loss in pre- and postmenopausal women with Graves' disease and Graves' orbitopathy

Advances in Our Understanding of Hyperthyroidism-associated Bone Loss

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