Effect of combined treatment with calcitonin on bone densitometry of patients with treated hypothyroidism

Stamato, Francisco Jose da Cunha; Amarante, E. C. J.; Furlanetto, Reinaldo P.

doi:10.1590/s0104-42302000000200013

Cited by 9 publications

(4 citation statements)

References 29 publications

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“…Consistent with histomorphometry data, two studies reported normal BMD in patients newly diagnosed with hypothyroidism (446,447). A cross-sectional cohort study of 49 patients with well-substituted hypothyroidism was compared to 49 age-and sex-matched controls investigated BMD by DXA, bone geometry by pQCT and bone strength by finite element analysis.…”

Section: Effect On Bmdmentioning

confidence: 64%

Role of Thyroid Hormones in Skeletal Development and Bone Maintenance

2016

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The skeleton is an exquisitely sensitive and archetypal T3-target tissue that demonstrates the critical role for thyroid hormones during development, linear growth, and adult bone turnover and maintenance. Thyrotoxicosis is an established cause of secondary osteoporosis, and abnormal thyroid hormone signaling has recently been identified as a novel risk factor for osteoarthritis. Skeletal phenotypes in genetically modified mice have faithfully reproduced genetic disorders in humans, revealing the complex physiological relationship between centrally regulated thyroid status and the peripheral actions of thyroid hormones. Studies in mutant mice also established the paradigm that T3 exerts anabolic actions during growth and catabolic effects on adult bone. Thus, the skeleton represents an ideal physiological system in which to characterize thyroid hormone transport, metabolism, and action during development and adulthood and in response to injury. Future analysis of T3 action in individual skeletal cell lineages will provide new insights into cell-specific molecular mechanisms and may ultimately identify novel therapeutic targets for chronic degenerative diseases such as osteoporosis and osteoarthritis. This review provides a comprehensive analysis of the current state of the art.

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Section: Effect On Bmdmentioning

confidence: 64%

Role of Thyroid Hormones in Skeletal Development and Bone Maintenance

2016

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“…Furthermore, the percentage reduction in b-CTX was not found to be associated with parameters of the disease in thalassemic patients such as ferritin levels, which is used as an index for iron overload, or hemoglobin levels (degree of anemia). Data of bone turnover markers in hypothyroid patients have presented inconclusive results reporting low or normal levels, although BMD is usually within normal limits (8,29). In histomorphometry studies, however, the bone remodeling cycle was found significantly prolonged associated with decreased bone turnover rate (25,30).…”

Section: Discussionmentioning

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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“…Hypothyroidism is known to result in delayed bone age, growth arrest and short stature when occurring in childhood [66,67]. Reduced bone turnover and increased fracture risk are the features of hypothyroidism during adulthood [68,69]. Hyperthyroidism during childhood, on the other hand, causes advanced bone age, accelerated growth, premature fusion of growth plates, short stature and craniosynostosis [64,70].…”

Section: Bone As a Th Target Tissuementioning

confidence: 99%

Thyroid Cathepsin K: Roles in Physiology and Thyroid Disease

Dauth

Arampatzidou

Rehders

et al. 2011

Clinic Rev Bone Miner Metab

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The human genome encodes 11 cysteine cathepsins belonging to the papain-like family of cysteine peptidases that are known predominantly as endo-lysosomal enzymes. However, it is now understood that the functions and activities of cysteine cathepsins are not limited to endo-lysosomal compartments, as they are also active in the peri-and extracellular space. The thyroid gland is an endocrine organ where such intra-and extracellular proteolytic activities are required to solubilize the prohormone thyroglobulin from its luminal, covalently cross-linked storage forms for subsequent processing into smaller protein fragments and thyroid hormone liberation. Cathepsin K has been identified as one of the cysteine cathepsins with a crucial role in thyroglobulin processing. However, cathepsin K has mainly been a key focus of attention in the last few years because of its high expression in osteoclasts and due to its essential role as collagenase and elastase important for bone remodelling. Besides its remarkable function as an endopeptidase acting on highmolecular mass, covalently cross-linked extracellular substrates such as type I collagen, elastin or thyroglobulin, cathepsin K is also one of the very few proteolytic enzymes that is able to directly liberate thyroxine from thyroglobulin fragments by exopeptidase action. Thus, thyroid cathepsin K is now accepted as a cysteine peptidase with a vital role in liberation of thyroid hormones, which in turn are essential for homoeostasis by triggering a number of important biological processes, ranging from growth and brain development in young vertebrates to tissue remodelling events during morphogenesis or wound healing, as well as control of metabolic pathways and thermoregulation in adults. This review focuses on thyroid cathepsin K and will discuss how localization and trafficking within thyroid epithelial cells explain its thyroid-specific functions. The effects of targeted cathepsin K gene ablation will be summarized from the perspective of the thyroid gland, and we will propose potential consequences of short-and long-term inhibition of thyroid cathepsin K activity for the main thyroid hormone target tissues, namely bone, cardiovascular and immune systems, intestine, and the central nervous system, in addition to the thyroid gland itself.

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Effect of combined treatment with calcitonin on bone densitometry of patients with treated hypothyroidism

Cited by 9 publications

References 29 publications

Role of Thyroid Hormones in Skeletal Development and Bone Maintenance

Role of Thyroid Hormones in Skeletal Development and Bone Maintenance

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

Thyroid Cathepsin K: Roles in Physiology and Thyroid Disease

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