Acceleration of growth and bone maturation in childhood thyrotoxicosis

Schlesinger, Stephen; MacGillivray, Margaret H.; Munschauer, Richard W.

doi:10.1016/s0022-3476(73)80481-0

Cited by 37 publications

(19 citation statements)

References 15 publications

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“…Advanced BA is generally accompanied by clinical features indicative of accelerated bone maturation such as extremely tall stature [19], obesity [18], hyperthyroidism [12], premature adrenarche [10,11,13] or early sexual maturation [9,14,15], as well as by elevated levels of hormones influencing the skeletal maturation rate. Indeed, in the vast majority of the 650 patients with the registered diagnosis of BA advancement, review of the medical files revealed the etiology for the accelerated bone maturation.…”

Section: Discussionmentioning

confidence: 99%

“…Delay or advance in the bone maturation rate may be associated with various endocrine disorders [1,2]. Among the most common causes for markedly accelerated bone maturation are prolonged exposure to elevated levels of estradiol, testosterone or adrenal androgens, as in precocious puberty [9] or congenital adrenal hyperplasia [10,11], and persistent hyperthyroidism [12]. Mildly advanced BA is found in precocious adrenarche [13] and to a lesser extent in premature thelarche [14,15].…”

Section: Introductionmentioning

confidence: 99%

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Natural History of Idiopathic Advanced Bone Age Diagnosed in Childhood: Pattern of Growth and Puberty

et al. 2010

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Background: Significant idiopathic bone age (BA) advancement is defined as BA >2 SD above the mean chronological age (CA) with no underlying etiology. BA advancement due to endocrinopathies is associated with early puberty and compromised adult height (AHt), necessitating treatment. The natural history of idiopathic BA advancement is not well-established. Aim: To determine the pattern of growth and puberty, and validity of AHt prediction in idiopathic BA advancement. Methods: Fifty-five prepubertal patients (20 boys aged 6.7 ± 2.2 years, 35 girls aged 6.4 ± 2.0 years) evaluated between 1985 and 2008 were found to have idiopathic BA advancement. Assessed during follow-up were: BA, height (Ht), weight (Wt), pubertal course and predicted AHt (PAHt). Attained AHt was compared to PAHt and to midparental Ht (MPHt). Results: Throughout follow-up, BA-SDS (SD score) significantly declined (p < 0.001), Ht-SDS significantly decreased (p = 0.006) and Wt-SDS did not change. Pubertal onset, duration and growth were within the normal range. Attained AHts did not differ significantly from MPHts (boys: 172 ± 6.7 vs. 171 ± 6.1 cm; girls: 160.5 ± 6.5 vs. 159.0 ± 6.8 cm). PAHts using the ‘accelerated’ tables of Bayley and Pinneau were accurate. Conclusion: Idiopathic BA advancement differs from BA advancement with underlying endocrinopathy in evolution of BA progression (decline in BA-SDS), growth pattern, validity of AHt prediction and uncompromised AHt. This indicates that it requires minimal clinical monitoring and usually does not mandate treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Natural History of Idiopathic Advanced Bone Age Diagnosed in Childhood: Pattern of Growth and Puberty

et al. 2010

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“…Thyrotoxicosis in childhood accelerates linear growth and advances bone age, but ultimately results in persistent short stature due to early fusion of the epiphyses. In severe cases, craniosynostosis results from premature closure of the skull sutures and fontanelles and may be associated with intellectual deficit [38,39] . Furthermore, in congenital hyperthyroidism resulting from constitutive activating mutations of the TSH receptor gene ( TSHR ), advanced bone age has been reported, although early thyroidectomy is effective to prevent long-term consequences of hyperthyroidism [40] .…”

Section: Thyroid Hormone Effects On Linear Growth and Skeletal Develomentioning

confidence: 99%

Thyroid Hormone Actions in Cartilage and Bone

Williams¹

2012

Eur Thyroid J

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T3 action in bone are considered in relation to mutant mouse models and to effects on bone mineral density and fracture susceptibility in humans. Finally, new studies identifying a putative role for thyroid hormone metabolism in articular cartilage maintenance and the pathogenesis of osteoarthritis are considered. The pharmacological context of these new findings is discussed, emphasising the importance of this emerging field of study in thyroid hormone pathophysiology.Copyright © 2012 European Thyroid Association Published by S. Karger AG, Basel Regulation of Thyroid Hormone Action Hypothalamic-Pituitary-Thyroid AxisThe thyroid gland produces mainly the pro-hormone T4 (3,5,3 ,5 -L -tetraiodothyronine, thyroxine) but also secretes smaller amounts of the active hormone T3 (3,5,3 -L -triiodothyronine). Most circulating T3 is derived via metabolism of T4, from which an outer-ring iodine atom is removed by activity of the type 1 iodothyronine deiodinase enzyme (Dio1) principally in liver and kidney [1] . The hypothalamic-pituitary-thyroid (HPT) axis senses circulating thyroid hormone concentrations and physiological thyroid status is controlled by negative feedback Key WordsThyroid hormone ؒ Cartilage ؒ Chondrocyte ؒ Ossification ؒ Osteoarthritis ؒ Bone ؒ Bone turnover ؒ Osteoblast ؒ Osteoclast ؒ Osteoporosis Abstract Thyroid hormones exert widespread and complex actions in almost all tissues during development, throughout childhood and in adults. The skeleton is an important T3-target tissue that exemplifies these processes, and yet understanding of the specific cellular and molecular mechanisms of T3 action in bone and cartilage remains incomplete. Here, the skeleton is considered as a T3-target tissue. The actions of thyroid hormones during skeletal development and in chondrocytes and growth plate cartilage during post-natal linear growth are outlined. The physiological importance of these actions are discussed in relation to patients with autosomal dominant mutations in genes encoding the thyroid hormone receptors TR ␣ 1 and TR ␤ , and in mice harbouring deletions or mutations of the orthologous genes. The role of thyroid hormones and the control of T3 action in bone turnover and maintenance are also outlined, and T3 action in boneforming osteoblasts and bone-resorbing osteoclasts discussed. The physiological and functional consequences of

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“…Mice with targeted disruption of TH receptors (THRs) exhibit reduced bone length and bone mass (5,12,13,44). By contrast, childhood thyrotoxicosis accelerates bone formation with premature closure of the growth plates and skull sutures, leading to short stature and craniosynostosis (15,19,37). The increase in TH levels during the prepubertal growth period is obligatory for the increase in IGF-I expression and trabecular bone mass during this period in mice (47,48).…”

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confidence: 99%

Thyroid hormone receptor-β1 signaling is critically involved in regulating secondary ossification via promoting transcription of the Ihh gene in the epiphysis

Xing

Aghajanian

Goodluck

et al. 2016

American Journal of Physiology-Endocrinology and Metabolism

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roid hormone (TH) action is mediated through two nuclear TH receptors, THR␣ and THR␤. Although the role of THR␣ is well established in bone, less is known about the relevance of THR␤-mediated signaling in bone development. On ther basis of our recent finding that TH signaling is essential for initiation and formation of secondary ossification center, we evaluated the role of THRs in mediating TH effects on epiphysial bone formation. Two-day treatment of TH-deficient Tshr Ϫ/Ϫ mice with TH increased THR␤1 mRNA level 3.4-fold at day 7 but had no effect on THR␣1 mRNA level at the proximal tibia epiphysis. Treatment of serum-free cultures of tibias from 3-day-old mice with T3 increased THR␤1 expression 2.1-and 13-fold, respectively, at 24 and 72 h. Ten-day treatment of Tshr Ϫ/Ϫ newborns (days 5-14) with THR␤1 agonist GC1 at 0.2 or 2.0 g/day increased BV/TV at day 21 by 225 and 263%, respectively, compared with vehicle treatment. Two-day treatment with GC1 (0.2 g/day) increased expression levels of Indian hedgehog (Ihh) 100-fold, osterix 15-fold, and osteocalcin 59-fold compared with vehicle at day 7 in the proximal tibia epiphysis. Gel mobility shift assay demonstrated that a putative TH response element in the distal promoter of mouse Ihh gene interacted with THR␤1. GC1 treatment (1 nM) increased Ihh distal promoter activity 20-fold after 48 h in chondroctyes. Our data suggest a novel role for THR␤1 in secondary ossification at the epiphysis that involves transcriptional upregulation of Ihh gene. thyroid hormones; ossification; bone formation; osteoblasts; chondrocytes; hypothyroidism; Indian hedge hog ENDOCHONDRAL OSSIFICATION is one of two essential processes required for fetal development of the mammalian skeletal system and for fracture healing. Unlike intramembranous ossification, which is the other process by which mesenchymal cells from the cranial neural crest, sclerotomes, and lateral plate mesoderm migrate and proliferate, forming mesenchymal condensations, cartilage is present and replaced by trabecular bone during endochondral ossification (16,35). There are two centers of ossification for endochondral ossification, a primary and a secondary center. The primary ossification center (POC) usually appears in the diaphysis of the long bones or in the body of the irregular bones during prenatal development while the secondary ossification center (SOC) occurs in the epiphysis of long bones at the time of birth in mammals (11). Endochondral ossification at the POC is tightly regulated by a number of growth factors (PTHrp, IHH, IGF-I, BMP/TGF␤, Wnt, VEGF) and transcription factors (Sox9, Runx2, osterix, ␤-catenin) (3, 10, 21-23, 29, 42, 53). Dysregulation in the production and/or actions of any of the factors that regulate endochondral ossification can result in skeletal diseases including chondrodysplasias and osteoarthritis (21, 40). Although the processes leading to POC formation have been well established, signaling pathways that stimulate SOC formation are not well understood.Thyroid hormone (TH) is known ...

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Acceleration of growth and bone maturation in childhood thyrotoxicosis

Cited by 37 publications

References 15 publications

Natural History of Idiopathic Advanced Bone Age Diagnosed in Childhood: Pattern of Growth and Puberty

Natural History of Idiopathic Advanced Bone Age Diagnosed in Childhood: Pattern of Growth and Puberty

Thyroid Hormone Actions in Cartilage and Bone

Thyroid hormone receptor-β1 signaling is critically involved in regulating secondary ossification via promoting transcription of the Ihh gene in the epiphysis

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