Interactions between GH, IGF-I, Glucocorticoids, and Thyroid Hormones during Skeletal Growth

Robson, Helen; Siebler, Thomas; Shalet, Stephen M; Williams, Graham R.

doi:10.1203/00006450-200208000-00003

Cited by 173 publications

(95 citation statements)

References 163 publications

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“…Although our data appear to provide a compelling temporal correlate of skeletal and sexual maturation, our study was not designed to relate our radiographic assays of skeletal maturation to the processes of puberty and sexual maturation. Thus, our data do not specifically address the commonly held notion that skeletal and sexual maturation processes are mutually responsive to endocrine influences governed by the hypothalamo-pituitary axis (Ojeda and Urbanski, 1994;Robson et al, 2002).…”

Section: Conclusion and Discussionmentioning

confidence: 57%

Ontogeny of Skeletal Maturation in the Juvenile Rat

Horton

Bariteau

Loomis

et al. 2008

The Anatomical Record

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Systemic regulation of the cellular processes that produce endochondral elongation and endochondral mineralization during postnatal skeletal maturation are not completely understood. In particular, a mechanism coupling the decline of cellular activity in the bone microenvironment to the onset of sexual maturity remains elusive. The purpose of this study was to empirically integrate the dynamic progression of bone mineral accrual and endochondral elongation as a function of animal age in growing male and female Sprague-Dawley rats. We used serial dual-energy X-ray absorptiometry (DXA) and radiography to study the temporal progression of bone growth and mineral accrual from weaning to adulthood. We observed that skeletal maturation proceeds in a pattern adequately described by the Gompertz function. During this period of growth, we found that serum markers of osteoblastic bone formation declined with age, while osteoclastic bone resorption activity remained unchanged. We also report a slight lag in the age at inflection in the rate of bone mineral accrual relative to the rate of tibial elongation and that both endochondral processes eventually come to asymptotic equilibrium by approximately 20 weeks of age. In addition, we studied tibial growth plate histomorphometry at select time points through 1 year of age. We report that, despite the histologic persistence of physeal cartilage, very little proliferative or elongative activity was measured in this tissue beyond 20 weeks of age. Taken together, these data provide insight to the temporal coordination of postnatal endochondral growth processes.

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Section: Conclusion and Discussionmentioning

confidence: 57%

Ontogeny of Skeletal Maturation in the Juvenile Rat

Horton

Bariteau

Loomis

et al. 2008

The Anatomical Record

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“…The epiphyseal plate is made up by two zones that have different morphofunctional characteristics (19)(20)(21), and is affected by several hormones, growth factors, and genes (22)(23)(24)(25)(26)(27). However, in spite of the years of research on bone formation and growth, the mechanisms by which specific transcription factors affect the development of the epiphyseal plate and formation of trabecular bones are still unclear, and the role of hypertrophic chondrocytes in the morphogenesis of the trabecular bone is still controversial.…”

Section: Discussionmentioning

confidence: 99%

Effects of excess maternal thyroxin on the bones of rat offspring from birth to the post-weaning period

Maia

Santos

Batista

et al. 2016

Arch. Endocrinol. Metab.

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Objective: To evaluate, in rat offspring, bone changes induced by excess maternal thyroxin during pregnancy and lactation, and to assess the reversibility of these changes after weaning. Material and methods: Twenty Wistar rats were distributed in two groups, hyperthyroid and control, that were treated daily with L-thyroxin (50 mcg/animal) and placebo, respectively. The treatment was initiated seven days before mating and continued throughout pregnancy and lactation. From every female of each of the two groups, two offspring were euthanized after birth, two at 21 days of age (weaning), and two at 42 days of age (21 days after weaning). In newborns, the length of pelvic and thoracic limbs were measured, and in the other animals, the length and width of the femur and humerus were measured. Bones were dissected, decalcified, embedded in paraffin, and analyzed histomorphometrically. Results: Excess maternal thyroxin significantly reduced the length of the pelvic limb in neonates. In 21-day-old individuals, excess maternal thyroxine reduced the length and the width of the femur and the humerus. It also increased thickness of the epiphyseal plate and the percentage of trabecular bone tissue. In 42-day-old individuals, there were no significant differences between groups in relation to the parameters evaluated in the previous periods. Conclusion: Excess maternal thyroxine reduced growth in suckling rats both at birth and at weaning, and it also increased the percentage of trabecular bone tissue in 21-day-old animals. These changes, however, were reversible at 42 days, i.e., 21 days after weaning. Arch Endocrinol Metab. 2016;60(2):130-7

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“…T3 has an indirect role on growth by influencing GH secretion and a direct role which has been shown by the presence of thyroid receptor a1 (TRa1) and thyroid receptor b (TRb) presence in proliferating chondrocytes in the physis. T3 also regulates osteoblast activity, bone turnover and vascular invasion [14,17,18,32,33].…”

Section: Thyroid Hormones and Scfementioning

confidence: 99%

Slipped capital femoral epiphysis and its association with endocrine, metabolic and chronic diseases: A systematic review of the literature

Witbreuk

Kemenade

Sluijs

et al. 2013

Journal of Children's Orthopaedics

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Purpose Puberty, obesity, endocrine and chronic systemic diseases are known to be associated with slipped capital femoral epiphysis (SCFE). The mechanical insufficiency of the physis in SCFE is thought to be the result of an abnormal weakening of the physis. However, the mechanism at the cellular level has not been unravelled up to now. Methods To understand the pathophysiology of endocrine and metabolic factors acting on the physis, we performed a systematic review focussing on published studies reporting on hormonal, morphological and cellular abnormalities of the physis in children with SCFE. In addition, we looked for studies of the effects of endocrinopathies on the human physis which can lead to cause SCFE and focussed in detail on hormonal signalling, hormone receptor expression and extracellular matrix (ECM) composition of the physis. We searched in the PubMed, EMBASE.com and The Cochrane Library (via Wiley) databases from inception to 11thSeptember 2012. The search generated a total of 689 references: 382 in PubMed, 232 in EMBASE.com and 75 in The Cochrane Library. After removing duplicate papers, 525 papers remained. Of these, 119 were selected based on titles and abstracts. After excluding 63 papers not related to the human physis, 56 papers were included in this review. Results Activation of the gonadal axis and the subsequent augmentation of the activity of the growth hormone-insulin-like growth factor 1 (GH-IGF-1) axis are important for the pubertal growth spurt, as well as for cessation of the physis at the end of puberty. The effects of leptin, thyroid hormone and corticosteroids on linear growth and on the physis are also discussed. Children with chronic diseases suffer from inflammation, acidosis and malnutrition. These consequences of chronic diseases affect the GH-IGF-1 axis, thereby, increasing the risk of the development of SCFE. The risk of SCFE and avascular necrosis in children with chronic renal insufficiency, growth hormone treatment and renal osteodystrophy remains equivocal. Conclusions SCFE is most likely the result of a multifactorial event during adolescence when height and weight increase dramatically and the delicate balance between the various hormonal equilibria can be disturbed. Up to now, there are no screening or diagnostic tests available to predict patients at risk.

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Interactions between GH, IGF-I, Glucocorticoids, and Thyroid Hormones during Skeletal Growth

Cited by 173 publications

References 163 publications

Ontogeny of Skeletal Maturation in the Juvenile Rat

Ontogeny of Skeletal Maturation in the Juvenile Rat

Effects of excess maternal thyroxin on the bones of rat offspring from birth to the post-weaning period

Slipped capital femoral epiphysis and its association with endocrine, metabolic and chronic diseases: A systematic review of the literature

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