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Abstract

Longitudinal bone growth occurs in the growth plate through a process called endochondral bone formation, a process where resting zone chondrocytes are recruited to start active proliferation and then undergo differentiation, followed by apoptosis and later mineralization. The balance between proliferation and differentiation is a crucial regulatory step controlled by various growth factors/hormones acting in both endocrine and paracrine/autocrine ways. From studies of individuals with aromatase deficiency and a boy with defective oestrogen receptor (ER)-alpha it has become clear that oestrogen action is indispensable for normal pubertal growth and growth plate fusion. Both oestrogen receptors, ER-alpha and ER-beta, are expressed in the growth plate in boys and girls throughout pubertal development. Any functional role of ER-beta has not yet been defined in the human growth plate. Increased understanding about the effects of oestrogen and the interactions between oestrogens and other endocrine factors within the growth plate is important for the development of new treatment strategies in different disorders affecting longitudinal bone growth. As new specific modulators of oestrogen receptors are developed, these could offer more specific ways to modulate longitudinal growth and growth plate fusion. (c) 2005 S. Karger AG, Basel.

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Systemic and local regulation of the growth plate.

B C J van der Eerden, M. Karperien, J Wit (2003)

The growth plate is the final target organ for longitudinal growth and results from chondrocyte proliferation and differentiation. During the first year of life, longitudinal growth rates are high, followed by a decade of modest longitudinal growth. The age at onset of puberty and the growth rate during the pubertal growth spurt (which occurs under the influence of estrogens and GH) contribute to sex difference in final height between boys and girls. At the end of puberty, growth plates fuse, thereby ceasing longitudinal growth. It has been recognized that receptors for many hormones such as estrogen, GH, and glucocorticoids are present in or on growth plate chondrocytes, suggesting that these hormones may influence processes in the growth plate directly. Moreover, many growth factors, i.e., IGF-I, Indian hedgehog, PTHrP, fibroblast growth factors, bone morphogenetic proteins, and vascular endothelial growth factor, are now considered as crucial regulators of chondrocyte proliferation and differentiation. In this review, we present an update on the present perception of growth plate function and the regulation of chondrocyte proliferation and differentiation by systemic and local regulators of which most are now related to human growth disorders.

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Effects of estrogen on growth plate senescence and epiphyseal fusion.

K Barnes, Flávio S J de Souza, J Barón … (2001)

Estrogen is critical for epiphyseal fusion in both young men and women. In this study, we explored the cellular mechanisms by which estrogen causes this phenomenon. Juvenile ovariectomized female rabbits received either 70 microg/kg estradiol cypionate or vehicle i.m. once a week. Growth plates from the proximal tibia, distal tibia, and distal femur were analyzed after 2, 4, 6, or 8 weeks of treatment. In vehicle-treated animals, there was a gradual senescent decline in tibial growth rate, rate of chondrocyte proliferation, growth plate height, number of proliferative chondrocytes, number of hypertrophic chondrocytes, size of terminal hypertrophic chondrocytes, and column density. Estrogen treatment accelerated the senescent decline in all of these parameters. In senescent growth plates, epiphyseal fusion was observed to be an abrupt event in which all remaining chondrocytes were rapidly replaced by bone elements. Fusion occurred when the rate of chondrocyte proliferation approached zero. Estrogen caused this proliferative exhaustion and fusion to occur earlier. Our data suggest that (i) epiphyseal fusion is triggered when the proliferative potential of growth plate chondrocytes is exhausted; and (ii) estrogen does not induce growth plate ossification directly; instead, estrogen accelerates the programmed senescence of the growth plate, thus causing earlier proliferative exhaustion and consequently earlier fusion.

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Localization of estrogen receptors-alpha and -beta and androgen receptor in the human growth plate at different pubertal stages.

Anders Boman, E M Ritzen, Lars Sävendahl … (2003)

Sex steroids are required for a normal pubertal growth spurt and fusion of the human epiphyseal growth plate. However, the localization of sex steroid receptors in the human pubertal growth plate remains controversial. We have investigated the expression of estrogen receptor (ER) alpha, ERbeta and androgen receptor (AR) in biopsies of proximal tibial growth plates obtained during epiphyseal surgery in 16 boys and eight girls. All pubertal stages were represented (Tanner stages 1-5). ERalpha, ERbeta and AR were visualized with immunohistochemistry and the number of receptor-positive cells was counted using an image analysis system. Percent receptor-positive chondrocytes were assessed in the resting, proliferative and hypertrophic zones and evaluated for sex differences and pubertal trends. Both ERalpha- and ERbeta-positive cells were detected at a greater frequency in the resting and proliferative zones than in the hypertrophic zone (64+/-2%, 64+/-2% compared with 38+/-3% for ERalpha, and 63+/-3%, 66+/-3% compared with 53+/-3% for ERbeta), whereas AR was more abundant in the resting (65+/-3%) and hypertrophic zones (58+/-3%) than in the proliferative zone (41+/-3%). No sex difference in the patterns of expression was detected. For ERalpha and AR, the percentage of receptor-positive cells was similar at all Tanner pubertal stages, whereas ERbeta showed a slight decrease in the proliferative zone during pubertal development (P<0.05). In summary, our findings suggest that ERalpha, ERbeta and AR are expressed in the human growth plate throughout pubertal development, with no difference between the sexes.

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PubMed ID:: 16286781

DOI:: 10.1159/000087764

ScienceOpen disciplines: Chemistry

Keywords: Androgens,physiology,Animals,Apoptosis,Bone Development,drug effects,Child,Estrogens,Growth Plate,Humans,Male,Selective Estrogen Receptor Modulators,pharmacology

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ScienceOpen disciplines: Chemistry

Keywords: Androgens, physiology, Animals, Apoptosis, Bone Development, drug effects, Child, Estrogens, Growth Plate, Humans, Male, Selective Estrogen Receptor Modulators, pharmacology

Hormonal regulation of growth plate cartilage.

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Karger: Endocrinology

Most cited references 16

Systemic and local regulation of the growth plate.

Effects of estrogen on growth plate senescence and epiphyseal fusion.

Localization of estrogen receptors-alpha and -beta and androgen receptor in the human growth plate at different pubertal stages.

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