Pubertal growth and epiphyseal fusion

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Abstract

The complex networks of nutritional, cellular, paracrine, and endocrine factors are closely related with pubertal growth and epiphyseal fusion. Important influencing factors include chondrocyte differentiation capacity, multiple molecular pathways active in the growth plate, and growth hormone-insulin-like growth factor-I axis activation and epiphyseal fusion through estrogen and its receptors. However, the exact mechanisms of these phenomena are still unclear. A better understanding of the detailed processes involved in the pubertal growth spurt and growth plate closure in longitudinal bone growth will help us develop methods to efficiently promote pubertal growth and delay epiphyseal fusion with fewer adverse effects.

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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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Endocrine Regulation of the Growth Plate

Ola Nilsson, Rose Marino, Francesco De Luca … (2005)

Longitudinal bone growth occurs at the growth plate by endochondral ossification. Within the growth plate, chondrocyte proliferation, hypertrophy, and cartilage matrix secretion result in chondrogenesis. The newly formed cartilage is invaded by blood vessels and bone cells that remodel the newly formed cartilage into bone tissue. This process of longitudinal bone growth is governed by a complex network of endocrine signals, including growth hormone, insulin-like growth factor I, glucocorticoid, thyroid hormone, estrogen, androgen, vitamin D, and leptin. Many of these signals regulate growth plate function, both by acting locally on growth plate chondrocytes and also indirectly by modulating other endocrine signals in the network. Some of the local effects of hormones are mediated by changes in paracrine factors that control chondrocyte proliferation and differentiation. Many human skeletal growth disorders are caused by abnormalities in the endocrine regulation of the growth plate. This review provides an overview of the endocrine signals that regulate longitudinal bone growth, their interactions, and the mechanisms by which they affect growth plate chondrogenesis.

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Sex steroid actions in male bone.

Dirk Vanderschueren, Michaël R Laurent, Frank Claessens … (2014)

Sex steroids are chief regulators of gender differences in the skeleton, and male gender is one of the strongest protective factors against osteoporotic fractures. This advantage in bone strength relies mainly on greater cortical bone expansion during pubertal peak bone mass acquisition and superior skeletal maintenance during aging. During both these phases, estrogens acting via estrogen receptor-α in osteoblast lineage cells are crucial for male cortical and trabecular bone, as evident from conditional genetic mouse models, epidemiological studies, rare genetic conditions, genome-wide meta-analyses, and recent interventional trials. Genetic mouse models have also demonstrated a direct role for androgens independent of aromatization on trabecular bone via the androgen receptor in osteoblasts and osteocytes, although the target cell for their key effects on periosteal bone formation remains elusive. Low serum estradiol predicts incident fractures, but the highest risk occurs in men with additionally low T and high SHBG. Still, the possible clinical utility of serum sex steroids for fracture prediction is unknown. It is likely that sex steroid actions on male bone metabolism rely also on extraskeletal mechanisms and cross talk with other signaling pathways. We propose that estrogens influence fracture risk in aging men via direct effects on bone, whereas androgens exert an additional antifracture effect mainly via extraskeletal parameters such as muscle mass and propensity to fall. Given the demographic trends of increased longevity and consequent rise of osteoporosis, an increased understanding of how sex steroids influence male bone health remains a high research priority.

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Author and article information

Journal

Journal ID (nlm-ta): Ann Pediatr Endocrinol Metab

Journal ID (iso-abbrev): Ann Pediatr Endocrinol Metab

Journal ID (publisher-id): APEM

Title: Annals of Pediatric Endocrinology & Metabolism

Publisher: The Korean Society of Pediatric Endocrinology

ISSN (Print): 2287-1012

ISSN (Electronic): 2287-1292

Publication date (Print): March 2015

Publication date (Electronic): 31 March 2015

Volume: 20

Issue: 1

Pages: 8-12

Affiliations

Department of Pediatrics, Kyung Hee University Hospital at Gangdong, Kyung Hee University School of Medicine, Seoul, Korea.

Author notes

Address for correspondence: Kye Shik Shim, MD, PhD. Department of Pediatrics, Kyung Hee University Hospital at Gangdong, Kyung Hee University School of Medicine, 892 Dongnam-ro, Gangdong-gu, Seoul 134-727, Korea. Tel: +82-2-440-6131, Fax: +82-2-440-6073, 64sks@ 123456khnmc.or.kr

Article

DOI: 10.6065/apem.2015.20.1.8

PMC ID: 4397276

PubMed ID: 25883921

SO-VID: 8eea3328-3464-444d-89d5-3948e3884cc3

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Pubertal growth and epiphyseal fusion

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Animal models of intrauterine growth restriction (IUGR)

Most cited references 34

Systemic and local regulation of the growth plate.

Endocrine Regulation of the Growth Plate

Sex steroid actions in male bone.

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