Impact of Growth Plate Senescence on Catch-up Growth and Epiphyseal Fusion

Overview

Journal Pediatr Nephrol

Specialties Nephrology
Pediatrics

Date 2005 Feb 22

PMID 15723267

Citations 10

Authors

Ola Nilsson

Jeffrey Baron

Affiliations

Soon will be listed here.

Abstract

In mammals, longitudinal bone growth occurs rapidly in prenatal and early postnatal life, but then slows and eventually ceases. This deceleration, which reflects a decline in chondrocyte proliferation, was previously attributed to a hormonal or other systemic mechanism. However, new evidence suggests that it is due to a local mechanism within the growth plate. In particular, recent findings suggest that growth plate chondrocytes have a finite proliferative capacity that is gradually exhausted, causing growth to slow and finally stop. This concept has provided insight into clinical phenomena including catch-up growth after transient growth inhibition, catch-down growth after transient estrogen exposure, and epiphyseal fusion.

Citing Articles

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Kvist O, Dallora A, Nilsson O, Anderberg P, Berglund J, Flodmark C Acta Paediatr. 2020; 110(4):1249-1256.

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Effect of dihydrotestosterone, 17-β-estrogen, genistein and equol on remodeling and morphology of bone in osteoporotic male rats during bone healing.

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Leptin induces osteocalcin expression in ATDC5 cells through activation of the MAPK-ERK1/2 signaling pathway.

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Genetically engineered flavonol enriched tomato fruit modulates chondrogenesis to increase bone length in growing animals.

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