Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2002;4(2):94-106.
doi: 10.1186/ar396. Epub 2001 Nov 8.

The life cycle of chondrocytes in the developing skeleton

Affiliations
Review

The life cycle of chondrocytes in the developing skeleton

Lillian Shum et al. Arthritis Res. 2002.

Abstract

Cartilage serves multiple functions in the developing embryo and in postnatal life. Genetic mutations affecting cartilage development are relatively common and lead to skeletal malformations, dysfunction or increased susceptibility to disease or injury. Characterization of these mutations and investigation of the molecular pathways in which these genes function have contributed to an understanding of the mechanisms regulating skeletal patterning, chondrogenesis, endochondral ossification and joint formation. Extracellular growth and differentiation factors including bone morphogenetic proteins, fibroblast growth factors, parathyroid hormone-related peptide, extracellular matrix components, and members of the hedgehog and Wnt families provide important signals for the regulation of cell proliferation, differentiation and apoptosis. Transduction of these signals within the developing mesenchymal cells and chondrocytes results in changes in gene expression mediated by transcription factors including Smads, Msx2, Sox9, signal transducer and activator of transcription (STAT), and core-binding factor alpha 1. Further investigation of the interactions of these signaling pathways will contribute to an understanding of cartilage growth and development, and will allow for the development of strategies for the early detection, prevention and treatment of diseases and disorders affecting the skeleton.

PubMed Disclaimer

Figures

Figure 1
Figure 1
A section through the growth plate of a fetal mouse metatarsal, 17 days post fertilization. Blue staining indicates endogenous alkaline phosphatase activity in the hypertrophic chondrocytes, diaphyseal perichondrium and bone collar, and primary spongiosa. Safranin O staining of chondromucin in the cartilage matrix is red. The regions populated by each stage of the chondrocyte lineage are shown.

Similar articles

Cited by

References

    1. Nuckolls GH, Shum L, Slavkin HC. Progress toward understanding craniofacial malformations. Cleft Palate Craniofac J. 1999;36:12–26. - PubMed
    1. Felson DT, Lawrence RC, Dieppe PA, Hirsch R, Helmick CG, Jordan JM, Kington RS, Lane NE, Nevitt MC, Zhang Y, Sowers M, McAlindon T, Spector TD, Poole AR, Yanovski SZ, Ateshian G, Sharma L, Buckwalter JA, Brandt KD, Fries JF. Osteoarthritis: new insights. Part 1: the disease and its risk factors. Ann Intern Med. 2000;133:635–646. - PubMed
    1. Loughlin J. Genetic epidemiology of primary osteoarthritis. Curr Opin Rheumatol. 2001;13:111–116. doi: 10.1097/00002281-200103000-00004. - DOI - PubMed
    1. Hill DJ, Logan A. Peptide growth factors and their interactions during chondrogenesis. Prog Growth Factor Res. 1992;4:45–68. - PubMed
    1. Underhill TM, Sampaio AV, Weston AD. Retinoid signalling and skeletal development. Novartis Found Symp. 2001;232:171–185. - PubMed

Publication types

MeSH terms