FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |   Search Term  Advanced Search

Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe

Previous Volume 347:210-212 July 18, 2002 Number 3 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

	Full Text PDF PDA Full Text Purchase this article Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited Related Article by Whyte, M. P. PubMed Citation

Over the past decade, we have learned a great deal about how skeletal development and remodeling are controlled.¹ Some of our knowledge has been derived from genetic analysis of diseases in humans, whereas other important information has come from targeting mutations in mice. In some instances, the two approaches have complemented each other, as occurred in the identification of core binding factor 1 as a major regulator of osteoblast differentiation in mice^2,3,4 and the nearly simultaneous demonstration of the mutation in one allele of the gene for core binding factor 1 as the cause of human cleidocranial dysplasia and the . . . [Full Text of this Article]

This article has been cited by other articles:

• Mosig, R. A., Dowling, O., DiFeo, A., Ramirez, M. C. M., Parker, I. C., Abe, E., Diouri, J., Aqeel, A. A., Wylie, J. D., Oblander, S. A., Madri, J., Bianco, P., Apte, S. S., Zaidi, M., Doty, S. B., Majeska, R. J., Schaffler, M. B., Martignetti, J. A. (2007). Loss of MMP-2 disrupts skeletal and craniofacial development and results in decreased bone mineralization, joint erosion and defects in osteoblast and osteoclast growth. Hum Mol Genet 16: 1113-1123 [Abstract] [Full Text]  
• Hamerman, D. (2005). Osteoporosis and atherosclerosis: biological linkages and the emergence of dual-purpose therapies. QJM 98: 467-484 [Abstract] [Full Text]