Get access

The Developing Mouse Dentition

A New Tool for Apoptosis Study

Authors

  • RENATA PETERKOVÁ,

    Corresponding author
    1. Institute of Experimental Medicine, Academy of Sciences CR, Videnska 1083, 142 20 Prague 4, Czech Republic
    • Address for correspondence: R. Peterková, Institute of Experimental Medicine, Academy of Sciences CR, Videnska 1083, 142 20 Prague 4, Czech Republic. Voice: +420-241-062-232; fax: +420-241-062-604. repete@biomed.cas.cz

    Search for more papers by this author
  • MIROSLAV PETERKA,

    1. Institute of Experimental Medicine, Academy of Sciences CR, Videnska 1083, 142 20 Prague 4, Czech Republic
    Search for more papers by this author
  • HERVÉ LESOT

    1. INSERM U-595, 11, rue Humann, 67085 Strasbourg, France
    Search for more papers by this author

  • Positional information specifies cells in a coordinate system.81 Reaction-diffusion processes generate spatial variation depending on interactions between activator and inhibitor substances.63,82

Abstract

Abstract: Developing limb or differentiating neural and blood cells are traditional models used to study programmed cell death in mammals. The developing mouse dentition can also be an attractive model for studying apoptosis regulation. Apoptosis is most extant during early odontogenesis in mice. The embryonic tooth pattern is comprised not only of anlagen of functional teeth (incisor, molars), but also of vestiges of ancestral tooth primordia that must be suppressed. Apoptosis is involved in (a) the elimination of vestigial tooth primordia in the prospective toothless gap (diastema) between the incisor and molars and (b) the shaping of germs in functional teeth. This type of apoptosis occurs in the dental epithelium according to a characteristic temporo-spatial pattern. Where apoptosis concentrates, specific signaling is also found. We proposed a hypothesis to explain the stimulation of apoptosis in the dental epithelium by integrating two concepts: (1) The regulation of epithelial budding by positional information generated from interactions between growth-activating and growth-inhibiting signals, and (2) apoptosis stimulation by the failure of death-suppressing signals. During the budding of the dental epithelium, local excess in growth inhibitors (e.g., Bmps) might lead to the epithelial cells' failure to receive adequate growth-activating (apoptosis-suppressing) signals (e.g., Fgfs). The resulting signal imbalance leads to cell “suicide” by apoptosis. Understanding of apoptosis regulation in the vestigial tooth primordia can help to elucidate the mechanism of their suppression during evolution and to identify factors essential for tooth survival. The latter knowledge will be important for developing a technology of tooth engineering.

Ancillary