Tooth development has attracted the attention of researchers since the 19th century. It became obvious even then that morphogenesis could not fully be appreciated from two-dimensional histological sections. Therefore, methods of three-dimensional (3D) reconstructions were employed to visualize the surface morphology of developing structures and to help appreciate the complexity of early tooth morphogenesis. The present review surveys the data provided by computer-aided 3D analyses to update classical knowledge of early odontogenesis in the laboratory mouse and in humans. 3D reconstructions have demonstrated that odontogenesis in the early stages is a complex process which also includes the development of rudimentary odontogenic structures with different fates. Their developmental, evolutionary, and pathological aspects are discussed. The combination of in situ hybridization and 3D reconstruction have demonstrated the temporo-spatial dynamics of the signalling centres that reflect transient existence of rudimentary tooth primordia at loci where teeth were present in ancestors. The rudiments can rescue their suppressed development and revitalize, and then their subsequent autonomous development can give rise to oral pathologies. This shows that tooth-forming potential in mammals can be greater than that observed from their functional dentitions. From this perspective, the mouse rudimentary tooth primordia represent a natural model to test possibilities of tooth regeneration.

• Keywords
• 3D reconstruction, Tooth, development, human, mouse, odontogenesis,
• MeSH
• Biological Evolution MeSH
• Dentition MeSH
• Diastema embryology   MeSH
• In Situ Hybridization methods   MeSH
• Humans MeSH
• Mice MeSH
• Odontogenesis * genetics   physiology   MeSH
• Image Processing, Computer-Assisted MeSH
• Regeneration MeSH
• Imaging, Three-Dimensional methods   MeSH
• Tooth, Supernumerary embryology   MeSH
• Tooth embryology   physiology   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH

An understanding of the factors that promote or inhibit tooth development is essential for designing biological tooth replacements. The embryonic mouse dentition provides an ideal system for studying such factors because it consists of two types of tooth primordia. One type of primordium will go on to form a functional tooth, whereas the other initiates development but arrests at or before the bud stage. This developmental arrest contributes to the formation of the toothless mouse diastema. It is accompanied by the apoptosis of the rudimentary diastemal buds, which presumably results from the insufficient activity of anti-apoptotic signals such as fibroblast growth factors (FGFs). We have previously shown that the arrest of a rudimentary tooth bud can be rescued by inactivating Spry2, an antagonist of FGF signaling. Here, we studied the role of the epithelial cell death and proliferation in this process by comparing the development of a rudimentary diastemal tooth bud (R(2)) and the first molar in the mandibles of Spry2(-/-) and wild-type (WT) embryos using histological sections, image analysis and 3D reconstructions. In the WT R(2) at embryonic day 13.5, significantly increased apoptosis and decreased proliferation were found compared with the first molar. In contrast, increased levels of FGF signaling in Spry2(-/-) embryos led to significantly decreased apoptosis and increased proliferation in the R(2) bud. Consequently, the R(2) was involved in the formation of a supernumerary tooth primordium. Studies of the revitalization of rudimentary tooth primordia in mutant mice can help to lay the foundation for tooth regeneration by enhancing our knowledge of mechanisms that regulate tooth formation.

• MeSH
• Adaptor Proteins, Signal Transducing MeSH
• Apoptosis * MeSH
• In Situ Hybridization MeSH
• Intracellular Signaling Peptides and Proteins MeSH
• Membrane Proteins genetics   physiology   MeSH
• Morphogenesis MeSH
• Mice, Knockout MeSH
• Mice MeSH
• Cell Proliferation * MeSH
• Protein Serine-Threonine Kinases MeSH
• Tooth growth & development   MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Research Support, N.I.H., Extramural MeSH
• Names of Substances
• Adaptor Proteins, Signal Transducing MeSH
• Intracellular Signaling Peptides and Proteins MeSH
• Membrane Proteins MeSH
• Protein Serine-Threonine Kinases MeSH
• Spry2 protein, mouse MeSH Browser

Craniopharyngioma is a rare benign tumour originating from Rathke's pouch. This paper reports a tumour case studied with a set of markers defining protein-carbohydrate recognition. Expression of endogenous lectins and their reactive glycoligands is under differentiation-dependent control in many cell types. These parameters can be related to the degree of cell differentiation in tumours. Therefore, the expression patterns of endogenous lectins, namely galectins-1, -3, and -7, in the craniopharyngioma case were determined. Galectins-1 and -3 were also used to reveal glycoconjugates in cells and extracellular matrices, an approach that has heretofore relied largely on plant lectins. The staining pattern of craniopharyngioma is compared with that of two other types of ectodermally derived tumours, namely basal and squamous cell carcinomas. Clusters of polygonal and flattened cells with morphological characteristics of differentiated cells in the craniopharyngioma and the majority of poorly differentiated cells in squamous cell carcinomas were reactive with galectin-3. No binding of this probe was observed in cells of basal cell carcinomas and the majority of craniopharyngioma cells. In view of the lack of accessible binding in the basal layer of normal squamous epithelia where proliferative cells (including stem cells) are located, galectin-3 binding could be used to distinguish basal from suprabasal cells of squamous epithelial cells.

• MeSH
• Neoplasms, Basal Cell metabolism   pathology   MeSH
• Cell Differentiation physiology   MeSH
• Adult MeSH
• Epithelium metabolism   pathology   MeSH
• Epitopes MeSH
• Phenotype MeSH
• Microscopy, Fluorescence MeSH
• Galectins metabolism   MeSH
• Histocytochemistry MeSH
• Keratins metabolism   MeSH
• Craniopharyngioma metabolism   pathology   MeSH
• Lectins MeSH
• Humans MeSH
• Antibodies, Monoclonal MeSH
• Biomarkers, Tumor MeSH
• Pituitary Neoplasms metabolism   pathology   MeSH
• Polysaccharides metabolism   MeSH
• Carcinoma, Squamous Cell metabolism   pathology   MeSH
• Binding Sites MeSH
• Check Tag
• Adult MeSH
• Humans MeSH
• Male MeSH
• Publication type
• Journal Article MeSH
• Case Reports MeSH
• Research Support, Non-U.S. Gov't MeSH
• Comparative Study MeSH
• Names of Substances
• Epitopes MeSH
• Galectins MeSH
• Keratins MeSH
• Lectins MeSH
• Antibodies, Monoclonal MeSH
• Biomarkers, Tumor MeSH
• Polysaccharides MeSH