The development of a tooth germ in a precise size, shape, and position in the jaw, involves meticulous regulation of cell proliferation and cell death. Apoptosis, as the most common type of programmed cell death during embryonic development, plays a number of key roles during odontogenesis, ranging from the budding of the oral epithelium during tooth initiation, to later tooth germ morphogenesis and removal of enamel knot signaling center. Here, we summarize recent knowledge about the distribution and function of apoptotic cells during odontogenesis in several vertebrate lineages, with a special focus on amniotes (mammals and reptiles). We discuss the regulatory roles that apoptosis plays on various cellular processes during odontogenesis. We also review apoptosis-associated molecular signaling during tooth development, including its relationship with the autophagic pathway. Lastly, we cover apoptotic pathway disruption, and alterations in apoptotic cell distribution in transgenic mouse models. These studies foster a deeper understanding how apoptotic cells affect cellular processes during normal odontogenesis, and how they contribute to dental disorders, which could lead to new avenues of treatment in the future.

• Keywords
• apoptosis, dental lamina, morphogenesis, odontogenesis, teeth,
• Publication type
• Journal Article MeSH
• Review MeSH

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

Apoptosis is an important morphogenetic event in embryogenesis as well as during postnatal life. In the last 2 decades, apoptosis in tooth development (odontogenesis) has been investigated with gradually increasing focus on the mechanisms and signaling pathways involved. The molecular machinery responsible for apoptosis exhibits a high degree of conservation but also organ and tissue specific patterns. This review aims to discuss recent knowledge about apoptotic signaling networks during odontogenesis, concentrating on the mouse, which is often used as a model organism for human dentistry. Apoptosis accompanies the entire development of the tooth and corresponding remodeling of the surrounding bony tissue. It is most evident in its role in the elimination of signaling centers within developing teeth, removal of vestigal tooth germs, and in odontoblast and ameloblast organization during tooth mineralization. Dental apoptosis is caspase dependent and proceeds via mitochondrial mediated cell death with possible amplification by Fas-FasL signaling modulated by Bcl-2 family members.

• MeSH
• Apoptosis * MeSH
• Caspases genetics   metabolism   MeSH
• Humans MeSH
• Mice MeSH
• Odontogenesis * MeSH
• Signal Transduction * MeSH
• Tooth Germ cytology   embryology   metabolism   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
• Names of Substances
• Caspases MeSH

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