The development and fate of the dental lamina of the mandibular first molar tooth in the rat.
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The lamina of the first mandibular molar teeth of rats, age range 13 d intrauterine (i.u.) to 16 d postnatal (p.n.), was examined by light and transmission electron microscopy to establish histological baselines of its development and fate. All material was obtained from animals anaesthetised with ether, killed by cervical dislocation and prepared by routine methods for both types of examination. Contrary to earlier reports that the lamina remains intact throughout development, mesenchymal elements disrupt the lamina. These were seen first at 19 d i.u., as collagen-filled bays in the basal epithelial layers, associated with partial loss of related basal lamina. In the early stages, collagen deposition was limited and it was not obviously preceded by epithelial cell death or transformation, even though many bay-related cells showed lipid and glycogen accumulations. Later disruption of the lamina showed more mesenchymal cells as well as collagen in deeper spaces. After the onset of tooth eruption, mesenchymal cells external to and within the lamina contained lysosomal bodies and these plus evidence of related epithelial cell death and capillaries in the laminar spaces became more and more apparent. Similar collagen deposits were observed in a successional tooth primordium, which appeared at term but eventually aborted between days 5 and 10 p.n. Thus disruption of the lamina by connective tissue began earlier than has been reported previously and progressed as the tooth erupted towards the oral cavity. The evidence suggests that this disruption is initiated and sustained by mesenchymal cell activity rather than by programmed cell death or transformation of the epithelium. (+info)
Immunohistochemically localization of vascular endothelial growth factor, vascular endothelial growth factor receptor-2, collagen I and fibronectin in the epithelia-mesenchymal junction of the human tooth germ.
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During tooth development, tooth shape is mediated by the ECM through epithelial-mesenchymal interactions mediated by the ECM at the epithelia-mesenchymal junction. Blood vessel endothelium growth is mainly regulated by vascular endothelial growth factor (VEGF) and the relationship between tooth shape formation and VEGF are unknown. We examined immunohistochemical localization of VEGF and its receptor VEGF receptor-2 (VEGFR-2), collagen I and fibronectin, (both representative protein of ECM) at the epithelia-mesenchymal junction of human deciduous teeth from the cap stage to late bell stages in a human fetus at 16, 20, 24, 28 and 32 weeks of gestation. Immunoreactivity at the basement membrane for VEGF was detected from the cap stage to the bell stage. Immunoreactivity to fibronectin was weak in the cap stage and increased in the bell stage; collagen I was negative in the cap stage and slightly expressed in the bell stage in the basement membrane. We suggest that VEGF and ECM affect cooperatively in tooth shape formation at the basement membrane. (+info)
Cytomegalovirus inhibition of embryonic mouse tooth development: a model of the human amelogenesis imperfecta phenocopy.
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Bioengineered dental tissues grown in the rat jaw.
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Our long-term objective is to develop methods to form, in the jaw, bioengineered replacement teeth that exhibit physical properties and functions similar to those of natural teeth. Our results show that cultured rat tooth bud cells, seeded onto biodegradable scaffolds, implanted into the jaws of adult rat hosts and grown for 12 weeks, formed small, organized, bioengineered tooth crowns, containing dentin, enamel, pulp, and periodontal ligament tissues, similar to identical cell-seeded scaffolds implanted and grown in the omentum. Radiographic, histological, and immunohistochemical analyses showed that bioengineered teeth consisted of organized dentin, enamel, and pulp tissues. This study advances practical applications for dental tissue engineering by demonstrating that bioengineered tooth tissues can be regenerated at the site of previously lost teeth, and supports the use of tissue engineering strategies in humans, to regenerate previously lost and/or missing teeth. The results presented in this report support the feasibility of bioengineered replacement tooth formation in the jaw. (+info)
Whole-tooth regeneration: it takes a village of scientists, clinicians, and patients.
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A team of senior scientists was formed in 2006 to create a blueprint for the regeneration of whole human teeth along with all of the supporting structure of the dentition. The team included experts from diverse fields, each with a reputation for stellar accomplishment. Participants attacked the scientific issues of tooth regeneration but, more importantly, each agreed to work collaboratively with experts from other disciplines to form a learning organization. A commitment to learn from one another produced a unique interdisciplinary and multidisciplinary team. Inspired by the Kennedy space program to send a man to the moon, with its myriad of problems and solutions that no one discipline could solve, this tooth regeneration team devised an ambitious plan that sought to use stem cell biology, engineering, and computational biology to replicate the developmental program for odontogenesis. In this manner, team members envisioned a solution that consisted of known or knowable fundamentals. They proposed a laboratory-grown tooth rudiment that would be capable of executing the complete program for odontogenesis when transplanted to a suitable host, recreating all of the dental tissues, periodontal ligament, cementum, and alveolar bone associated with the canonical tooth. This plan was designed to bring regenerative medicine fully into the dental surgery suite, although a lack of funding has so far prevented the plan from being carried out. (+info)
Ectodermal Smad4 and p38 MAPK are functionally redundant in mediating TGF-beta/BMP signaling during tooth and palate development.
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Differential expression of type I and type III collagen genes during tooth development.
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Collagen gene expression during mouse molar tooth development was studied by quantitative in situ hybridization techniques. Different expression patterns of type I and type III collagen mRNAs were observed in the various mesenchymal tissues that constitute the tooth germ. High concentration for pro-alpha 1(I) and pro-alpha 2(I) collagen mRNAs were found within the osteoblasts. We found that the cellular content of type I collagen mRNAs in the odontoblasts varies throughout the tooth formation: whereas mRNA concentration for pro-alpha 1(I) collagen decreases and that of pro-alpha 2(I) increases, during postnatal development. Moreover, different amounts of pro-alpha 1(I) and pro-alpha 2(I) collagen mRNAs were observed in crown and root odontoblasts, respectively. Type III collagen mRNAs were detected in most of the mesenchymal cells, codistributed with type I collagen mRNAs, except in odontoblasts and osteoblasts. Finally, this study reports differential accumulation of collagen mRNAs during mouse tooth development and points out that type I collagen gene expression is regulated by distinct mechanisms during odontoblast differentiation process. These results support the independent expression of the collagen genes under developmental tissue-specific control. (+info)