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Odontogenic Epithelium and its Residues
Published in Roger M. Browne, Investigative Pathology of the Odontogenic Cysts, 2019
Progression from the bud to cap stage leads to differentiation of four regions in the enamel organ; (a) inner enamel epithelium: low columnar cells; (b) outer enamel epithelium: low cuboidal cells; (c) stratum intermedium: squamous shaped cells; (d) stellate reticulum: stellate shaped cells. The inner and outer enamel epithelium are continuous at the cervical loop and are derived from the basal cells of the tooth bud. This histogenesis appears to be controlled by epithelial-mesenchymal interactions since it has been shown that outer enamel epithelium can acquire the histogenic specificity of an inner enamel epithelium when cultured in heterotopic association with dental papilla.22 In such an association, a new stratum intermedium was observed in contact with the newly differentiated inner enamel epithelium reinforcing the concept of the interdependence of these two cell layers upon one another. It has been postulated that the epithelial-mesenchymal interactions involved in these histogenic modifications are matrix mediated through the dental basement membrane, which controls the cell kinetic changes and histogenesis.22,23 The extent to which tooth histogenic properties can be conserved by isolated cells is still in question.24,26
Bone, Muscle, and Tooth
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
John L. Vahle, Joel R. Leininger, Philip H. Long, D. Greg Hall, Heinrich Ernst
Ameloblastomas (Ernst and Mirea 1995) do not produce dental hard tissues; this is their most distinguishing feature from odontomas. They arise from the epithelium of dentigerous cysts, remnants of the dental lamina and of the enamel organ, and the basal cell layer of the oral mucosa. Ameloblastomas are usually large and grow concentrically. They tend to be locally invasive and destructive but do not metastasize. They are composed of islands or nests or anastomosing strands of epithelial cells embedded in a collagenous stroma. The epithelium consists of a peripheral layer of tall columnar cells resembling the inner enamel epithelium and loosely arranged central cells similar to stellate reticulum. The epithelial islands may be solid (solid type) or may show degenerative changes in the stellate cells resulting in cyst formation (cystic type). The stroma may be focally hyalinized, but dental hard tissues (enamel, dentin, or cementum) are not produced. In one variant (acanthomatous ameloblastoma), epithelial cells of the stellate reticulum may undergo squamous metaplasia.
Differentiation of Ameloblasts and Its Regulation by Epithelial-Mesenchymal Interactions
Published in Colin Robinson, Jennifer Kirkham, Roger Shore, Dental Enamel, 2017
The process whereby the oral epithelial cells undergo progressive determination and finally differentiate into ameloblasts can be viewed schematically in Figure 6. It can be speculated that there are developmental transition points at which the cells acquire higher levels of determination. Such transition points could include the formation of the dental bud from the oral epithelium and the specialization of the inner enamel epithelium from other dental epithelial cells during the cap stage. The final transition points are characterized by the differentiation of the inner enamel epithelial cells into preameloblasts and their terminal differentiation into ameloblasts during the bell stage. This progressive determination of cells in the ameloblast cell lineage is regulated by epigenetic signals from the mesenchyme, i.e., epithelial-mesenchymal interactions. This model is, of course, much simplified; in reality there are likely to be many more transition points and reciprocal signals.
Mesenchymal Wnt/β-catenin signaling induces Wnt and BMP antagonists in dental epithelium
Published in Organogenesis, 2019
Xiaoyan Chen, Jing Liu, Nan Li, Yu Wang, Nan Zhou, Lei Zhu, Yiding Shi, Yingzhang Wu, Jing Xiao, Chao Liu
To clarify the epithelial responses to the persistent Wnt/β-catenin signaling in the Osr2-creKI;Ctnnb1ex3f dental mesenchyme, gene expression was checked in the E14.5 tooth germs. In the E14.5 Osr2-creKI;Ctnnb1ex3f incisor epithelium, the Pitx2 expression was still active throughout the regressing enamel organs (Fig. 5A’,A’’), displaying no difference from the WT control (Fig. 5A). However, Noggin, a BMP antagonist which was silenced in WT oral epithelium (Fig. 5B), was ectopically activated in the Osr2-creKI;Ctnnb1ex3f oral epithelium, especially the regressing incisor epithelium (Fig. 5B’). In contrast, although actively transcribed in the inner enamel epithelium of WT incisors (Fig. 5C,D), the expression of Shh was abrogated in the Osr2-creKI;Ctnnb1ex3f incisor epithelium (Fig. 5C’,D’).
Focusing on Hippo Pathway in Stem Cells of Oral Origin, Enamel Formation and Periodontium Regeneration
Published in Organogenesis, 2022
Tianyi Wang, Kehan Li, Hanghang Liu, En Luo
Continuous growth of cap stage will transfer into the bell stage, where several cell groups could be seen, involving inner enamel epithelium, outer enamel epithelium, stratum intermedium and stellate reticulum. During this stage, ameloblasts and odontoblasts formed, making the hard tissues of the crown (Figure 4).41