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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
The Cell Biology of Amelogenesis
Published in Colin Robinson, Jennifer Kirkham, Roger Shore, Dental Enamel, 2017
Ziedonis Skobe, Doris N. Stern, Kenneth S. Prostak
The secretory-stage enamel organ consist of tour cell layers: the outer enamel epithelium, the stellate reticulum, the stratum intermedium, and secretory stage ameloblasts (Figure 5). The outer enamel epithelial cells are squamous and delineate the developing tooth bud from the connective tissue and vasculature of the jaw.64,65 Subjacent to the outer cells are loosely arranged star-shaped cells, the stellate reticulum. The thickness of this layer is species dependent (Figures 5,6, and 7), consisting of only a few layers in the rat,64,65 but is "quite extensive" in cats,66'67 mini-pig,42 monkey,68 and human.28 The extracellular spaces of the stellate reticulum usually contained floccular material in all species examined, except the rat.67
Experimental Oral Carcinogenesis
Published in Samuel Dreizen, Barnet M. Levy, Handbook of Experimental Stomatology, 2020
Samuel Dreizen, Barnet M. Levy
As early as 1964, Stanley and co-workers76 injected polyoma virus into mice and reported on some 70 tumors present in 11 mouse heads in one study and a large number of tumors in a different strain of mouse using a substrain of the virus in another study.77 Lucas78 injected newborn C3H strain mice subcutaneously with the LID/I strain polyoma virus. Animals were killed at varying intervals up to 1 year, and the tumors were carefully studied. (Precise numbers of animals used were not given in the publication.) Tumors occurred in close connection with the incisor and molar teeth of both the mandible and the maxilla. In some cases, there were multiple tumors. In general, they resembled those described by Stanley et al. Almost all of the tumors appeared to have a connection with the gingival epithelium. Some of the tumors which appeared to have a connection with the incisor teeth gave an appearance somewhat reminiscent of the follicles of human ameloblastoma, with central areas of stellate reticulumlike cells. Lucas pointed out that any possible analogy between the human ameloblastoma and this tumor should not be pursued too far, since in the mouse tumor the cells were not really stellate in type, and in fact the appearances could be due to intercellular edema. The other feature comparable to ameloblastomas was cyst formation. Small cysts were quite frequently seen, but larger ones surrounded by a thin layer of tumor tissue also developed. Tumors of that type seemed to have quite a noticeable resemblance to the monocystic type of ameloblastoma in man, with areas of squamous change and keratin production. Even in these tumors and cysts, a connection could be found between the tumor and the gingival epithelium. Stanley and his group considered that the tumors arose from gingival epithelium, though often the growths were so extensive by the time of autopsy that the actual site of origin could not be detected. Lucas’ study indicated that the tumors do arise from gingival epithelium, although the possibility of an origin from epithelial rests was also considered. Main and Dawe,79 on the basis of ingenious and carefully executed transplantation experiments, believed that the tumors arose from the outer enamel epithelium. Under sterile conditions, 14-day mouse embryos were removed from the uterus, and the maxillary and mandibular incisor tooth buds were dissected out. These were then placed in virus suspension and subsequently transplanted s.c. into newborn syngeneic mice. Tumors appeared in the transplants after 20 days and were identical to those described by Stanley et al.76 Early tumors could be seen arising from the outer enamel epithelium. Interestingly enough, tumors also appeared in the host mice, arising in the outer enamel epithelium. In the tumors described by Lucas, the origin, where it could be detected, appeared to be the fully differentiated squamous epithelium of the gingiva. There is still considerable work to be done concerning the role of the polyoma virus in odontogenic tumorigenesis in various strains of mice.
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