scholarly journals Papilliferous Keratoameloblastoma: An Extremely Rare Case Report

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Neeta Mohanty ◽  
Varun Rastogi ◽  
Satya Ranjan Misra ◽  
Susant Mohanty

Odontogenic tumors develop in the jaw bones from the odontogenic tissue-oral epithelium in tooth germ, enamel organ, dental papilla, reduced enamel epithelium, remnants of Hertwig’s root sheath or dental lamina, and so forth. Hence, a bewildering variety of tumors are encountered in the maxilla and mandible. Ameloblastoma is the second most common odontogenic neoplasm after odontomes, and it has numerous clinical and histologic variants. We report a very rare histologic variant: the papilliferous keratoameloblastoma which is the fifth reported case in the English literature.

2013 ◽  
Vol 3 ◽  
pp. 11 ◽  
Author(s):  
Satya Ranjan Misra ◽  
Sthitaprajna Lenka ◽  
Sujit Ranjan Sahoo ◽  
Sobhan Mishra

Odontogenic tumors develop in the jaws from odontogenic tissues such as enamel organ, Hertwig epithelial root sheath, dental lamina, and so on. A variety of tumors unique to the maxilla and mandible are therefore seen. Calcifying epithelial odontogenic tumor (CEOT) is a rare, aggressive, benign odontogenic tumor of epithelial origin accounting for only about 1% of all odontogenic tumors. It is eponymously called “Pindborg tumor”, as it was first described by Pindborg in 1955. The origin of this locally invasive tumor remains unknown. It is thought to arise from stratum intermedium. It commonly affects the posterior mandible manifesting as a slow-growing asymptomatic swelling often associated with an impacted tooth. We report a case of CEOT, for which, owing to its huge size we have proposed the term “giant” Pindborg tumor (CEOT). This is probably the largest case of this tumor reported so far in the English literature. The present case also has the classic yet rare “driven snow” appearance of the tumor on radiographs.


Author(s):  
Max Robinson ◽  
Keith Hunter ◽  
Michael Pemberton ◽  
Philip Sloan

Odontogenic cysts and tumours arise from inclusion of tooth-forming epithelium and mesenchyme in the jaw bones during development. Cysts also arise from non-odontogenic epithelium trapped during fusions or from vestigial structures. In addition, bone cysts that can arise at other skeletal sites may also occur in the jaws. Odontogenic cysts and tumours may be classified according to their putative developmental origins and biology. The classification of jaw cysts is shown in Fig. 6.1. Odontomes are hamartomatous develop­mental lesions of the tooth-forming tissues. Odontogenic tumours are uncommon and are usually benign. Ameloblastoma is the most com­mon odontogenic tumour and is described in detail. The other odon­togenic tumours are rare and only the principal features are presented. Very rare congenital lesions of possible odontogenic origin are men­tioned in the final section. A cyst may be defined as pathological cavity lined by epithelium with fluid or semi-fluid contents. However, clinically, the term encompasses a broader range of benign fluid-filled lesions, some of which do not possess an epithelial lining. The preferred definition is, therefore, ‘a pathological cavity having fluid or semi-fluid contents that has not been created by the accumulation of pus’. Cysts are commonly encountered in clinical dentistry and are generally detected on radiographs or as expansions of the jaws. Most cysts have a radiolucent appearance and are well circumscribed, often with a corticated outline. At least 90% of jaw cysts are of odontogenic origin. The clinico-pathological features of jaw cysts are summarized in Table 6.1. The incidence of the four most common jaw cysts are provided in Table 6.2. The epithelial lining of odontogenic cysts originates from residues of the tooth-forming organ. • Epithelial rests of Serres are remnants of the dental lamina and are thought to give rise to the odontogenic keratocyst, lateral periodon­tal, and gingival cysts. • Reduced enamel epithelium is derived from the enamel organ and covers the fully formed crown of the unerupted tooth. The dentiger­ous (follicular) and eruption cysts originate from this tissue, as do the mandibular buccal and paradental cysts. • Epithelial rests of Malassez form by fragmentation of Hertwig’s epi­thelial root sheath that maps out the developing tooth root. Radicular cysts originate from these residues.


Author(s):  
Hermes Pretel ◽  
Sebastião Hetem ◽  
Celina Antônio Prata ◽  
Marlei Seccani Galassi ◽  
Lizeti Toledo Oliveira Ramalho ◽  
...  

The aim of this work was to analyse the behaviour of the dental lamina during the development process of first molar teeth. The offspring of female mice were analysed at the 16th day of intra-uterine life and since birth till 17 days old with the aim to evaluate the dental lamina evolution of upper and lower first molars. The animals were sacrificed, and the heads embedded in paraffin in order to get frontal or sagittal sections whose were stained by hematoxylin and eosin method. The results showed a very clear presence of the dental lamina in all periods under analysis, without the occurrence of its disorganization, in other words, it was permanently connecting the developing tooth germ to the oral epithelium until advanced dental eruption.


2006 ◽  
Vol 121 (1) ◽  
pp. 72-75 ◽  
Author(s):  
D Bray ◽  
A Michael ◽  
D T Falconer ◽  
H S Kaddour

Ameloblastoma is an odontogenic neoplasm of enamel organ type tissue which does not undergo transformation to the point of enamel formation. We present the second case in the English literature of maxillary ameloblastoma that presented with nasal obstruction and rhinorrhoea, and the first to be excised using a combined maxillotomy and endoscopic ethmoidectomy. The patient had no previous dental history. The unusual presenting symptoms, as well as the highly destructive nature of these lesions when arising in the maxilla, make them worthy of consideration in the differential diagnosis of nasal and maxillary masses. We discuss the clinical features, pathology and management of these lesions and review the literature.


Development ◽  
1992 ◽  
Vol 115 (2) ◽  
pp. 403-420 ◽  
Author(s):  
A. MacKenzie ◽  
M.W. Ferguson ◽  
P.T. Sharpe

We have studied the expression patterns of the newly isolated homeobox gene, Hox-8 by in situ hybridisation to sections of the developing heads of mouse embryos between E9 and E17.5, and compared them to Hox-7 expression patterns in adjacent sections. This paper concentrates on the interesting expression patterns of Hox-8 during initiation and development of the molar and incisor teeth. Hox-8 expression domains are present in the neural crest-derived mesenchyme beneath sites of future tooth formation, in a proximo-distal gradient. Tooth development is initiated in the oral epithelium which subsequently thickens in discrete sites and invaginates to form the dental lamina. Hox-8 expression in mouse oral epithelium is first evident at the sites of the dental placodes, suggesting a role in the specification of tooth position. Subsequently, in molar teeth, this patch of Hox-8 expressing epithelium becomes incorporated within the buccal aspect of the invaginating dental lamina to form part of the external enamel epithelium of the cap stage tooth germ. This locus of Hox-8 expression becomes continuous with new sites of Hox-8 expression in the enamel navel, septum, knot and internal enamel epithelium. The transitory enamel knot, septum and navel were postulated, long ago, to be involved in specifying tooth shape, causing the inflection of the first buccal cusp, but this theory has been largely ignored. Interestingly, in the conical incisor teeth, the enamel navel, septum and knot are absent, and Hox-8 has a symmetrical expression pattern. Our demonstration of the precise expression patterns of Hox-8 in the early dental placodes and their subsequent association with the enamel knot, septum and navel provide the first molecular clues to the basis of patterning in the dentition and the association of tooth position with tooth shape: an association all the more intriguing in view of the evolutionary robustness of the patterning mechanism, and the known role of homeobox genes in Drosophila pattern formation. At the bell stage of tooth development, Hox-8 expression switches tissue layers, being absent from the differentiating epithelial ameloblasts and turned on in the differentiating mesenchymal odontoblasts. Hox-7 is expressed in the mesenchyme of the dental papilla and follicle at all stages. This reciprocity of expression suggests an interactive role between Hox-7, Hox-8 and other genes in regulating epithelial mesenchymal interactions during dental differentiation.(ABSTRACT TRUNCATED AT 400 WORDS)


1964 ◽  
Vol 04 (02) ◽  
pp. 186-192
Author(s):  
Leonel Costacurta

SummaryDental germs of the upper incisors of six-days old rats were studied for the uptake of leucine-H3 by different layers of the enamel organ in correlation to the various stages of the development of enamel.The longitudinal section of the tooth germ was divided into 15 zones of about equal length in order to facilitate the description and interpretation of results. Autoradiographic images of the histologic preparations from rats sacrificed 30 minutes, 1 hour, 1 day and 3 days after the injection were made. The strongest reactions were observed in dental germs of rats sacrificed 1 hour, and particularly one day, after the leucine-H3 injection.The uptake of this compound by the enamel matrix increases progressively up to the young enamel and then decreases to the distal extremity; the greatest quantity of this labeled amino-acid was observed in the primary and young enamel. The reactions were present in the transitional enamel only along a thin band close to the dentine-enamel junction.In the enamel organ leucine-H3 incorporation was greatest in the three layers, the zones corresponding to primary and young enamel. In zones corresponding to transitional enamel, the inner epithelium showed a small quantity, and the stellate reticulum a blackening only in its superficial part, were the blood vessels reach the enamel organ.


2021 ◽  
Vol 9 (1) ◽  
pp. 7
Author(s):  
Yusuke Makino ◽  
Kaoru Fujikawa ◽  
Miwako Matsuki-Fukushima ◽  
Satoshi Inoue ◽  
Masanori Nakamura

Tooth eruption is characterized by a coordinated complex cascade of cellular and molecular events that promote tooth movement through the eruptive pathway. During tooth eruption, the stratum intermedium structurally changes to the papillary layer with tooth organ development. We previously reported intercellular adhesion molecule-1 (ICAM-1) expression on the papillary layer, which is the origin of the ICAM-1-positive junctional epithelium. ICAM-1 expression is induced by proinflammatory cytokines, including interleukin-1 and tumor necrosis factor. Inflammatory reactions induce tissue degradation. Therefore, this study aimed to examine whether inflammatory reactions are involved in tooth eruption. Reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed sequential expression of hypoxia-induced factor-1α, interleukin-1β, and chemotactic factors, including keratinocyte-derived chemokine (KC) and macrophage inflammatory protein-2 (MIP-2), during tooth eruption. Consistent with the RT-PCR results, immunohistochemical analysis revealed KC and MIP-2 expression in the papillary layer cells of the enamel organ from the ameloblast maturation stage. Moreover, there was massive macrophage and neutrophil infiltration in the connective tissue between the tooth organ and oral epithelium during tooth eruption. These findings suggest that inflammatory reactions might be involved in the degradation of tissue overlying the tooth organ. Further, these reactions might be induced by hypoxia in the tissue overlying the tooth organ, which results from decreased capillaries in the tissue. Our findings indicate that bacterial infections are not associated with the eruption process. Therefore, tooth eruption might be regulated by innate inflammatory mechanisms.


Development ◽  
1977 ◽  
Vol 41 (1) ◽  
pp. 279-287
Author(s):  
J. A. Sofaer

The semidominant gene ‘crooked’ (Cd) in the mouse produces anomalies of the axial skeleton (resulting in a crooked tail), microphthalmia and dental abnormalities, including small molars with simplified cusp patterns that are equivalent to patterns passed through during normal morphodifferentiation. A series of embryonic litters from Cd/ + × Cd / + matings was used to investigate the embryological basis for the dental abnormalities. Microphthalmic embryos were classed as Cd/Cd, and their most normal litter mates were selected as controls (+ / + or Cd / +). An additional set of control embryos came from the inbred strain CBA/Cam (+ / +). Serial sagittal sections of the heads of these embryos were examined microscopically, and the maximum anteroposterior diameters of the developing upper and lower first molars were measured. Reduction in the rates of growth and morphodifferentiation of Cd/Cd first molars, relative to those of litter mate controls, was associated with the appearance of an adjacent abnormal proliferation of the dental lamina. Some proliferations in older embryos showed signs of early tooth germ formation, but many were seen to have regressed and no examples of supernumerary teeth have been found in Cd/Cd adults. Small size of Cd/Cd molars may therefore result from competitive inhibition of molar growth by a transient abnormal laminal proliferation, and Cd/Cd cusp patterns from the relatively premature onset of hard tissue formation during normal but retarded sequences of morphodifferentiation.


2009 ◽  
Vol 20 (5) ◽  
pp. 365-369 ◽  
Author(s):  
Elizabeth Ferreira Martinez ◽  
Luciana Alves Herdy da Silva ◽  
Cristiane Furuse ◽  
Ney Soares de Araújo ◽  
Vera Cavalcanti de Araújo

Dentin matrix protein 1 (DMP1) is an acidic phosphoprotein that plays an important role in mineralized tissue formation by initiation of nucleation and modulation of mineral phase morphology. The purpose of the present study was to examine the immunoexpression of DMP1 in tooth germs of 7 human fetuses at different gestational ages (14, 16, 19, 20, 21, 23 and 24 weeks) comparing with completed tooth formation erupted teeth. The results showed the presence of DMP1 in the dental lamina, as well as in the cells of the external epithelium, stellate reticulum and stratum intermedium of the enamel organ. However, in the internal dental epithelium, cervical loop region and dental papilla some cells have not labeled for DMP1. In the crown stage, DMP1 was expressed in the ameloblast and odontoblast layer, as well as in the dentinal tubules of coronal dentin near the odontoblast area. Erupted teeth with complete tooth formation exhibited immunolabeling for DMP1 only in the dentinal tubules mainly close to the dental pulp. No staining was observed in the enamel, predentin or dental pulp matrix. DMP1 is present in all developing dental structures (dental lamina, enamel organ, dental papilla) presenting few immunoexpression variations, with no staining in mineralized enamel and dentin.


1981 ◽  
Vol 18 (5) ◽  
pp. 684-689 ◽  
Author(s):  
R. R. Dubielzig ◽  
R. J. Higgins ◽  
S. Krakowka

Ten 7-day-old gnotobiotic Beagle puppies were inoculated intraperitoneally with virulent canine distemper virus (R252-CDV). The dogs were killed and perfused with paraformaldehyde/glutaraldehyde from eight to 36 days after inoculation. The developing teeth of the mandibles were examined by light microscopy, and the teeth from three dogs were examined by electron microscopy. Necrosis of individual cells in the stratum intermedium of the developing tooth was the first change, detectable at day 9 post-inoculation. At day 16 post-inoculation, there was disorganization of the ameloblasts. In the stratum intermedium, multinucleate giant cells and large eosinophilic cytoplasmic viral inclusions were prominent. Ultrastructurally, these inclusions consisted of clusters of tubular aggregates typical of canine distemper virus nucleocapsids. At 28 to 36 days post-inoculation, the changes were seen in the reduced enamel epithelium. Multinucleate cells were seen, but no inclusions. Some necrotic cells were seen. In these teeth, ameloblastic cells of the root were morphologically normal. Our results suggest that distemper virus affects developing teeth by direct infection of the enamel organ.


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