Academic literature on the topic 'Odontogenic epithelium'
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Journal articles on the topic "Odontogenic epithelium"
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Kundi, Jawad Ahmad, Muhammad Ilyas, Salman Khan, Faryal Gul, and Muhammad Umar. "Calcifying Epithelial Odontogenic Tumor." Journal of Gandhara Medical and Dental Science 3, no. 01 (September 1, 2016): 42–46. http://dx.doi.org/10.37762/jgmds.3-01.48.
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ABSTRACTCalcifying epithelial odontogenic tumor (CEOT) is a rare odontogenic tumor, accounts 0.4% to 3 % of all odontogenic tumors arising from odontogenic epithelium. Dr. Jens JorgenPindborg first described this unusual lesion; subsequently Shafer et al coined the term Pindborg tumor. It occurs most commonly in the 4th to 6th decade and bears no gender predilection. A case of CEOT in a 55 years old female extending from themesial aspect of right lower canine to the contralateral third molar region is described.
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Cserni, Dorottya, Tamás Zombori, Anette Stájer, Annamária Rimovszki, Gábor Cserni, and Zoltán Baráth. "Immunohistochemical Characterization of Reactive Epithelial Changes in Odontogenic Keratocysts." Pathology & Oncology Research 26, no. 3 (October 18, 2019): 1717–24. http://dx.doi.org/10.1007/s12253-019-00749-3.
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Abstract Odontogenic keratocysts (OKCs) have a diagnostic thin epithelial lining characterised by a linear epithelial connective tissue interface generally lacking inflammatory changes, basal palisading of the nuclei and a wavy parakeratotic layer on the surface. This typical epithelium may convert to a thicker non-keratinizing one with rete pegs and a relatively flat surface after operative decompression. The aim was to characterize this type of epithelial change by immunohistochemistry for bcl2, keratin17, 10 and 19. Eleven out of 33 archived OKCs demonstrated an altered epithelium related to previous biopsy, decompressing drainage or inflammation. The typical basal bcl2 staining was lost in 10/11 cases; transepithelial CK17 was lost or markedly reduced in 9/11 cases. CK10 displayed a segmental upper layer staining in OKCs, and its loss or partial loss in the altered epithelium did not differ from negative areas of OKCs. CK19 displayed various staining patterns in the altered epithelium from lost to maintained in a patchy transepithelial distribution, the latter of which did not differ from the typical OKC staining pattern. Three of four non-keratinizing epithelial linings with basal palisading displayed immunostaining reminiscent of typical OKC epithelium. The lack of a typical epithelium is not sufficient to exclude the diagnosis of OKC if the sampling is not generous (e.g. biopsy), and the presence of non-keratinizing epithelium with basal palisading and an immunophenotype characteristic of OKC (basal bcl2, patchy or diffuse CK17 and upper layer CK10 positivity) may be consistent with the OKC diagnosis even in the absence of typical epithelial lining.
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Soares, Ciro Dantas, Wilson Delgado-Azañero, Thayná Melo de Lima Morais, Oslei Paes de Almeida, and Hugo Ghersi Miranda. "Odontogenic Carcinosarcoma: Clinicopathologic Features of 2 Cases." International Journal of Surgical Pathology 28, no. 4 (December 1, 2019): 421–26. http://dx.doi.org/10.1177/1066896919888578.
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This study reports 2 odontogenic carcinosarcomas, including the clinicopathologic and immunoprofile characteristics of these rare tumors. The first case occurred in a 22-year-old male presenting a bilobular mass involving the gingiva and bone of the premolar region of the left mandible, with paresthesia of the lower lip. Microscopic examination revealed a tumor similar to ameloblastic fibrosarcoma, with atypical mesenchymal cells; however, the odontogenic epithelium also showed atypia. In the second case, a 16-year-old female had a painless, asymptomatic, large intraosseous mandibular lesion. The patient received radiotherapy to treat a rhabdomyosarcoma of the parotid 13 years before. The tumor was composed of atypical spindle cells, positive for vimentin and smooth muscle actin, intermingled with malignant odontogenic epithelium. Both epithelial and mesenchymal components of the tumors showed high index of p53- and Ki67-positive cells. The first case was diagnosed as odontogenic carcinosarcoma possibly originated from an ameloblastic fibrosarcoma, and the second as de novo odontogenic carcinosarcoma possibly caused by previous radiotherapy.
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Cimadon, Natalia, Isabel Silva Lauxen, Vinicius Coelho Carrard, Manoel Sant'Ana Filho, Pantelis Varvaki Rados, and Márcia Gaiger Oliveira. "Analysis of the Proliferative Potential of Odontogenic Epithelial Cells of Pericoronal Follicles." Journal of Contemporary Dental Practice 15, no. 6 (2014): 761–65. http://dx.doi.org/10.5005/jp-journals-10024-1613.
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ABSTRACT Aim To evaluate the proliferative potential and the cell proliferation rate of odontogenic epithelial cells. Materials and methods Forty-two cases of pericoronal follicles of impacted third molars were submitted to silver impregnation technique for quantification of argyrophilic nucleolar organizer regions (AgNOR) and immunohistochemical staining for EGFR and Ki-67. For AgNOR quantification, the mean number of active nucleolar organizer regions per nucleus (mAgNOR) and the percentage of cells with 1, 2, 3 and 4 or more AgNORs per nucleus (pAgNOR) were quantified. Ki-67 immunolabeling was quantified, whereas for EGFR, a descriptive analysis of staining patterns (membrane, cytoplasm or membrane + cytoplasm positivity) was performed. We evaluated the reduced epithelium of the enamel organ and/or islands of odontogenic epithelium present in the entire connective tissue. Results mAgNOR were 1.43 (1.0-2.42) and were significantly different among pericoronary follicles from upper and lower teeth (p = 0.041). Immunostaining of Ki-67 was negative in all cases. EGFR immunolabeling was found mainly in the cytoplasm and was more intense in islands and cords when compared to reduced epithelium of the enamel organ. Conclusion Odontogenic epithelial cells of some pericoronal follicles have proliferative potential, suggesting their association with the development of odontogenic lesions. Clinical significance The authors suggest that nonerupted, especially of the lower teeth, should be monitored and if necessary removed. How to cite this article Cimadon N, Lauxen IS, Carrard VC, Filho MSA, Rados PV, Oliveira MG. Analysis of the Proliferative Potential of Odontogenic Epithelial Cells of Pericoronal Follicles. J Contemp Dent Pract 2014;15(6):761-765.
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Poulet, F. M., B. A. Valentine, and B. A. Summers. "A Survey of Epithelial Odontogenic Tumors and Cysts in Dogs and Cats." Veterinary Pathology 29, no. 5 (September 1992): 369–80. http://dx.doi.org/10.1177/030098589202900501.
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A retrospective histologic study of 12 canine and eight feline epithelial odontogenic tumors and cysts was conducted from oral masses ( n = 3,917) obtained between 1980 and 1990. No sex or breed predilection was identified. Ameloblastoma was observed in two dogs (case Nos. 1, 2) 6 and 8 months of age. Calcifying epithelial odontogenic tumors were seen in a dog (case No. 3) and in two cats (case Nos. 4, 5) between 8 and 16 years of age. Ameloblastic fibroma (or fibroameloblastoma) was observed in cats (case Nos. 6–10) only. Inductive fibroameloblastoma was observed in four cats (case Nos. 6–9) up to 1 year of age, whereas ameloblastic fibroma was seen in a 14-year-old cat (case No. 10). A single ameloblastic odontoma was identified in a 20-month-old dog (case No. 11). Two complex odontomas occurred in a 6-month-old (case No. 12) and a 4-year-old (case No. 13) dog. Odontogenic cysts were identified in five dogs (case Nos. 14–18) aged 4.5 months to 16 years and in a 1-year-old cat (case No. 19) and have not been previously reported in these species. These cysts were lined by a stratified epithelium reminiscent of the appearance of ameloblastic epithelium. An odontogenic keratocyst with prominent central parakeratotic keratinization was identified in one 9-year-old female dog (case No. 20). Almost all epithelial odontogenic tumors were circumscribed, benign tumors that warranted a good prognosis for survival, although local recurrence may have followed (or may follow) incomplete excision. Calcifying epithelial odontogenic tumors may be locally invasive. Of six odontogenic cysts (case Nos. 14–19), two (case Nos. 15, 18) gave rise to basi-squamous carcinomas. The classification and behavior of epithelial odontogenic tumors and cysts in human beings, dogs, and cats are discussed.
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Saraçoğlu, U., B. Kurt, Ö. Günhan, and O. Güven. "MIB-1 expression in odontogenic epithelial rests, epithelium of healthy oral mucosa and epithelium of selected odontogenic cysts." International Journal of Oral and Maxillofacial Surgery 34, no. 4 (June 2005): 432–35. http://dx.doi.org/10.1016/j.ijom.2004.09.005.
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Shah, Shreyas N., and Falguni Patel. "Erupting Compound Odontome - A Case Report." Journal of Evolution of Medical and Dental Sciences 10, no. 18 (May 3, 2021): 1361–64. http://dx.doi.org/10.14260/jemds/2021/287.
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Odontomas are asymptomatic, benign odontogenic tumours comprised of dental tissue. Most of the cases usually get detected on routine radiographic evaluation. Odontoma can be classified according to morphology in two different variants, compound odontoma showing anatomic similarity or miniature version of the tooth and complex odontoma having irregular masses with different type of dental tissues. Early detection of such type of silent lesion is mandatory to rule out certain silent but aggressive pathologies. Here, we present a case of erupting compound odontoma of maxillary area in 15-year-old male patient. Development of tooth is a result of complicated interaction between ectodermal and ecto mesenchymal tissue. Sometimes the remnants of such tissues are left behind in the jaw after development and eruption of tooth, which can become a source of development of odontogenic lesions later on.1 As revealed by World Health Organization (WHO), Odontogenic tumours can be classified in three different categories according to their histopathological form.2 1. Odontogenic tumours which develop from odontogenic epithelium without involvement of odontogenic ectomesenchyme, 2. Odontogenic tumours which develop from odontogenic epithelium with involvement of odontogenic ectomesenchyme, with or without formation of dental hard tissue and 3. Odontogenic tumours which develop from odontogenic ectomesenchyme with or without involvement of odontogenic epithelium.2 For such lesions “Odontoma” word was initially given by Paul Broca in 1866, who revealed the term as tumour occurred by the overgrowth of entire dental tissue. The growth of absolutely differentiated epithelial cells as functional ameloblast and mesenchymal cells as functional odontoblast can give rise to a different developmental anomaly coined as Odontomas.3 According to their behaviour and composition, odontomas can be considered as malformations or hamartomas rather than a true neoplasm. 4,5,6 In 2005, World Health Organization (WHO) classified two variants of odontomas, 1. Compound odontomas, which typically appears as unilocular lesions containing multiple radiopaque, tiny tooth like structures commonly known as denticles; and 2. Complex odontomas, which is comprised of an irregular mass of soft and hard dental tissues.
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Murphy, Brian, Cynthia Bell, Amanda Koehne, and Richard R. Dubielzig. "Mandibular odontoameloblastoma in a rat and a horse." Journal of Veterinary Diagnostic Investigation 29, no. 4 (May 26, 2017): 536–40. http://dx.doi.org/10.1177/1040638717711996.
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Odontoameloblastoma (OA) is a mixed odontogenic tumor that is an ameloblastoma with concurrent histologic evidence of odontoma differentiation. As a mixed tumor, OA is a tripartite lesion comprised of neoplastic odontogenic epithelium, induced dental ectomesenchyme (dental pulp), and mineralized dental matrix. Although rare, OA represents a diagnostic conundrum, as it is histologically closely related to 2 other mixed odontogenic tumors: odontoma (complex and compound) and ameloblastic fibro-odontoma. Herein we describe an OA arising from the mandible of a 4-mo-old Fischer 344 rat that had been exposed in utero to the mutagen ENU (N-ethyl-N-nitrosourea), and a naturally occurring lesion in a 2-y-old Appaloosa horse. In order to satisfy the diagnostic criteria for this lesion, mineralized dental matrix in relationship to neoplastic odontogenic epithelium must be identifiable within the OA lesion. This group of odontogenic tumors is differentiated by the degree to which the dental matrix is organized and the relative proportions of pulp ectomesenchyme, odontogenic matrix, and odontogenic epithelium.
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Pindborg, J. J., and Jes Hansen. "STUDIES ON ODONTOGENIC CYST EPITHELIUM." Acta Pathologica Microbiologica Scandinavica 58, no. 3 (August 17, 2009): 283–94. http://dx.doi.org/10.1111/j.1699-0463.1963.tb01572.x.
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Chen, Hsin-Ming. "Langerhans cells in odontogenic epithelium." Journal of the Formosan Medical Association 112, no. 9 (September 2013): 586. http://dx.doi.org/10.1016/j.jfma.2013.07.004.
Full textDissertations / Theses on the topic "Odontogenic epithelium"
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Wassberger, Johanna, and Mahtab Yarahmadi. "Proliferation and expression of p53 in odontogenic tumours - An immunohistochemical analysis." Thesis, Malmö högskola, Odontologiska fakulteten (OD), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-19756.
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Introduktion: Ameloblastom (AB), adenomatoid odontogen tumör (AOT), ameloblastiskt fibrom (AF) och odontogent fibrom (OF) är odontogena tumörer som innehåller epiteliala komponenter. Frekvensen av recidiv hos dessa varierar från låg förekomst till relativt hög förekomst. Syftet med denna studie är att undersöka om Ki-67, p53 och BRAF kan användas som prognostiska markörer i recidivmönstret hos dessa tumörer.Material och metod: Studien genomfördes genom immunohistokemi med monoklonala antikroppar av Ki-67, p53 och BRAF på respektive tumör. Tumörerna hämtades från avdelningen för Oral patologi på Malmö högskola. En statistisk analys utfördes med hjälp av Kruskal-Wallis envägs-ANOVA.Resultat: I de tio AB-fallen kunde en hög proliferation och en hög prevalens av muterade p53 ses. I de sju fallen av AOT kunde en måttligt hög proliferation och en generellt hög prevalens av muterade p53, jämförbara med värden för AB, ses. De sju fallen med AF och de fem fallen med OF visade båda en låg proliferation och en låg förekomst av muterade p53. Skillnaden mellan gruppen AB och AOT och gruppen AF och OF visade en signifikant högre infärgningsintensitet för både Ki-67 (p<0.001) och p53(p=0.001) för gruppen med AB och AOT.Konklusion: Proliferations index med Ki-67 och förekomst av p53-mutationer kan användas som en prognostisk markör för recidiv hos AB och AOT. Det är å andra sidan inte tillämpbart för AF och OF.Introduction: Ameloblastoma (AB), adenomatoid odontogenic tumour (AOT), ameloblastic fibroma (AF) and odontogenic fibroma (OF) are all odontogenic tumours with an epithelial component. The recurrence rate for these odontogenic tumours varies from low frequencies to quite high frequencies. The aim of this study is to evaluate the expression of Ki-67, p53 and BRAF and the possibility of these antibodies acting as prognostic markers in the recurrence pattern of odontogenic tumours.Material and method: An immunohistochemical study using Ki67, p53 and BRAF monoclonal antibodies was performed on 29 paraffin blocks from the respective tumours obtained at the department of Oral Pathology in the Faculty of Odontology at Malmö University. Statistical analysis was performed with Kruskal-Wallis one-way ANOVA.Results: In the series of ten AB cases high proliferation activity and a high prevalence of p53 mutations was observated. In the seven AOT cases a moderately high proliferative activity as well as a generally high prevalence of p53 mutation, comparable to AB, was observed. The seven cases of AF and the five cases of OF demonstrated a low proliferative activity and a low prevalence of p53 mutation. The difference between AB and AOT versus AF and OF as two separate groups, showed a significantly higher staining intensity for both Ki-67 (p < 0.001) and p53 (p = 0.001) in AB and AOT as a group.Conclusion: Ki-67 proliferation index and p53-mutation status can be considered to be a prognostic marker for AB and AOT recurrence. This is, however, not applicable to AF and OF.
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Nickolaychuk, Brent R. "Evidence for a role of MAP kinases (ERK1 and pERK) in proliferating and differentiating odontogenic epithelia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ57566.pdf.
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Parikka, M. (Mataleena). "Collagen XVII and TIMP-1 in epithelial cell migration." Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:951427198X.
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Abstract
Collagen XVII (BP180) is a transmembrane component of hemidesmosomes, which connect basal keratinocytes to the basement membrane. The extracellular domain of collagen XVII is proteolytically shed from the cell surface and released to the extracellular matrix. Apart from its function in epithelial cell adhesion, collagen XVII has been suggested to participate in keratinocyte motility. The collagen XVII expression pattern was studied in wounds of oral mucosa and in epithelial tumors. During re-epithelialization, collagen XVII was expressed in the keratinocytes distal to the wound edge, but not in the leading cells of the epithelial tip. Collagen XVII upregulation was observed in moderate/severe dysplasias of oral mucosa. In follicular ameloblastomas and basal cell carcinomas, collagen XVII expression was reduced in peripheral cells, whereas cytoplasmic staining was detected in central tumor cells. Tongue squamous cell carcinomas showed increased collagen XVII expression in grade II/III tumors, particularly in areas of invasive growth. The results suggest a correlation between overexpression of collagen XVII and the invasive potential of the tumor.
For the first time, the role of collagen XVII in the regulation of malignant migration was explored. The presence of COL15, the cell adhesion domain of collagen XVII, induced migration of tongue squamous cell carcinoma cells in transmigration assays. Experiments with specific function-blocking integrin antibodies revealed that the promigratory function of COL15 is mediated by αv and α5 integrins.
The role of the matrix metalloproteinase (MMP) family of proteolytic enzymes in wound re-epithelialization was studied in a transgenic mouse model. In these mice, a specific inhibitor of MMPs, TIMP-1, was overexpressed in cells that normally produce MMP-9. The healing of cutaneous wounds was found to be significantly delayed, but not prevented, due to the impaired ability of keratinocytes to migrate to the wound area.
These results suggest that collagen XVII may participate in epithelial tumor progression and invasion by promoting migration of tumor cells. Based on the present study, epithelial cell-derived MMPs play a significant role in the migration of wound keratinocytes during re-epithelialization.
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Togo, Yumiko. "Antagonistic functions of USAG-1 and RUNX2 during tooth development." Kyoto University, 2017. http://hdl.handle.net/2433/218004.
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Prosdócimi, Fábio César. "Perfil de expressão das metaloproteinases de matriz (MMPs) e seus inibidores (TIMPs e RECK) em tumores odontogênicos benignos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/23/23141/tde-29052013-152333/.
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Os tumores odontogênicos benignos compreendem um grupo de neoplasias originárias dos tecidos dentários. Pesquisas vêm buscando identificar moléculas envolvidas nos mecanismos moleculares que regulam a remodelação da matriz extracelular (MEC) e como isto influencia no comportamento localmente invasivo presente em alguns destes tumores. A Transição Epitélio-Mesenquimal (TEM conversão do fenótipo epitelial em mesenquimal) é bem caracterizada em diversos carcinomas, culminando em mestástase. MMPs são enzimas que degradam os componentes da MEC, geram moléculas bioativas, participam da TEM e o controle da remodelação da MEC dá-se pelo balanço entre elas, seus inibidores (TIMPs e RECK) e seu ativador (EMMPRIN). Assim, o objetivo deste trabalho foi delinear o perfil de expressão das MMPs (-2, -7, -9 e -14), seus inibidores (TIMPs -2, -3, -4 e RECK), seu ativador (EMMPRIN) e marcadores da TEM (Snail, Slug, N-caderina, Fibronectina, a-Actina de músculo liso e Vimentina) em Ameloblastomas (AB) e Tumores Odontogênicos Cístico Calcificantes (TOCC). Ainda, realizamos a comparação da expressão de cada molécula avaliada em cada compartimento celular (epitélio e estroma) e correlação entre as moléculas avaliadas no mesmo tumor. Utilizamos 19 casos de AB e 18 casos de TOCC (Serviço de Anatomia Patológica da FOUSP), localização das enzimas/proteínas por imunoistoquímica e analisadas nos compartimentos epitelial e estromal. Todas as proteínas/enzimas analisadas foram detectadas tanto nos AB quanto nos TOCC, sendo a maioria expressa em ambos os compartimentos. A N-caderina foi localizada apenas no epitélio dos AB e a Vimentina somente no estroma em ambos os tumores. Na comparação entre o epitélio x estroma dos ameloblastomas, verificamos que houve diferença estatisticamente significante (p<0,05) para a MMP-2, MMP-7, EMMPRIN/CD147, Fibronectina, a-Actina de músculo liso, N-caderina, Vimentina, Snail e Slug. Na comparação entre o epitélio x estroma dos TOCC, verificamos que houve diferença estatisticamente significante (p<0,05) para a MMP-9, RECK, EMMPRIN/CD147, Vimentina, N-caderina, Snail e Slug. Assim, entre o epitélio x estroma dos ameloblastomas e TOCC, verificamos que houve diferença estatisticamente significante (p<0,05) para a MMP-2, MMP-7, MMP-9, RECK, EMMPRIN/CD147, Fibronectina, Vimentina, a-Actina de músculo liso, N-caderina, Snail e Slug. Esta é a primeira vez que a EMMPRIN, RECK, TIMP-3, TIMP-4, Ncaderina, Snail e Slug são descritas em TOCC e TIMP-3, TIMP-4, Snail e Slug em ameloblastomas. Concluímos que estas proteínas/enzimas estão diferencialmente expressas tanto no epitélio quanto no estroma destes tumores e sugerimos que estes podem participar do comportamento localmente invasivo.Odontogenic tumors comprise a group of benign neoplasms originating from dental tissues. Research looking for identify molecules involved in the molecular mechanisms that regulate extracellular matrix remodeling (ECM) and how this impacts on locally invasive behavior present in some of these tumors. Epithelial-Mesenchymal Transition (EMT - conversion of epithelial phenotype into mesenchymal phenotype) is well characterized in several carcinomas, leaving to metastasis. MMPs are enzymes that degrade ECM components, generate bioactive molecules, participating in the EMT and control ECM remodeling is given by the balance between them, their inhibitors (TIMPs and RECK) and its activator (EMMPRIN). The aim of this study was evaluate expression profile of MMPs (-2, -7, -9 and - 14), their inhibitors (TIMPs -2, -3, -4 and RECK), its activator (EMMPRIN) and EMT markers (Snail, Slug, N-cadherin, Fibronectin, -smooth muscle actin and Vimentin) in ameloblastomas (AB) and Calcifying Cystic Odontogenic Tumor (CCOT). We also compared the expression of each molecule assessed in each cellular compartment (epithelium and stroma) and correlation between molecules evaluated in the same tumor. We used 19 AB cases and 18 CCOT cases from files of Pathology Laboratory (FOUSP), localization of enzymes/proteins and analyzed by immunohistochemistry in epithelial and stromal compartments. All proteins/enzymes were detected in both AB and CCOT, mostly expressed in both compartments. N-cadherin was localized only in the epithelium of AB and Vimentin only in stromal in both tumors. Comparing \"epithelium vs stroma\" of AB, we observed a statistically significant difference (p <0.05) for MMP-2, MMP-7, EMMPRIN/CD147, Fibronectin, -smooth muscle actin, N-cadherin, Vimentin, Snail and Slug. Comparing \"epithelium vs stroma\" of CCOT, we observed a statistically significant difference (p <0.05) for MMP-9, RECK, EMMPRIN/CD147, Vimentin, N-cadherin, Snail and Slug. Analizing epithelium vs stroma\" between AB and CCOT, we observed a statistically significant difference (p <0.05) for MMP-2, MMP-7, MMP-9, RECK, EMMPRIN/CD147, Fibronectin, Vimentin , -smooth muscle actin, N-cadherin, Snail and Slug. This is the first time that EMMPRIN, RECK, TIMP-3, TIMP-4, N-cadherin, Snail and Slug are described in CCOT and TIMP-3, TIMP-4, Snail and Slug in AB. We conclude that these proteins/enzymes are differentially expressed in both epithelium and stroma of these tumors and suggest that they may participate locally invasive behavior.
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Nel, Sulette. "Immunohistochemical profile of odontogenic epithelium of developing dog teeth (Canis Familiaris)." Diss., 2009. http://hdl.handle.net/2263/28704.
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Similarities between the acanthomatous epulis and ameloblastomas resulted in debate regarding the nature and origin of the acanthomatous epulis found in dogs. In an attempt to elucidate the origin and character of the acanthomatous epulides, this study aimed to find suitable cell markers to identify odontogenic epithelium versus oral epithelium in developing dog teeth in order to use in future research on the pathogenesis and pathology of odontogenic neoplasms in dogs. As specific markers for odontogenic epithelium have not been described in dog tissue, proposed markers of odontogenic epithelium of human and rat tissues were tested on developing dog teeth. Keratin 14, keratin 19, amelogenin, p75 neurotrophin receptor and calretinin have been proposed as markers for inner enamel epithelium and/or ameloblasts in human and rat tissue and was therefore included in this study. Keratin 14 and keratin 19 can not be regarded as specific markers of odontogenic epithelium as various other types of epithelium also stained positive with these markers. Amelogenin could be a promising marker to distinguish between odontogenic tumours and non-odontogenic tumours as it was only detected in odontogenic tissues in this study. However, amelogenin has also been observed in other tissues in dogs and rats, and therefore further studies on this protein will be needed to elucidate the expression profile of amelogenin in odontogenic versus non-odontogenic tissues in dogs. p75 Neurotrophin receptor expression was restricted to certain regions of the inner enamel epithelium and no staining was observed in other epithelial cells. It therefore seems to be a promising marker to differentiate between odontogenic and non-odontogenic epithelium, but the widespread staining observed in the mesenchymal tissue makes differentiation between odontogenic and non-odontogenic stromal elements impossible. Calretinin staining was observed in the alveolar epithelial cells directly overlying the developing tooth germ, proposed as the oral epithelium where the dental lamina takes origin from, as well as the dental laminae and Serres rests. No staining was observed in the rest of the oral epithelium and it can therefore be proposed that calretinin could be a useful marker to distinguish between odontogenic and non-odontogenic epithelial cells. In light of the results found in this study on foetal tissue, the expression profile may be different in adult tissue. Odontogenic tumours in adult dogs may originate from remnants of odontogenic tissue like Serres rests and Malassez rests. It is therefore proposed that this study be repeated on adult dog tissue with specific reference to Serres rests, Malassez rests and the associated gingiva CopyrightDissertation (MSc)--University of Pretoria, 2009.
Oral Pathology and Oral Biology
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Mendonça, Soraia Juliana Leite. "Patologia cística de origem odontogénica: classificação, histologia e embriologia." Master's thesis, 2018. http://hdl.handle.net/10284/7602.
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Grande parte das lesões diagnosticadas na cavidade oral correspondem a cistos odontogénicos. Estes cistos surgem do epitélio de um gérmen dentário durante ou após a odontogénese se completar, podendo ser de origem inflamatória ou de desenvolvimento. Estas lesões intra-ósseas costumam ser assintomáticas, e o paciente só procura ajuda quando a lesão já se encontra desenvolvida. Esta narrativa bibliográfica tem como objetivo determinar a diferente classificação, prevalência, histologia e a apresentação clínica das diferentes patologias císticas odontogénicas. A metodologia consistiu numa pesquisa efetuada nas bases de dados PubMed, Medline, Scielo, B-on, google académicos. No período entre Março e Julho de 2018, as palavras chave utilizadas foram: odontogenic cysts, odontogenic epithelium, histology, clinical features, embryology. A sensibilização da população e das classes médicas para as lesões císticas que possam estar presentes na cavidade oral poderia fazer diferença no sucesso antecipado destas patologias. Neste sentido, é necessário o clínico conhecer bem as lesões da cavidade oral, fazer uma análise sistemática e cuidadosa das lesões radiolucentes e realizar todos os exames complementares necessários para chegar a um diagnóstico correto.Most of the lesions diagnosed in the oral cavity correspond to odontogenic cysts. These cysts arise from the epithelium of a dental germ, during or after odontogenesis when is completed, and it can be of inflammatory or developmental origin. These intraosseous lesions are usually asymptomatic, and the patient only seeks for help when the lesion is already developed. This bibliographic narrative aims to determine the different classification, prevalence, histology and clinical presentation of different odontogenic cystic pathologies. The methodology consisted on a research carried out in the databases; PubMed, Medline, Scielo, B-on, google academic. In the period between March and July 2018, the keywords used were: odontogenic cysts, odontogenic epithelium, histology, clinical features, embryology. The sensibilization of the population and of the medical classes for the cystic lesions that are present in the oral cavity could make a difference in the early success of these pathologies. In this sense, it is necessary for the clinician to know well the lesions of the oral cavity, to make a systematic and careful analysis of the radiolucent lesions and to perform all the complementary exams necessary to arrive at a correct diagnosis.
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Nickolaychuk, Brent R. "Evidence for a role pf MAP kinases (ERK1 and pERK) in proliferating and differentiating odontogenic epithelia." 2001. http://hdl.handle.net/1993/1987.
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The epithelial rests of Malassez (ERM), remnants of odontogenic epithelium, have been implicated in maintaining the periodontal space by stimulating osteoclastic bone resorption and interstitial matrix degradation. While the binding of epidermal growth factor (EGF) to its receptor (EGFr) on ERM appears to play a central role in the functional activation of these cells, the nature of intracellular signaling pathways downstream of EGFr remains unclear. Mitogen-activated protein (MAP) kinases (or extracellular signal-regulated kinases - ERKs) have been described as downstream mediators of EGF-induced cellular activation in other tissues. The purpose of this study was to determine the expression pattern of ERK1 and its phosphorylated form (pERK) in proliferating and differentiating odontogenic epithelia, including ERM, in the presence or absence of inflammation. To this end, immunohistochemistry for ERK1, pERK, PCNA (marker for cycling cells), and PAN-cytokeratin (marker for epithelial differentiation) was performed on paraffin-embedded sections of dental follicles and odontogenic cysts. (Abstract shortened by UMI.)
Books on the topic "Odontogenic epithelium"
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Li, Tie-jun. Immunocytochemical studies of proliferation markers in pathological odontogenic epithelium. Birmingham: University of Birmingham, 1995.
Find full textBook chapters on the topic "Odontogenic epithelium"
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Chi, Angela. "Odontogenic Epithelial Hamartoma." In Encyclopedia of Soil Science, 266–69. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-3-319-28085-1_750.
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Slootweg, Pieter. "Epithelial Odontogenic Tumors." In Pathology of the Maxillofacial Bones, 33–59. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16961-3_3.
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Prein, Joachim, Wolfgang Remagen, Bernd Spiessl, and Erwin Uehlinger. "Calcifying Epithelial Odontogenic Tumor." In Atlas of Tumors of the Facial Skeleton, 54–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70949-4_14.
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Chi, Angela. "Calcifying Epithelial Odontogenic Tumor." In Dental and Oral Pathology, 52–56. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28085-1_660.
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Chi, Angela. "Odontogenic Gingival Epithelial Hamartoma." In Encyclopedia of Soil Science, 278. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-3-319-28085-1_753.
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Slootweg, Pieter. "Odontogenic Tumors: Mixed Epithelial and Mesenchymal." In Pathology of the Maxillofacial Bones, 77–97. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16961-3_5.
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Isobe, Takashi, Takanori Miki, Fuyuki Kametani, and Tomotaka Shinoda. "Amyloid Associated with Calcifying Epithelial Odontogenic Tumor — A New Type of Amyloid Fibril Protein CEOT." In Amyloidosis, 805–11. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2199-6_100.
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Robinson, Max, Keith Hunter, Michael Pemberton, and Philip Sloan. "Jaw cysts and odontogenic tumours." In Soames' & Southam's Oral Pathology. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199697786.003.0011.
Full textAbstract:
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.
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Smith, A. J., and J. B. Matthews. "Odontogenic Epithelium and its Residues." In Investigative Pathology of the Odontogenic Cysts, 53–86. CRC Press, 2019. http://dx.doi.org/10.1201/9780429274329-3.
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"Calcifying Epithelial Odontogenic Tumor." In Diagnostic Pathology: Head and Neck, 660–61. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-39255-6.50210-6.
Full textConference papers on the topic "Odontogenic epithelium"
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Diniz, Marina Goncalves, Carolina Cavalieri Gomes, Bruna Viana Antonini Guimaraes, Alessandra Pires Duarte, and Ricardo Santiago Gomez. "Abstract 702: BRAF V600E mutation in benign and malignant epithelial odontogenic tumors." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-702.
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