52 resultados para unicystic ameloblastoma


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We investigated the immunohistochemistry expression of claudins -1 and -7 in ameloblastoma and in human dental germs on the pattern of distribution (focal, regional or diffuse), the cells that expressed (if central or peripheral) and the location of that expression in the cell components recital membrane, cytoplasm and nucleus. Among the 29 cases of ameloblastoma, 24 were type solid and 6 unicystic. In 7 mandibular specimens of human fetuses found dental germs from the stage of bud to the crown. We note that the pattern of expression in the dental germs was variable for claudinas studied according to the cell type and stage of differentiation and was invariate only in the cells of stellate reticulum. In epithelium internal of enamel organ, claudin-1 has been decreasing with the progression of differentiation as to claudina-7 that was found in the cells of the peripheral papilla. For ameloblastoma the expression was more significant than that observed in dental germs. Fisher s exact test no found association between the expression of claudinas cells in central and peripheral and the type of ameloblastoma (solid or unicystic). Thus, in general the claudin-1 was positive in the central cell of 93,1% of the cases and in peripheral cells of 51,7%. The claudin-7 was expressed in the cells of all cases central and peripheral cells from 89,7%. For both claudins the distribution was predominantly diffuse cells both in central and peripheral cells. Given our findings it is suggested that the expression of claudins may be indicative of the involvement of these molecules in morphogenetics events culminating with the dental development and that possibly influence the development of neoplastic ameloblastoma

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BMPs are components superfamily ligands transformation growth fator-β (TGF-β) secreted into the extracellular environment, with mechanisms of intercellular communication through specific ligands and receptors in various target cells, being recognized for its influence in osteogenic induction, also play an important role in tissue homeostasis, cell proliferation, differentiation control , in addition to being present in the development of various malignancies. The aim of this study was to compare the immunohistochemical expression of BMP-2, BMP-4 and its receptors BMPRIA and BMPRII in cases of ameloblastoma and adenomatoid odontogenic tumor. The sample consisted of 20 cases of solid ameloblastoma (SA), 10 cases of ameloblastoma unicystic (UA) and 16 cases of adenomatoid odontogenic tumor (AOT). The expression of BMPs and their receptors was evaluated in the parenchyma and stroma of lesions, establishing the percentage of immunopositive cells (0 - negative; 1-1 % to 10 % of cells positive; 2 - 11% to 25% of positive cells; 3 - 26% to 50% of cells positive; 4 - 51% to 75 % of positive cells; 5 - more than 75% positive cells). Analysis of the expression of BMP-2 revealed no statistically significant differences in parenchymal (p = 0.925) and stromal component (p = 0.345) between the groups, as well as BMP-4 (p = 0.873 / p = 0.131). In the epithelial component, SA and AOT had a higher frequency of score 5. In turn, all cases of UA were classified as score 5. The analysis of the stromal component showed no statistically significant difference between groups with respect to median scores BMPRIA positivity (p = 0.768) and BMPRII (p = 0.779). In the epithelial component of SA and UA, no statistically significant correlations between imunoexpression proteins analyzed were observed. In turn, the group of AOT, statistically significant positive correlations between the scores of expression of all studied proteins were found. In the stromal component, statistically significant positive correlations were found only in the SA group in BMP -4 and BMPRII (r = 0.476; p = .034), in the UA in BMP-4 and BMPRIA (r = 0.709; p = 0.022). The results of this study suggest that the BMPs and their receptors are involved in the development process odontogenic tumors. BMP-4, in turn, besides being present in odontogenic tumors have the capacity to form mineralized material.

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Myofibroblasts are cells that exhibit a hybrid phenotype, sharing the morphological characteristics of fibroblasts and smooth muscle cells, which is acquired during a process called differentiation. These cells then start to express -SMA, a marker that can be used for their identification. Studies suggest that myofibroblasts are related to the aggressiveness of different tumors and that TGF-1 and IFN- play a role in myofibroblast differentiation, stimulating or inhibiting this differentiation, respectively. The objective of this study was to investigate the role of myofibroblasts in epithelial odontogenic tumors, correlating the presence of these cells with the aggressiveness of the tumor. Immunohistochemistry was used to evaluate the expression of TGF-1 and IFN- in myofibroblast differentiation, as well as the expression of MMP-13, which is activated by myofibroblasts, and of EMMPRIN (extracellular matrix metalloproteinase inducer) as a precursor of this MMP. The sample consisted of 20 solid ameloblastomas, 10 unicystic ameloblastomas, 20 odontogenic keratocysts, and 20 adenomatoid odontogenic tumors. For evaluation of myofibroblasts, anti- -SMA-immunoreactive cells were quantified in connective tissue close to the epithelium. Immunoexpression of TGF-1, IFN-, MMP-13 and EMMPRIN was evaluated in the epithelial and connective tissue components, attributing scores of 0 to 4. The results showed a higher concentration of myofibroblasts in solid ameloblastomas (mean of 30.55), followed by odontogenic keratocysts (22.50), unicystic ameloblastomas (20.80), and adenomatoid odontogenic tumors (19.15) (p=0.001). No significant correlation between TGF-1 and IFN- was observed during the process of myofibroblast differentiation. There was also no correlation between the quantity of myofibroblasts and MMP-13 expression. Significant correlations were found between MMP-13 and TGF-1 (r=0.087; p=0.011), between MMP- 13 and IFN- (r=0.348; p=0.003), as well as between EMMPRIN and MMP-13 (r=0.474; p<0.001) and between EMMPRIN and IFN- (r=0.393; p=0.001). The higher quantity of myofibroblasts observed in solid ameloblastomas, odontogenic keratocysts and unicystic ameloblastomas suggests that these cells are one of the factors responsible for the more aggressive biological behavior of these tumors, although the myofibroblast population was not correlated with TGF-1, IFN-, MMP-13 or EMMPRIN. The correlation between MMP- 13 and TGF-1 suggests that the latter induces the expression of this metalloproteinase. The present results also support the well-established role of EMMPRIN as an inducer of MMP-13. Furthermore, the relationship between EMMPRIN and IFN- and between MMP-13 and IFN- suggests synergism in the antifibrotic effect of these markers

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Ameloblastoma is an odontogenic tumor, usually benign, which rarely metastasizes to distant organs. The case of a 27-year-old white woman is described, who presented a metastatic pulmonary ameloblastoma 7 years after the removal of a mandibular ameloblastoma. She presented no pulmonary symptoms, but a lung nodule was found in a chest x-ray during a routine check-up for job admission. Computed tomography (CT) revealed a 2-cm well-defined solitary round nodule without calcifications, leading to the hypothesis of a metastatic tumor. Clinical and CT investigation confirmed no ameloblastoma recurrence in the jaw and no other primary tumor. The diagnosis of metastatic ameloblastoma was confirmed by microscopic evaluation of the pulmonary nodule.

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Short-term cultures of a collagenase disaggregated ameloblastoma previously diagnosed as an adenoid cystic carcinoma of the salivary gland were shown by cytogenetic analysis to have the clonal karyotype 45,XY,del(10)(p12), -22. The data may indicate that the loss of genes of chromosome 22, as well as of 10p, could be a critical event in the evolutionary pattern of odontogenic neoplasias. (C) Elsevier B.V., 1996

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A case of peripheral ameloblastoma in a 57-years-old woman is presented, along with a discussion of the clinical and histological characteristics of the lesion. After clinical and radiographic examinations, and with a differential diagnosis of pyogenic granuloma, an excisional biopsy was performed and the material collected was sent for histological examination. On the basis of the histopathological diagnosis, a second operation was performed with a wide safety margin, including bone tissue, which did not show any involvement with the odontogenic neoplasm.

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Odontogenics tumors are uncommon in the dog. Ameloblastoma is considered a benign, aggressive and non-inductive odontogenic neoplasia commonly located in the incisor teeth. Its conclusive diagnosis is obtained by histopathological examination. Due to the expansive nature of this neoplasia, its resection needs to have an adequate surgical margin so it will have excellent prognostics. A canine, male, Pekingese, 8 years old had an increased volume in the rostral region of the mandible, adhered, consistency moderately firm. Radiography revealed extensive mandibular bone lysis caused by the neoplasia. Biopsy identified the tumor as ameloblastoma. Combining data from the clinical, radiographic and histopatological study and after explain to the owner regarding the postoperative esthetic it was held a bilateral rostral mandibulectomy. The fragment removed was assessed radiographically and histopathologically for evidence of tumor at its edges. The patient is active and healthy without evidence of metastasis or recurrence. The radiographic and histopathologic evaluation of edges of the fragment showed no tumor evidence. The patient is active and healthy without evidence of metastasis or recurrence since January 2010 when mandibulectomy was performed.

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O ameloblastoma e o tumor odontogênico cístico calcificante (TOCC) são tumores odontogênicos que tem origem do epitélio odontogênico, porém ainda não é conhecido o estímulo ou gatilho que leva à transformação neoplásica desses tumores. O comportamento biológico das lesões é distinto, pois o ameloblastoma é um tumor mais agressivo e com taxa de recorrência significativa. Já o TOCC é um tumor menos agressivo e raramente há recorrência e por esse motivo foi utilizado como controle no estudo. Portanto, a elucidação completa dos mecanismos pelos quais esses tumores odontogênicos apresentam tais comportamentos biológicos continua sendo um desafio para os pesquisadores. As c (A Disintegrin and Metalloproteinase with ThromboSpondin) são metaloendopeptidases que são dependentes de zinco em seu domínio catalítico. Essas enzimas possuem ampla atividade catalítica contra uma variedade de substratos como os proteoglicanos (agrecan, brevican e versican), que são proteínas presente na matriz extracelular (MEC). As ADAMTS exibem características estruturais que lhes conferem um grande potencial para exibir múltiplas funções. Exibem função crucial em vários processos como proliferação, adesão, invasão e sinalização celular. As alterações nessas enzimas estão presentes em diversos tumores, o que sugere que estas proteínas podem estar envolvidas no processo carcinogênico em diferentes caminhos. Especificamente a ADAMTS-1 tem sido correlacionada com a tumorigênese de algumas neoplasias como no câncer de mama, pulmão e pâncreas. Assim como a ADAMTS, agrecan, brevican e versican são expressos em vários tumores e a regulação alterada desses proteoglicanos pode contribuir para o desenvolvimento da carcinogênese. Neste trabalho foram estudadas ADAMTS-1, agrecan, brevican e versican no ameloblastoma e TOCC. Foram incluídos 20 casos de ameloblastoma e 6 casos de TOCC, utilizados como controle. A expressão de ADAMTS-1, agrecan, brevican e versican foi avaliada por imunohistoquímica e as áreas de marcação foram mensuradas e analisadas. Para análise de correlação entre as proteínas estudadas utilizou-se o teste de Spearman. Todas as amostras de ameloblastoma expressaram ADAMTS-1, agrecan, brevican e versican. Todas as amostras de TOCC também expressaram as mesmas proteínas, porém numa quantidade significativamente menor que no ameloblastoma. A diferença de expressão de ADAMTS-1 e brevican no epitélio do ameloblastoma e do TOCC foi significante estatisticamente (p<0,0105). Assim como a expressão de agrecan e versican, no epitélio do ameloblastoma e do TOCC, também foi estatisticamente significante (p<0,0067) e (p<0,0148), respectivamente. Não houve correlação entre as proteínas estudadas.

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Ameloblastomas are benign, invasive locally and highly recurrent. It is an odontogenic tumor, characterized by the proliferation of epithelial ameloblastic in a fibrous stroma. This paper reports a case of mandibular ameloblastoma, in patients 27 years of age without pain with developments around 4 years, with about 20 mm at its greatest extent, sessile base and surface coatings full. The treatment of choice was the surgical conservative

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Dental lesions represent about 1% of oral cavity tumors being ameloblastoma the most common one. It is a tumor of epithelial origin that mainly affects the jaw, and less commonly the maxilla. Its clinical presentation is that of an asymptomatic slow-growing tumor. Despite being a benign tumor, it has an invasive behavior with a high rate of recurrence if not treated properly. Objective: To describe the cases of ameloblastoma in a reference department. Methods: Retrospective analysis of 40 cases. The variables analyzed were: age, gender, ethnicity, tumor location, type of treatment, complications and recurrence. Results: The most affected gender was male - 21 cases (52.5%); with a predominance of Caucasians - 24 cases (60%). The mean age was 35.45 years; the most common location was in.the jaw - 37 cases (92.5%). Facial asymmetry was the most frequent complaint. Of the 40 cases, 33 were submitted to surgery. Of those submitted to surgery, 24 (72.72%) underwent segmental resection, with recurrence in 4 (12.12%) cases. Conclusion: Ameloblastoma may relapse when treatment is not performed with broad surgical resection of the lesion with wide safety margins.

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Rho GTPases are proteins that regulate cell cycle, shape, polarization, invasion, migration, and apoptosis, which are important characteristics of normal and neoplastic cells. Rho GTPases expression has been reported in normal tooth germ and several pathologies; however, it has not been evaluated in ameloblastomas. The aim of this study was to analyze the expression and distribution of RhoA, RhoB, Rac1, and Cdc42 Rho GTPases in solid and unicystic ameloblastomas. Three-micrometer sections from paraffin- embedded specimens were evaluated by using an avidin- biotin immunohistochemical method with antibodies against the proteins mentioned above. RhoA and RhoB staining was observed in a high number of cells (P < 0.05) and greater intensity in non-polarized ones. Rac1 was not observed, andCdc42 didnot showany statistical differences between the number of non-polarized and basal positive cells (P > 0.05). Upon comparing the studied ameloblastomas, a higher number of positive cells in the unicystic variant was observed than that in the solid one (P < 0,05). The results obtained suggest that theseGTPases could play a role in the ameloblastoma neoplastic epithelial cell phenotype determination (polarized or non-polarized), as well as in variant (solid or unicystic) and subtype (follicular or plexiform) determination. Furthermore, they could participate in solid ameloblastoma invasion mechanisms. J Oral Pathol Med (2012) 41: 400-407

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OBJECTIVE: The aim was to analyze the expression of E-cadherin and beta-catenin in ameloblastomas and tooth germs to determine their roles in cell differentiation processes and invasiveness compared with odontogenesis. STUDY DESIGN: Twenty-one ameloblastoma cases (16 solid and 5 unicystic tumors) and 5 tooth germs were submitted to the immunohistochemical detection of E-cadherin and beta-catenin. Immunoreactivity was evaluated using descriptive and semiquantitative analysis, investigating the location and intensity of staining. The Fisher exact test was performed, and P values of <.05 were considered to indicate statistical significance. RESULTS: There was no statistically significant difference in the expression of E-cadherin and beta-catenin between solid and unicystic ameloblastomas (P = .59; P = .63; respectively). The same was found when comparing solid and unicystic ameloblastomas with the tooth germs for both E-cadherin (P = .53; P = .44; respectively) and beta-catenin (P = .12; P = .16; respectively). Nuclear staining of beta-catenin was observed in only 4 cases (3 solid and 1 unicystic tumor). CONCLUSION: The results showed no differences in the expression of E-cadherin or beta-catenin between tooth germs and solid and unicystic ameloblastomas. The expression of these molecules seems mainly to be related to the process of cell differentiation.

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El ameloblastoma es una neoplasia odontogénica que muestra un comportamiento agresivo local. Algunas variantes como la uniquística y la desmoplásica tienen un mejor pronóstico que la sólida/multiquística. Presentamos un caso en un varón de 76 años con una lesión radiolúcida interradicular mandibular de apariencia quística, la cual se enucleó quirúrgicamente. Histológicamente correspondió a una lesión desmoplásica con una amplia zona quística que fue diagnosticada como ameloblastoma desmoplásico con predominio quístico. Trascurridos 30 meses no se evidencia recidiva. En este artículo se discuten los principales aspectos clinicopatológicos de estas entidades.

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Ameloblastic fibrosarcoma (AFS), regarded as the malignant counterpart of the benign ameloblastic fibroma, is an extremely rare odontogenic neoplasm with only 68 cases reported in the English literature up to 2009. It is composed of a benign odontogenic epithelium, resembling that of ameloblastoma, and a malignant mesenchymal part exhibiting features of fibrosarcoma. Due to the rarity of the lesion, little is known about its molecular pathogenesis; therefore, in the current study, we sought to evaluate the immunoexpression of Ki67, proliferative cell nuclear antigen, and Bcl-2 proteins in AFS, comparing the results obtained with its benign counterpart, as well as to report a new case of this rare entity affecting a 19-year-old female patient. The results obtained revealed that all the proteins evaluated were overexpressed in the malignant mesenchymal portion of AFS if compared with ameloblastic fibroma, suggesting that nuclear proliferative factors such as Ki67 and proliferative cell nuclear antigen, in association to histopathologic features, may be useful markers for identifying the malignancy and that, despite the lack of molecular analysis in the case reported, Bcl-2 alteration may play a role in AFS pathogenesis. (C) 2010 Elsevier Inc. All rights reserved.