A moesina, uma das proteínas do complexo ERM (ezrina, radixina e moesina), está envolvida nos processos de migração e invasão tumoral, participando da dinâmica do citoesqueleto na movimentação celular associada à ativação da GTPase Rho-A. O objetivo desse estudo foi avaliar a correlação da imunoexpressão da moesina e da Rho-A em tumores odontogênicos benignos, diagnosticados no Serviço de Anatomia Patológica da Faculdade de Odontologia de Bauru (USP), no período de 1963 a 2009. Um total de 45 tumores odontogênicos benignos incluindo 7 ameloblastomas, 8 tumores odontogênicos adenomatóides, 19 tumores odontogênicos queratocísticos, 2 cistos odontogênicos ortoqueratinizantes, 1 tumor odontogênico epitelial calcificante, 2 fibromas ameloblásticos, 4 fiboodontomas ameloblásticos e 2 tumores odontogênicos císticos calcificantes, foram avaliados quanto a expressão imunohistoquímica da moesina e da Rho-A pelas células odontogênicas. A correlação entre as expressões membranosa e citoplasmática da moesina e da Rho-A pelo epitélio odontogênico nos diferentes tumores foi avaliada pelo teste de correlação de Spearman, com nível de significância de 5%. Os resultados mostraram uma forte expressão membranosa de moesina e citoplasmática de Rho-A em 66,7% e 62,2% dos tumores odontogênicos benignos, respectivamente. Houve uma correlação positiva e estatisticamente significativa entre a expressão membranosa e citoplasmática da moesina (ρ=0,000) e de Rho-A (ρ=0,048) nos tumores. Entretanto, não houve correlação entre as expressões demoesina e de Rho-A nos tumores odontogênicos benignos. Estes resultados comprovam que a moesina e a Rho-A são fortemente expressas pelo epitélio odontogênico neoplásico e, sugerem que ambas proteínas provavelmente participamdo crescimento e expansão local destes tumores odontogênicos benignos. / The moesin, one of the proteins of the ERM complex (ezrin, radixin and moesin), is involved in the migration and tumor invasion processes participating in the cytoskeleton dynamics in cell movement associated with the activation of the GTPase Rho-A. The aim of this study was to evaluate the immunoexpression orrelation of moesin and Rho-A in benign odontogenic tumors, diagnosed at the Bauru School of Dentistry Oral Pathology Biopsy Service of the University of São Paulo in the period of 1963-2009. A total of 45 benign odontogenic tumors including 7 ameloblastomas, 8 adenomatoid odontogenic tumors, 19 keratocystic odontogenic tumors, 2 orthokeratinized odontogenic cyst, 1 calcifying epithelial odontogenic tumor, 2 ameloblastic fibroma, 4 ameloblastic fibroodontoma and 2 calcifying cystic odontogenic tumors, were evaluated for immunohistochemical expression of moesin and Rho-A by odontogenic cells. The correlation between the membranous and cytoplasmic expression of moesin and Rho-A by the odontogenic epithelium in different tumors was evaluated by the Spearman correlation test, with a significance level of 5%. The results showed strong membranous expression of moesin and cytoplasmic expression of Rho-A in 66.7% and 62.2% of the benign odontogenic tumors, respectively. There was a positive and statistically significant correlation between membranous and cytoplasmic expression of moesin (ρ=0.000) and Rho-A (ρ=0.048) in the tumors. However, there was no correlation between the expression of moesin and Rho-A in benign odontogenic tumors. These results show that the moesin and Rho-A are strongly expressed by neoplastic odontogenic epithelium and suggest that both proteins probably participate in the growth and local expansion of these benign odontogenic tumors.

Tumores odontogênicos constituem grupo abrangente de afecções tumorais, sendo ameloblastomas e tumores odontogênicos queratocísticos as lesões benignas de maior frequência, cujas características biológicas são pouco conhecidas. Objetivo do presente estudo foi avaliar o perfil imuno-histoquímico das proteínas pRB e p53 em ameloblastoma e tumor odontogênico queratocístico. Foram avaliadas amostras de material parafinado de 21 casos de ameloblastoma e de 20 casos de tumor odontogênico queratocístico para ensaio de imuno-histoquímica com os anticorpos anti-pRB e anti-p53. A contagem da imuno-marcação foi realizada a partir de fotografias de alta resolução processadas no software ImageJ para quantificação manual em campo de 1000 células. A localização da imuno-marcação para ambos anticorpos foi semelhante, sendo em ameloblastomas predominantemente nas células da periferia e, em tumores odontogênicos queratocísticos, nas camadas suprabasais. Quantitativamente, as porcentagens de células marcadas foram estatisticamente maior nos ameloblastoma para anti-p53 (p=0,01) e maior nos tumores odontogênicos queratocísticos para anti-pRB (p=0,04). Não houve correlação estatística entre a porcentagem de células marcadas para anti-p53 e anti-pRB nos ameloblastomas, porém, esta correlação foi positiva e moderada nos tumores odontogênicos queratocísticos (r=0,537; p=0,018). Nota-se ligeira diferença na quantificação das imuno-marcações para o anti-p53 e anti-pRB. Tais resultados devem ser ponderados pela reduzida casuística, porém, sugerem perfis distintos em mecanismos biológicos determinantes para ambos os tumores. / Odontogenic tumors are a comprehensive group of tumor diseases, being ameloblastomas and keratocystic odontogenic tumors the most frequent benign odontogenic tumors. Their biological characteristics are little unknown. The aim of present study was to evaluate the immunohistochemical profile of pRB and p53 proteins in 21 cases of ameloblastomas and 20 cases of keratocystic odontogenic tumors for anti-pRB and anti-p53 antibodies. The quantification of immunostaining was performed manually with high-resolution photographs processed in the ImageJ software to quantify positive cells in a 1000 cells-field. The location of immunostaining for both antibodies was similar. In ameloblastomas, positive cells are located mainly in the peripheral layers, whereas in keratocystic odontogenic tumors the positive cells are located in the suprabasal layers. Quantitatively, the percentage of labeled cells was statistically higher in ameloblastomas for anti-p53 (p = 0.01) and higher in keratocystic odontogenic tumors for anti-pRB (p = 0.04). There was no statistical correlation between the percentage of labeled cells to anti-p53 and anti-pRB in ameloblastomas, however, its correlation was positive and moderate in keratocystic odontogenic tumors (r = 0.537; p = 0.018). It is possible to identify a slight difference in immuno-quantification for anti-p53 and anti-pRB among these lesions. These results must be pondered by the small sample, however, is suggests a different profile in a preponderant key biological mechanisms for odontogenic tumors.

Thesis (M.D.S.)--University of Hong Kong, 2005.

Made available in DSpace on 2014-06-11T19:32:06Z (GMT). No. of bitstreams: 0 Previous issue date: 2007-09-21Bitstream added on 2014-06-13T18:42:58Z : No. of bitstreams: 1 jardim_ptc_dr_araca.pdf: 424188 bytes, checksum: e24b02b831793bae90189f19233a46f6 (MD5) / O tumor odontogênico adenomatóide (TOA) é um tumor benigno composto de epitélio odontogênico com uma variedade de padrões arquiteturais histológicos, embebido em um estroma de tecido conjuntivo maduro e caracterizado por um crescimento lento, porém progressivo. O tumor odontogênico epitelial calcificante (TOEC) é definido como uma neoplasia odontogênica epitelial localmente invasiva, caracterizada pela presença de material amilóide que pode se tornar calcificado. Ambos recentemente reclassificados pela Organização Mundial da Saúde como tumores de epitélio odontogênico, com estroma fibroso maduro e sem ectomesênquima odontogênico. Com o objetivo de contribuir para o estabelecimento de tratamentos e prognósticos mais precisos, através de um melhor entendimento do comportamento biológico destes tumores, este estudo se propôs aavaliar o potencial proliferativo dos dois tumores que por vezes apresentam aspectos histológicos coincidentes, utilizando a técnica histoquímica do AgNOR e a imunohistoquímica de evidenciação de PCNA, P53 e Ki-67. Foram utilizados 5 espécimes de cada tumor. A análise comparativa dos resultados quantitativos/ qualitativos da histoquímica de evidenciação das NORs e dos resultados imunohistoquímicos para os três anticorpos estudados confirmam o comportamento patológico neoplásico benigno do tumor odontogênico adenomatóide e do tumor odontogênico epitelial calcificante. Foi observada distribuição positiva do PCNA nas células epiteliais das áreas sólidas e adenomatóides do TOA e nas áreas sólidas de células epiteliais poliédricas do TOEC, o que permite sugerir estes sítios como os responsáveis pelo crescimento dos respectivos tumores. / The adenomatoid odontogenic tumor (OAT) is a benign tumor composed of odontogenic epithelium in a variety of histoarquitectural patterns, embedded in a mature connective tissue stroma and characterized by slow but progressive growth. The calcifying epithelial odontogenic tumor (CEOT) is defined as an epithelial odontogenic neoplasia locally invasive, characterized by the presence of amiloyd material that may become calcified. Both were recently reclassified by World Health Organization as tumors of odontogenic epithelium, with mature fibrous stroma without odontogenic ectomesenchyme. With the aim of contributing to the achievement of more precise treatments and prognosis, based on a better understanding of the biological behavior of these tumors, this study proposed evaluation of the proliferative potential of both tumors that sometimes present similar histological patterns, using AgNOR histochemistry and imunohistochemical expression of PCNA, P 53 and Ki- 67. There were analyzed 5 specimens of each tumor. Comparative analysis of quantitative/qualitative results of the NORs staining and the histochemical expression results of the antibodies studied confirm the benign neoplastic pathological behavior of the AOT and CEOT and the positive expression of PCNA distributed among epithelial cells of solid nodules and adenomatoid structures of AOT and among the polyhedral epithelial CEOT cells allowed suggest these sites as the responsible ones for respective tumoral growth.

A relação da podoplanina com a proliferação celular tem sido demonstrada, porém ainda é tema de controvérsia. O objetivo deste estudo foi investigar a expressão da podoplanina em ameloblastomas e remanescentes de epitélio odontogênico (REO) de folículos pericoronários de dentes não-irrompidos e verificar a relação da imunomarcação da podoplanina com a proliferação celular. A amostra incluiu 33 pacientes submetidos à biópsia incisional ou à exérese de ameloblastomas e 32 folículos de pacientes submetidos à extração de dentes não-irrompidos. Todos os espécimes selecionados foram corados pela técnica imuno-histoquímica com os anticorpos anti-podoplanina e anti-Ki-67. A expressão da podoplanina foi avaliada por um método semi-quantitativo de escores. Já o índice de proliferação celular foi obtido pela porcentagem de células positivas (no mínimo 500 células/ameloblastoma e todas as células do REO foram avaliadas). Todos os ameloblastomas apresentaram imunomarcação pela podoplanina nas células periféricas. Nas células centrais, a expressão foi ausente ou fraca. Nos REO, a podoplanina apresentou expressão predominantemente nas células em contato com o tecido conjuntivo. A expressão membranosa da podoplanina foi superior nos ameloblastomas em relação aos REO (!=0,001). Também houve diferença significante entre a imunomarcação citoplasmática e membranosa da podoplanina nos REO (!=0,001). A expressão do Ki-67 foi mais acentuada nos ameloblastomas do que nos REO (!<0,001). A correlação entre a expressão citoplasmática (r= -0,15, != 0, 396) e membranosa (r= 0,00, != 0, 989) da podoplanina e do Ki-67 nos ameloblastomas não foi estatisticamente significante, tampouco entre a imunomarcação citoplasmática (r= 0,15, != 0, 421) e membranosa (r= -0, 09, ! = 0, 629) da podoplanina e do Ki-67 nos REO. Os resultados sugerem que não há associação da podoplanina com a proliferação celular e reforçam a necessidade da elucidação do papel desta proteína em tumores odontogênicos benignos. / The association between podoplanin and cellular proliferative activity has been demonstrated but is still source of debate. The aim of this study was to investigate the expression of podoplanin in ameloblastomas and remnants of odontogenic epithelium (ROE) from dental follicles of unerupted teeth and verify the relation between the podoplanin expression and proliferative activity of the odontogenic cells. Thirty-three patients submitted to the incisional biopsy or resection of ameloblastoma and 32 patients submitted to the extraction of unerupted tooth were selected for analysis. Archived paraffin-embedded ameloblastomas and dental follicles specimens were sectioned and stained with anti-human podoplanin and anti-Ki-67 antibodies. The podoplanin expression by odontogenic epithelial cells was evaluated using a score method and the Ki-67 labelling index was obtained by the percentage of positive odontogenic cells (at least 500 cells/ameloblastoma and all ROE cells). All ameloblastomas showed podoplanin expression in ameloblast-like cells of the epithelial islands. Weak or absent immunostaining was observed in the central cells resembling stellate reticulum. Podoplanin expression in ROE was mainly found in the cells in contact with the connective tissue. Membranous expression of podoplanin in ameloblastomas was stronger than its expression in ROE (!=0.001). Statistically significant difference between cytoplasmic and membranous expression of podoplanin in ROE was observed (!=0.001). The index of cellular odontogenic proliferative activity, verified by Ki-67 expression, was highest in ameloblastomas when compared with ROES (!<0.001). No statistically significant correlation between podoplanin and cellular odontogenic proliferative activity in ameloblastomas and dental follicles was found (!>0.05). These results support the evidence that there is no connection between podoplanin expression and odontogenic cellular proliferative activity in ameloblastomas and reinforce that the exact role of this protein in benign odontogenic tumor needs to be elucidated.

Orientador: Marcio de Moraes / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba / Made available in DSpace on 2018-08-04T00:42:43Z (GMT). No. of bitstreams: 1 MauretteO¿Brien_PaulEdward_M.pdf: 2138527 bytes, checksum: 184b6be2a89636c5de2b0ea675777d7a (MD5) Previous issue date: 2004 / Resumo: O propósito deste estudo foi avaliar retrospectivamente os casos de queratocistos odontogênicos (QO) tratados pela Área de Cirurgia Buco-Maxilo-Facial da Faculdade de Odontologia de Piracicaba da Universidade Estadual de Campinas (FOP-Unicamp), entre os anos 1995 e 2004. Foram avaliadas as características clínicas, histológicas e a eficácia do protocolo de tratamento em 28 pacientes com diagnóstico histológico de queratocisto odontogênico. Observou-se maior prevalência em mulheres (67,9%) de cor branca (57,1%), com idade média de 30 anos. A maioria das lesões estavam localizadas na região de ângulo e ramo mandibular (53,3%) e tinham padrão histológico paraqueratinizado (70%). Do total dos 28 pacientes, 13 (46,4%) apresentavam dente incluso envolvido na lesão. Inicialmente todos os pacientes foram submetidos a biópsia e tratados principalmente por descompressão e posterior curetagem da lesão remanescente (67,85%). O tempo médio de descompressão foi de 9,27 meses. Houve recorrência em 4 pacientes (14,3%), os quais tinham sido tratados com descompressão e curetagem (2 casos) ou unicamente com descompressão (2 casos). Todos os casos de recorrência foram tratados por meio de enucleação e curetagem associado a ostectomia periférica da cavidade óssea remanescente. O tempo médio de proservação de todos os pacientes da amostra foi de 24 meses, (mais ou menos 9,74). De acordo com os resultados podemos concluir que, dentro das características da amostra atendida, os pacientes são em sua maioria, mulheres adultas de cor branca, tratadas principalmente por meio de descompressão da lesão e apresentando taxas de recorrência similares à relatadas na literatura, demonstrando que o tratamento conservador do queratocisto odontogênico por meio do protocolo utilizado mostrou-se eficaz, de baixa morbidade e com índices de recorrências dentro da média relatada na literatura. No entanto, é necessário a contínua proservação buscando os resultados em longo prazo / Abstract: The aim of our study was to retrospectively evaluate all odontogenic keratocysts (OKC) cases treated in the Oral and Maxillofacial Surgery Department of Piracicaba Dental School at Campinas State University in Sao Paulo, Brazil between 1995 and 2004. This study evaluated clinical and histological characteristics of 28 patients all diagnosed with OKC by histopathology analysis and compared the data with that published in the literature. OKC was more prevalent in white (57.1%) and young (average age 30 years) females (67.9%). Most of the lesions (53.3%) occurred in the angle of the mandible and mandibular ramus. The most common histological pattern of OKC was parakeratinazed (70%) and 13 (46.4%) out of 28 patients presented impacted teeth associated with the lesion. Initial biopsy was performed in all patients and all cases were treated according to the Department of Oral and Maxillofacial Surgery Protocol, which consists mainly of decompression followed by curettage of the remaining lesion. The mean time for decompression was 9.27 months. Recurrence occurred in 4 patients (14.3%), who were initially treated with decompression and curettage (2 cases), or with decompression only (2 cases). All recurrent cases were submitted to enucleation and curettage of the remaining bone cavity. The average follow-up time for the 28 cases was 24 months (more or less 9,74). According to these results, we can conclude that adult white females treated for OKC with decompression, present similar recurrence rates to those reported in the literature. This Department of Oral and Maxillofacial Surgery¿s treatment protocol for OKC offers a conservative and effective option with low morbidity and similar recurrence rates to those reported in the literature. However, a long term follow-up is necessary to confirm these conclusions / Mestrado / Cirurgia e Traumatologia Buco-Maxilo-Faciais / Mestre em Clínica Odontológica

Magister Scientiae Dentium - MSc(Dent) / Over the last few decades, and throughout the world, there would seem to have been an increase in the number and severity of infections affecting the maxillofacial region. In the South African setting this seems to be especially evident in the state health system. Maxillofacial infection of odontogenic origin is largely preventable. If treated appropriately and early in the pathological process, the progression of the disease process is generally prevented and complications avoided. Management of maxillofacial infections once established has serious implications for patients and an already stressed health system. The reasons for this perceived increase in infections are likely multifactorial and it is hoped that this study may aid in understanding factors contributing to this burden.

Necrotizing fasciitis (NF) is a critical and rapidly progressive infection of the skin and soft tissue, and it is associated with a high mortality rate. NF of the cervicofacial region is uncommon due to the rich vascular supply of the head and neck, which promotes an efficient immune response to infection. Patients who are immunocompromised or have comorbidities affecting the vasculature, such as diabetes mellitus or peripheral vascular disease, are at an increased risk of more severe disease and outcome. Cervicofacial necrotizing fasciitis (CNF) is most frequently attributed to mucosal damage, such as those related to dental infections or local trauma including medical procedures. Due to its ability to quickly spread to the neck and mediastinum, CNF must be diagnosed and treated expeditiously. In this report, we present a case of a 28-year-old female with a past medical history significant for obesity and tobacco abuse who presented to the emergency department (ED) with fever, left-sided facial pain, cervical pain, and swelling. She had worsening symptoms despite current treatment with clindamycin for a dental abscess. A CT scan of the head and neck revealed an odontogenic abscess complicated by CNF. Intravenous antibiotics were initiated and she underwent prompt surgical intervention. She remained nasally intubated following her surgery due to concern for postoperative edema leading to airway compromise. Following extubation, she experienced an uncomplicated recovery. This case demonstrates that NF is a complication of dental infection that may occur even in young and relatively healthy patients. Additionally, due to the swiftly destructive nature and high mortality rate of CNF, early diagnosis and aggressive medical and surgical therapy are essential to reduce morbidity and mortality.

Statins, hydroxymethylglutaryl-coenzyme-A reductase inhibitors (HMG-Co-A), are known to reduce plasma cholesterol levels. Interestingly, Simvastatin was previously reported to have a positive effect on the proliferation and odontoblastic differentiation of human dental pulp cells. However, the biocompatibility of Simvastatin has not been studied thoroughly. The purpose of this study was to further compare the effectiveness of different concentrations of Simvastatin on the attachment, proliferation, differentiation, toxicity, mineralization, and flow cytometry of human dental pulp cells (HDPCs) and osteoblasts. HDPCs and osteoblasts were cultured with Simvastatin at various concentrations of 1, 10, 25, 50, 75, 100 μmol/L, and 0 μmol/L was used as a control. The cell attachment was evaluated at 16 hours for HDPCs and 9 hours for osteoblasts. The proliferation rate, differentiation, cytotoxicity, and mineralization were investigated at 7, 14 and 21 days. Cell cycle and apoptosis were assessed at 1 and 3 days. Statistical analysis was performed using ANOVA. P-values ≤0.05 were considered statistically significant. The results showed that 25 μmol/L demonstrated the highest cell attachment efficiency when compared to the control in HDPCs (P<0.05). There was no statistical significance (P>0.05) amongst the groups in the cell attachment efficiency in osteoblasts. All tested concentrations showed a significant decrease in the proliferation rate and mineralization (P<0.001) and an increase in cytotoxicity and cytostasis (P<0.001) in both cell types. ALP levels increased in HDPCs and osteoblasts (P<0.001). DSP and RUNX2 levels decreased in HDPCs (P<0.001). OSC levels were increased in osteoblasts, but RUNX2 was decreased (P<0.001). Cell cycle and apoptosis significantly increased as time increased (P<0.001) in both cell types. In conclusion, the present findings showed that Simvastatin adversely affects the proliferation, cell viability of HDPCs and osteoblasts by inducing apoptosis, which were confirmed by flow cytometry results. There was an increase in the odontogenic and osteogenic markers hinting at early differentiation, which decreased as time increased. / 2025-07-10T00:00:00Z

No description available.