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O presente estudo propôs critérios histopatológicos para o diagnóstico diferencial entre as entidades patológicas. Materiais e métodos: Cortes histológicos de lesões diagnosticadas microscopicamente como Fibroma Oral (n=61) e Hiperplasia Fibrosa Inflamatória (n=75) foram submetidos a diferentes técnicas de coloração (Hematoxilina-eosina, Tricrômio de Masson e Ácido Fosfomolibidico- Vermelho de Picrosírius) para permitir análises quantitativa e qualitativa. A análise qualitativa da densidade do colágeno foi baseada nas lâminas coradas em Hematoxilina- eosina e observada no centro e periferia de cada lesão. Resultados: Fibras colágenas enoveladas eram mais frequentes e mais densas no Fibroma Oral, enquanto as fibras paralelas eram observadas na Hiperplasia Fibrosa Inflamatória (teste exato de Fisher, p, Oral Fibroma and Inflammatory Hyperplasia display similarities in their clinical and histopathological appearance. The present study proposed histopathological criteria for the differential diagnosis between those pathological entities. Histological sections of lesions histopathologically diagnosed as Oral Fibroma (n=61) and Inflammatory Hyperplasia (n=75) and were submitted to different techniques (Hematoxylin-Eosin; Masson Trichrome and Phosphomolybdic acid - Picrosirius red) to allow quantitative and qualitative analysis. The qualitative analysis of collagen density was based on sections stained by Hematoxylin-Eosin and focused in the center and periphery of each lesion. Wound and collagen fibers were more frequent and higher in Oral Fibroma, while parallel fibers were more frequent in Inflammatory Hyperplasia (Fisher’s exact test, p

Objective: the role of p53 expression in odontogenic lesions has not been fully determined, but has been associated with cell proliferation. The purpose of this study was to analyze p53 and proliferating cell nuclear antigen (PCNA) expression in 4 different odontogenic lesions. Design: expression of p53 and PCNA was analyzed in radicular and dentigerous cysts, odontogenic keratocysts, and calcifying odontogenic cysts (Gorlin cysts) using monoclonal antibodies for detection of p53 and PCNA. Results: PCNA expression was significantly greater in the basal layer of radicular cysts and in the suprabasal layer of odontogenic keratocysts; the percentage of p53 positive cells was significantly greater in the suprabasal layer of odontogenic keratocysts. Conclusions: The patterns of p53 and PCNA expression in dentigerous and radicular cysts were similar although the two lesions are of different origin. In odontogenic keratocysts and Gorlin cysts, results indicate a different pattern of tumor growth.

O propósito do presente estudo foi analisar as células epiteliais odontogênicas procurando um entendimento maior sobre a natureza e conseqüentemente o comportamento de algumas lesões odontogênicas. A expressão imunoistoquímica de p53 e PCNA foi analisada em cisto radicular, cisto dentígero, ceratocisto odontogênico e cisto odontogênico calcificante (Cisto de Gorlin) onde verificou-se que no cisto radicular e cisto dentígero a expressão dos marcadores está relacionado com proliferação e stress celular causado pelo estímulo inflamatório e em ceratocisto odontogênico e Cisto de Gorlin a expressão dos marcadores corresponde a proliferação celular não descartando também a presença de mutação no gene TP53. Também foi observada a expressão de Ki-67, EGFR e Survivin em folículo pericoronário, ceratocisto odontogênico e cisto dentígero que mostrou que as células epiteliais dos folículos pericoronários têm potencial proliferativo para formar lesões odontogênicas e que a proliferação das células do cisto dentígero é relacionada com o estímulo inflamatório. Todos os marcadores estudados comprovaram a natureza neoplásica do ceratocisto odontogênico. The purpose of this study was to analyze odontogenic epithelial cells to contribute to the knowledge about their nature and, consequently, about the behavior of certain odontogenic lesions. Immunohistochemical expressions of p53 and PCNA were analyzed in radicular cysts, dentigerous cysts, odontogenic keratocysts and calcifying odontogenic cysts (Gorlin cyst). In radicular and dentigerous cysts, the expression of these markers was associated with cell proliferation and stress caused by an inflammatory stimulus. In keratocysts and Gorlin cysts, the expression of markers corresponded to cell proliferation. Results also showed possible mutation in TP53 gene. Also, Ki-67, EGFR and Survivin were expressed in pericoronal follicles, odontogenic keratocysts and dentigerous cysts, which demonstrated that epithelial cells of pericoronal follicles may proliferate to form odontogenic lesions and that cell proliferation in dentigerous cysts was associated with an inflammatory stimulus. The analysis of all markers under study confirmed the neoplastic nature of odontogenic keratocysts.