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|Title:||﻿Avaliação da freqüência de displasia epitelial em hiperplasias fibrosas inflamatórias e leucoplasias: aspectos histopatológicos e imuno-histoquímicos|
|Keywords:||Hiperplasia Fibrosa Inflamatória; Displasia epitelial; Leucoplasia; Histopatologia; Imuno-histoquímica; Proteína p53; Antígeno Ki-67; inflammatory Fibrous Hyperplasia; Leukoplakia; Epithelial dysplasia; Histopathology; Immunohistochemistry; P53 protein; Ki-67 antigen|
|Abstract:||﻿Cancer development in the oral mucosa may be preceded by epithelial abnormalities ranging from hyperplasia to intraepithelial neoplasia termed histologically epithelial dysplasia. Epithelial dysplasia is characterized by architectural disturbance accompanied by cytological atypia and is generally regarded as one of the most important predictors of malignant transformation in the potentially malignant oral lesions. Dysplasia is a spectrum and no criteria exist to precisely divide this spectrum into mild, moderate and severe categories. It is accepted that the more severe the dysplasia the greater the likelihood is of progression to malignancy. The presence of epithelial dysplasia and its classification must be reported. However, evaluation of dysplastic features is subjective and considerable inter-and intra-observer variations in the scoring of epithelial dysplasia have been reported. In the last decades, several studies have been evaluating the expression of molecular markers that may identify high-risk lesions. The aim of this study was to investigate the frequency and degree of epithelial dysplasia in inflammatory fibrous hyperplasia and leukoplakias, as well as to compare the immunostaining of the antibodies against Ki-67 protein and p53 protein in cases with and without epithelial dysplasia. A retrospective study was performed with 138 specimens diagnosed as inflammatory fibrous hyperplasia and 19 as compatible with the clinical diagnosis of leukoplakia . Blocks of Tissue Microarray (TMA) modified for bigger specimens were constructed for the cases of inflammatory fibrous hyperplasia. Immunohistochemical staining method was used to evaluate the expression of Ki-67 and p53 proteins and the quantification and localization of the immunostaining were related with the presence of epithelial dysplasia. A p value ≤ .05 was considered to indicate statistical significance. Presence of epithelial dysplasia was observed in 13.8% and 52.6% of inflammatory fibrous hyperplasias and leukoplakias, respectively. Moderate epithelial dysplasia was noted in three cases of inflammatory fibrous hyperplasia and all of the remains were graded as mild dysplasia. Ki-67 and p53 proteins were expressed in 97.1% and 97.8% of the inflammatory fibrous hyperplasias, respectively, and in all of leukoplakias. It was noted that the labeling index and the ratio of cases with suprabasal Ki-67 immunoexpression in the hyperplasias with dysplasia were significantly bigger than cases without dysplasia. The p53 labeling index was bigger in leukoplakias with dysplasia than in leukoplakias without dysplasia. However, suprabasal p53 immunostaining was not able to distinguish cases with dysplasia from these without dysplasia. In conclusion, the frequency of epithelial dysplasia in inflammatory fibrous hyperplasia is greater than specified in literature and our results suggest that increase and localization of Ki-67 immunostaining can assist in the diagnosis of the presence/absence of epithelial dysplasia in this group of lesions. The increase of p53 expression in potentially malignant lesions can be associated with early events of oral carcinogenesis|
|Appears in Collections:||TEDE sem arquivo|
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