Name: Susy Carmelita Pereira do Nascimento
Type: MSc dissertation
Publication date: 06/09/2012
Advisor:
Name |
Role |
|---|---|
| Liliana Aparecida Pimenta de Barros | Advisor * |
Examining board:
| Name |
Role |
|---|---|
| Danielle Resende Camisasca Barroso | External Examiner * |
| Leticia Nogueira da Gama de Souza | Internal Examiner * |
| Liliana Aparecida Pimenta de Barros | Advisor * |
Summary: The oral leukoplakia, which is a potentially malignant disorder commonly found in the oral cavity and the Squamous Cell Carcinoma (SCC), the most common neoplasm in the maxillofacial region, are the main lesions in the understanding of oral arcinogenesis. The study of the transition from oral epithelial dysplasia for SCC involves not only histopathological aspects, but also the presence of biomarkers that complement the prognostic parameters of pathology services. OBJECTIVE: Describe the socio-demographic data), exposure to risk factors and site of injury in different lesions and determine the degree of dysplasia and differentiation for leukoplakia and SCC, respectively;; correlate dysplastic features with clinical data;; evaluate the profile of TIMP-1 expression and correlate with dysplasia. MATERIAL AND METHODS: Files of patients with the clinical and histological diagnosis of leukoplakia and SCC from 2004 to 2010 were reviewed retrospectively in the Oral Pathology Lab, Dentistry
College, Federal University of Espírito Santo, Brazil. All clinical history data were obtained from those files. For histopathological study, HE slides were analyzed to etermine epithelial dysplasia degree to leukoplakia and carcinoma degree. New slides were obtained and submitted to immunohistochemical assay to determine expression profile of TIMP-1. Parenchyma and stroma were evaluated, and different layers of the epithelium. RESULTS: There were 32 cases of leukoplakia and 23 cases of SCC. Patients ranged 26-77 and 42-89 years were diagnosed with eukoplakia and SCC respectively. The jugal mucosa was the most frequently site in leukoplakia, although tongue represent the main site to SCC. According to dysplasia grade, 6 cases of leukoplakia were diagnosed with mild-grade, 17 with moderate and 9 with severe-grade. In SCC cases, 7 were level I, 14 level II and 2 level III. Some representative correlation were achieved between clinical and microscopic data. In all
cases was detected presence of TIMP-1 in the stroma and parenchyma. In mild
leukoplakia the basal layer with hyperplasia showed intense immunostaining, on the other hand, cells with loss of polarity had lower expression. In moderate leukoplakia all epithelium layers, except the cornea, presented labeling. Spinous layer of severe leukoplakia was the most intensely marked. In SCC grade I, the deeper layer showed ntense cells labeling in areas of pleomorphism and mitoses, and tumor islands the
less differentiated cells were pour marked. In SCC grade II labeling was observed in basal cell and in spinous layer, however, parabasal layer was not marked. Also less differentiated cells did not express the protein. CONCLUSION: For better understanding of malignant and aggressive behavior of SCC, it is important to search or correlations between clinical, histopathological and molecular features. Epithelial ysplasia is an important aspect that sould be analyzed, WHEREas TIMP-1 could
represent a valuable tool in other to sstudy oral mucosa carcinogenesis.
