Thiago Fonseca-Silva1, Marina G Diniz1, Sílvia F de Sousa1, Ricardo S Gomez1, Carolina C Gomes2. 1. Department of Oral Surgery and Pathology, School of Dentistry, Biological Sciences Institute, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. 2. Department of Pathology, Biological Sciences Institute, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Abstract
AIMS: Oral leukoplakia (OL) dysplasia is graded on the basis of architectural and cytological features, and grade does not correlate well with malignant transformation. Loss of heterozygosity (LOH) profiles have been validated as risk predictors of OL malignant transformation. We aimed to assess whether the histological parameters used to grade dysplasia show different LOH profiles. METHODS AND RESULTS: Areas of epithelial dysplasia of 29 OL samples were microdissected, and LOH was assessed by use of a panel of 11 microsatellite markers located on chromosomes 3, 9, 11, and 17. Dysplasia was graded, and the cytological and architectural parameters were scored. Dysplasia was graded as mild in 18 samples, moderate in nine, and severe in two. The moderate/severe dysplasias and the mild dysplasias did not show different frequencies of allelic loss. Irregular epithelial stratification was associated with LOH at marker D3S1234 (3p14.2). In addition, the presence of drop-shaped rete ridges and premature keratinization in single cells showed associations with LOH at D9S162 (9p22) and P53 (17p13.1), respectively. CONCLUSIONS: We provide evidence that architectural and cellular changes in OL have different LOH patterns.
AIMS: Oral leukoplakia (OL) dysplasia is graded on the basis of architectural and cytological features, and grade does not correlate well with malignant transformation. Loss of heterozygosity (LOH) profiles have been validated as risk predictors of OL malignant transformation. We aimed to assess whether the histological parameters used to grade dysplasia show different LOH profiles. METHODS AND RESULTS: Areas of epithelial dysplasia of 29 OL samples were microdissected, and LOH was assessed by use of a panel of 11 microsatellite markers located on chromosomes 3, 9, 11, and 17. Dysplasia was graded, and the cytological and architectural parameters were scored. Dysplasia was graded as mild in 18 samples, moderate in nine, and severe in two. The moderate/severe dysplasias and the mild dysplasias did not show different frequencies of allelic loss. Irregular epithelial stratification was associated with LOH at marker D3S1234 (3p14.2). In addition, the presence of drop-shaped rete ridges and premature keratinization in single cells showed associations with LOH at D9S162 (9p22) and P53 (17p13.1), respectively. CONCLUSIONS: We provide evidence that architectural and cellular changes in OL have different LOH patterns.