Elastin Accumulation in Actinic Cheilitis with Different Degrees of Epithelial Dysplasia

The extracellular matrix (ECM) plays an important role in the regulation of biological events such as the development of cell migration, proliferation and differentiation. Chronic sun exposure causes changes present in the ECM of actinic cheilitis (AC), a premalignant lesion of the lower lip which h...

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Published inInternational journal of morphology Vol. 30; no. 2; pp. 627 - 633
Main Authors Araújo, Caliandra Pinto, Xavier, Flávia Caló de Aquino, Gurgel, Clarissa Araújo Silva, Ramos, Eduardo Antônio Gonçalves, Freitas, Valéria Souza, Schlaepfer-Sales, Caroline Brandi, Ramalho, Luciana Maria Pedreira, dos Santos, Jean Nunes
Format Journal Article
LanguageEnglish
Portuguese
Published Sociedad Chilena de Anatomía 01.06.2012
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Summary:The extracellular matrix (ECM) plays an important role in the regulation of biological events such as the development of cell migration, proliferation and differentiation. Chronic sun exposure causes changes present in the ECM of actinic cheilitis (AC), a premalignant lesion of the lower lip which helps to understand the carcinogenesis of the lip. This study aimed to investigate elastin, the main component of solar elastosis alternating current in an attempt to establish the relationship between this protein and ECM in epithelial dysplasia. Paraffin embedded tissue sections of the lesions of 35 cases of AC were analyzed by immunohistochemistry for elastin, and became the association with the degree of epithelial dysplasia and age. Highest scores of elastin (+3) was predominant in 45.7% of cases of AC, especially in cases of severe dysplasia (n = 3). When comparing the scores of elastin between the different grades of epithelial dysplasia showed no significant difference (P> 0.05, Kruskal-Wallis). This study was not able to demonstrate the influence of elastin on the severity of epithelial dysplasia in AC. Additional studies on other ECM proteins must be conducted in an attempt to better understand the mechanism of malignant progression of the AC.
ISSN:0717-9502
0717-9502
DOI:10.4067/S0717-95022012000200044