Angiogênese (WT1, CD31 e CD105) e mutação (Gene H3F3A) em lesões centrais de células gigantes agressivas e não agressivas

• Ano de defesa: 2019
• Autor(a) principal: Oliveira Filho, Sérgio Alves de
• Orientador(a): Mendonça, Elismauro Francisco de
• Banca de defesa: Mendonça, Elismauro Francisco de, Silva, Fernanda Paula Yamamoto, Costa, César Augusto Sam Tiago Vilanova
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Goiás
• Programa de Pós-Graduação: Programa de Pós-graduação em Odontologia (FO)
• Departamento: Faculdade de Odontologia - FO (RG)
• País: Brasil
• Palavras-chave em Português: Granuloma de células gigantes; Proteínas WT1; Molécula-1 de adesão celular endotelial de plaquetas; Endoglina; Tumor de células gigantes do osso; Platelet endothelial cell adhesion molecule-1; Histonas
• Palavras-chave em Inglês: WT1 Proteins; Endoglin; Giant cell tumor of bone; Histones; Giant cell granuloma
• Área do conhecimento CNPq: ODONTOLOGIA::CLINICA ODONTOLOGICA
• Link de acesso: http://repositorio.bc.ufg.br/tede/handle/tede/10108

A central giant cell lesion (CGCL) is a benign osteolytic lesion that affects gnathic bones and has a controversial etiology, a variable biological behavior, and can be classified as aggressive or nonaggressive. Although it is highly vascularized, there is no consensus about its neoplastic or proliferative vascular origin or whether it is a distinct lesion from a giant cell tumor (GCT). It is speculated that a GCT shares histological features and has a biological behavior similar to aggressive CGCLs. A genetic mutation located in the H3F3A gene codon G34W of the histone H3.3 protein has been found in GCTs; however, little is known about this mutation in CGCLs. The purpose of this study was to evaluate aggressive (n = 9) and nonaggressive (n = 29) CGCL specimens using WT1, CD31 and CD105 (angiogenic) and histone H3.3 G34W (mutational) markers using an immunohistochemistry technique. WT1 was positively expressed in all specimens, both in mononuclear and giant cells, with higher expression in aggressive CGCL mononuclear cells. CD31 and CD105 were expressed on microvessels, and their microvascular density (MVD) was higher in aggressive lesions. The CD105 MVD was higher than the CD31 MVD, indicating a higher degree of neoangiogenesis in both groups compared to the preexisting vascularization. There was no statistically significant difference between angiogenic marker expressions between groups. There was no expression of histone H3.3 gene mutation in aggressive or nonaggressive lesions. In summary, the results indicate that CGCLs are proliferative neoplastic vascular lesions that present a high proliferative angiogenic profile in aggressive and nonaggressive lesions and, despite their biological behavior, do not express histone H3.3 mutation, which characterizes the distinction of GCTs.