Angiogenesis pattern and H3.3 histone mutation in aggressive and non-aggressive central giant cell lesions. (October 2021)

• Record Type: Journal Article
• Authors: de Oliveira Filho, Sérgio Alves; Martins, Allisson Filipe Lopes; Mosconi, Carla; de Paula, Henrique Moura; Mendonça, Elismauro Francisco
• Is Part Of: Archives of oral biology. Volume 130(2021)
• Publication Date: 2021-10
• Subjects: CD105 Endoglin -- CD31 Platelet endothelial cell adhesion molecule -- CGCL Central giant cell lesion -- GCT Giant cell tumor -- WT1 Wilm's Tumor Protein 1; central giant cell granuloma -- angiogenisis -- histone; Mouth -- Periodicals; Mouth -- Diseases -- Periodicals; Dentistry -- Periodicals; Electronic journals; 617.6005
• DOI: 10.1016/j.archoralbio.2021.105218
• Languages: English
• ISSNs: 0003-9969

Abstract

Highlights: We evaluated angiogenesis and H3F3A mutation in central giant cell lesions. Central giant cell lesions have a tumoral vascular pattern. Angiogenesis status is similar in the variants of the central giant cell lesions. H3F3A mutation does not occur in central giant cell lesions. Giant cell lesions of gnathic bones and of long bones are not the same entity. Abstract: Objective: The aim of this study was to evaluate angiogenesis in central giant cell lesions (CGCL) and its association with biological behavior. In addition, investigation of the histone H3.3 mutation was performed. Design: Thirty-eight cases of CGCL were classified as aggressive (n = 9) or nonaggressive (n = 29). Cases were submitted to immunohistochemistry to compare angiogenesis using Wilms' tumor protein 1 (WT1), platelet endothelial cell adhesion molecule (CD31) and endoglin (CD105) between groups. To verify the presence of genic mutation, histone H3.3 was investigated. Results: WT1 was expressed in mononuclear and giant cells of all cases. CD31 and CD105 were expressed in CGCL microvessels, with a higher CD105 microvascular density than CD31. No statistically significant difference was observed between groups. None of the cases studied showed the histone mutation. Conclusions: There was no difference between aggressive and nonaggressive lesions regarding the angiogenic markers. The expression of WT1 and CD105 suggests that CGCL presents a tumoral vascular pattern with high neoangiogenic activity. The absence of histone mutation may indicate that CGCL is not a true giant cell tumor.