ASSOCIATION OF THE PI3K/AKT/mTOR/NF-κB PATHWAY WITH CELLULAR CANNIBALISM IN GIANT CELL LESION: AN IMMUNOHISTOCHEMICAL STUDY
Giant Cells; Giant Cell Tumors; Granuloma, Giant Cell; PTEN Phosphohydrolase; Regulatory-Associated Protein of mTOR; Immunohistochemistry
BACKGROUND: The maxillofacial region may be affected by giant cell lesions (GCLs) that exhibit distinct clinical behavior and nature. Among them, the central giant cell granuloma (CGCG) is a benign lesion, sometimes destructive osteolytic lesion composed of giant cell type osteoclast, cannibal and mononuclear cells. Cell cannibalism molecular mechanism is not clear in this lesion. However, an association between the PI3K/AKT/mTOR/NF-κB signaling pathway and this process is suggested. OBJECTIVE: To evaluate the association between PI3K/AKT/mTOR/NF-κB signaling pathway and cell cannibalism in giant cell lesions, as well as with CGCGs aggressiveness. METHODS: The sample will be composed of 20 cases of peripheral giant cell granuloma (PGCG), 40 cases of CGCG (20 non-aggressive CGCG and 20 aggressive CGCGs), and 18 cases of giant cell tumor of bone (GCT). The sample will be submitted to immunohistochemical analysis using mTOR, PTEN, NF- κB, and p63 antibodies. Five independent fields will be photographed in light microscopy in a ×400 magnification. Afterward, positive multinucleated giant cells, mononuclear cells, and cannibal multinucleated giant cells will be quantified, and the result will be expressed by percentage using the labeling index. Subsequently, the result will be submitted to the appropriate statistical test through the software SPSS for Windows (Statistical Package for Social Sciences; IBM, USA, 22.0 version), and the statistical significance will be set at 5% (α = 0.05).