The transverse and anteroposterior widths of the maxillary sinus on axial CT are convenient indices for its size. The height of the sinus floor altered with changes in sinus volume, but was not directly influenced by the status of the dentition.
Ameloblastoma is an epithelial benign tumor of the odontogenic apparatus and its growth mechanisms are not well understood. Fibroblast growth factor (FGF) 3, FGF7 and FGF10, which are expressed by the neural crest-derived ectomesenchymal cells, induce the proliferation of odontogenic epithelial cells during tooth development. Therefore, we examined the expression and function of these FGFs in ameloblastoma. We examined 32 cases of ameloblastoma as well as AM-1 cells (an ameloblastoma cell line) and studied the expression of FGF3, FGF7, FGF10 and their specific receptors, namely, FGF receptor (FGFR) 1 and FGFR2. Proliferation, mitogen-activated protein kinase (MAPK) signaling and PI3K signaling were examined in AM-1 cells after the addition of FGF7, FGF10 and these neutralizing antibodies. The expression of FGF7, FGF10, FGFR1 and FGFR2 was detected in ameloblastoma cells and AM-1 cells, while that of FGF3 was not. FGF7 and FGF10 stimulated AM-1 cell proliferation and phosphorylation of p44/42 MAPK. However, Akt was not phosphorylated. Blocking the p44/42 MAPK pathway by using a specific mitogen-activated protein/extracellular signal-regulated kinase (MEK) inhibitor (U0126) completely neutralized the effects of FGF7 and FGF10 on AM-1 cell proliferation. However, Anti FGF7 and FGF10 neutralizing antibodies did not decrease cell proliferation and MAPK phosphorylation of AM-1 cells. These results suggested that FGF7 and FGF10 are involved in the proliferation of ameloblastoma cells through the MAPK pathway.
SUMMARYThe muscle membrane and contractile properties of placental and non-placental regions of pregnant and postpartum myometria of the rat were investigated.
An increased attenuation area (IAA) is sometimes seen in the cystic cavity of odontogenic keratocysts (OKCs) on CT scans. The significance of IAA was compared radiologically and histologically in 26 cysts in which a provisional diagnosis of OKC had been made. First, the presence of IAA in the cystic cavity was assessed. Then, relationship between the presence of IAA and data obtained from the cysts, including the CT and histological findings and the visual appearance of the cyst contents, was evaluated. An IAA was frequently seen in large multilocular cysts. There was no relationship between the presence of IAA and aggressive features of the cyst on CT or the cyst contents. Histologically, subepithelial inflammation was often observed in the cysts with IAA. In order to ascertain whether the IAA was due to the keratin mass, a CT scan of a bundle of hair in a water bath was performed and shown to have a similar density. Our study demonstrated that IAA in cystic cavities results from desquamated keratin. Since this seems to occur in long-standing or inflamed multilocular OKCs, it could be used as a significant finding in the diagnosis of OKC.
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