Expression of CD34, VEGFR3 and eosinophil density in selected odontogenic tumors- a pilot study

Abstract

Background: Limited statistically and clinically significant studies have been down on connective tissue factors in the odontogenic tumors. Therefore, the aim of this study was to determine the biological behavior of two selected epithelial odontogenic tumors (Ameloblastoma and Adenomatoid odontogenic tumor) by detecting CD34, VEGFR3 and eosinophil densities. Methods: In this cross-sectional study, paraffin blocks including 20 cases of ameloblastoma and 20 (AOT), were selected. Totally, 4 sections were prepared for hematoxylin-eosin, Congo red staining, immunohistochemistry with CD34 and VEGFR3. Expression of VEGFR3, CD34 and lymphatic, blood vessels and eosinophil densities was examined. Results: The mean of blood, lymphatic vessels and eosinophils densities in ameloblastoma were 14.9 ± 6.4, 4.4 ± 2 and 3.2 ± 2.7, respectively; and in AOT, they were 8.9 ± 3.4, 3.6 ± 1.3 and 1.2 ± 07, respectively. There was a significant difference in eosinophils and blood vessels densities between the two lesions (p = 0.005; p = 0.003). By increasing the density of eosinophils, the density of the blood vessels increased in both lesions (r = 0.539, P = 0.001) There was no positive relationship between eosinophils and lymphatic vessels densities in the two above mentioned odontogenic lesions (p = 0.288, R = 0.191) Conclusion: It can be suggested that tumor angiogenesis and eosinophil densities may play a more effective role than lymphangiogenesis in local invasive behavior of ameloblastoma rather than AOT.

Contrast-enhanced multidetector computed tomography features and histogram analysis can differentiate ameloblastomas from central giant cell granulomas

“…The difference in enhancement patterns may be explained based on microvascular density (MVD) of these two tumours. While there are no studies directly comparing MVD of these two entities, separate studies have shown that ameloblastomas had an MVD of 14.9 ± 6[ 27 ] compared to 24.5 ± 5.8 in CGCGs[ 28 ]. This difference, we hypothesise, would result in a faster and a more considerable peak enhancement in CGCGs than in ameloblastomas, which would then translate to differences in the maximum and minimum venous phase-contrast enhancement of CGCGs.…”