The detection and comparison of angiogenesis-associated factors in pyogenic granuloma by immunohistochemistry

Background: Pyogenic granuloma is a benign inflammatory lesion demonstratin g obvious activity of angiogenesis. Female steroid hormones are believed to play important roles in the etiology because the lesion is frequently foun d in females with high levels of sex hormones. Few molecular mechanisms of the pathogenesis have been proposed and proven. The purpose of this study w as to detect and compare the expression of angiogenesis-associated factors among healthy gingiva, gingiva from periodontitis, and pyogenic granuloma t o clarify the pathogenesis of pyogenic granuloma. Methods: Fifteen specimens were collected from each of 3 groups of gingiva (healthy gingiva, periodontitis, and pyogenic granuloma). The subjects were age and gender matched. The specimens were processed for immunohistochemis try to detect and compare the expression of 2 angiogenesis enhancers, i.e., vascular endothelial growth factor (VEGF) and basic fibroblast growth fact or (bFGF), 2 angiogenesis inhibitors, i.e., angiostatin and thrombospondin- 1 (TSP-1), and estrogen receptor (ER). Using the subject as the unit of sta tistical analysis, either analysis of variance or chi-square analysis was e mployed to show the statistically significant difference at a level P <0.05 . Results: The pyogenic granuloma group expressed significantly more VEGF and bFGF than healthy gingiva and periodontitis. The positive staining of VEGF was mostly localized in the cytoplasm of macrophages and fibroblasts while that of bFGF was in the extracellular matrix of lamina propria. Angiostati n was expressed significantly less in pyogenic granuloma than the other 2 g roups and was mostly localized in the nuclei of endothelial cells and epith elial cells. There was no significant difference in the expression of TSP-1 and ER among the 3 groups. Conclusions: The results of this research suggest that the etiology of pyog enic granuloma is due to the imbalance between angiogenesis enhancers and i nhibitors. Whether and how the angiogenesis-associated factors are regulate d by female steroid hormones remain to be answered.