The detection and comparison of angiogenesis-associated factors in pyogenic granuloma by immunohistochemistry.
BACKGROUND
Pyogenic granuloma is a benign inflammatory lesion demonstrating obvious activity of angiogenesis. Female steroid hormones are believed to play important roles in the etiology because the lesion is frequently found in females with high levels of sex hormones. Few molecular mechanisms of the pathogenesis have been proposed and proven. The purpose of this study was to detect and compare the expression of angiogenesis-associated factors among healthy gingiva, gingiva from periodontitis, and pyogenic granuloma to 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 immunohistochemistry to detect and compare the expression of 2 angiogenesis enhancers, i.e., vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), 2 angiogenesis inhibitors, i.e., angiostatin and thrombospondin-1 (TSP-1), and estrogen receptor (ER). Using the subject as the unit of statistical analysis, either analysis of variance or chi-square analysis was employed 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. Angiostatin was expressed significantly less in pyogenic granuloma than the other 2 groups and was mostly localized in the nuclei of endothelial cells and epithelial 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 pyogenic granuloma is due to the imbalance between angiogenesis enhancers and inhibitors. Whether and how the angiogenesis-associated factors are regulated by female steroid hormones remain to be answered.
Yuan
K
K
Dental Department, National Cheng-Kung University Hospital, Tainan, Taiwan.
Jin
Y T
YT
Lin
M T
MT
D000328:Adult; D000704:Analysis of Variance; D043168:Angiostatins; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D016228:Endothelial Growth Factors / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D005881:Gingiva / Q000098:blood supply / Q000378:metabolism; D005882:Gingival Diseases / Q000209:etiology* / Q000378:metabolism*; D017789:Granuloma, Pyogenic / Q000209:etiology* / Q000378:metabolism*; D006801:Humans; D007124:Immunoenzyme Techniques; D008222:Lymphokines / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000378:metabolism*; D010446:Peptide Fragments / Q000378:metabolism; D010518:Periodontitis / Q000378:metabolism; D010958:Plasminogen / Q000378:metabolism; D011960:Receptors, Estrogen / Q000378:metabolism; D019700:Thrombospondin 1 / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
D016228:Endothelial Growth Factors; D008222:Lymphokines; D010446:Peptide Fragments; D011960:Receptors, Estrogen; D019700:Thrombospondin 1; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D016222:Fibroblast Growth Factor 2; D043168:Angiostatins; D010958:Plasminogen