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Increased expression of vascular endothelial growth factor in cyclosporin A-induced gingival overgrowth in rats

Date

2006

Author

Cetinkaya, Burcu Ozkan
Acikgoz, Gokhan
Ayas, Bulent
Aliyev, Eldar
Sakallioglu, Elif Eser

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Abstract

Background: Gingival overgrowth is a side effect associated with cyclosporin A (CsA) therapy. The lesion is characterized by increased epithelial thickness, enlargement of connective tissue, and increased vascularization. The aim of this experimental study was to examine the role of vascular endothelial growth factor (VEGF) in the pathogenesis of CsA-induced gingival overgrowth. Methods: Twenty male Wistar rats were divided into two groups of 10 animals each. For the development of gingival overgrowth, one group received CsA therapy subcutaneously in a daily dose of 10 mg/kg for 60 days, and the other group was used as a control. At the end of the experimental period, rats were subsequently decapitated, and the mandibles with the surrounding gingiva and soft tissue were removed. Half of each sample was used for histomorphometric analysis, and the other half was used for biochemical analysis. Histomorphometric analysis included the measurements of the number and diameter of blood vessel profiles under a microscope, and biochemical analysis included the assessment of VEGF concentration by enzyme-linked immunosorbent assay (ELISA). Results: The histomorphometric findings showed that the number of blood vessel profiles increased in the CsA group compared to the control group (P < 0.001), although the increase in the diameter of blood vessel profiles was not significant (P > 0.05). The biochemical findings showed that in vivo VEGF expression was higher in the CsA group compared to the control group (P < 0.001). Conclusion: The results of this study suggest that increased VEGF expression may be associated with the pathogenesis of CsA-induced gingival overgrowth.

Source

Journal of Periodontology

Volume

77

Issue

1

URI

https://doi.org/10.1902/jop.2006.77.1.54
https://hdl.handle.net/20.500.12712/20802

Collections

  • PubMed İndeksli Yayınlar Koleksiyonu [6144]
  • Scopus İndeksli Yayınlar Koleksiyonu [14046]
  • WoS İndeksli Yayınlar Koleksiyonu [12971]



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