Methods: Gingivitis was provoked by placing ligature around and between the lower incisors next to the gingiva and building light-curing resin composite material upon it in order to make plaque retention in anaesthetized Wistar male rats (n=7). Seven days later VEGFR2 antagonist ZM323881 was dripped (10 µl, 20 μg/ml) upon the gingiva next to the lower incisors. Diameter changes of the selected gingival venule were observed by vital microscopy combined with digital photography at the lower incisors in specified times. Animals with healthy gingiva served as control using the same protocol. Venule diameter changes were compared to the start-up and to the values of the control group as well (mean ± SE; p<0.05). Immunohistochemical analysis was utilized to localize VEGFR2. Repeated Measures ANOVA was applied for statistical analysis.
Results: There was a significant vasodilation in experimental gingivitis as compared to the diameter of the same venule under normal circumstances (1013 ± 157 µm and 407 ± 51 µm, respectively). After the local application of ZM323881 there was a significant vasoconstriction in the venules of the inflamed gingiva as compared to the start-up in the 15., 30. and in the 60. minutes (84.81 ± 6.01 %, 81.81 ± 6.44 %, 82.47 ± 4.77 %, respectively). There was no change of venule diameter in the control group. Immunohistochemical analysis showed strong reaction in the endothelium of the venules in gingivitis, i.e. VEGFR2 expression was grown as compared to the control, where no reaction was found.
Conclusion: Our findings suggest, that VEGF has an important role in the vasodilation of the gingival venules in gingivitis.
This study was supported by grants OTKA T042584 and T049708.