Microvascular regulatory role and increased expression of vascular endothelial growth factor receptor type 2 in experimental gingivitis Gyurkovics M, Lohinai Z, Gy } orfi A, Bodor C, Sze´kely AD, Dinya E, Rosivall L. Microvascular regulatory role and increased expression of vascular endothelial growth factor receptor type 2 in experimental gingivitis. J Periodont Res 2012; doi: 10.1111/j.1600-0765.2012.01520.x. © 2012 John Wiley & Sons A/S Objective: The aim of the present study was to investigate the possible microvas- cular regulatory role of vascular endothelial growth factor receptor type 2 (VEGFR2) in experimental gingivitis in rats. Background: Our previous results demonstrated that functionally active VEGFR2s are located in the venules of rat gingiva. While there is no remarkable endogenous gingival VEGF production under normal circumstances, exogenous VEGF, via VEGFR2, shows venodilatory effects. We assumed that VEGF plays an important role in vasoregulatory processes (vasodilation, increased permeability, angiogenesis) of gingival inflammation. Methods: Gingivitis was induced by placing ligatures and composite material around and between the lower incisors of anesthetized Wistar rats next to the gingival margin. Seven days later, VEGFR2 antagonist (ZM323881), was dripped upon the labial gingiva next to the lower incisors. Diameter changes of the selected gingival venules were measured by vital microscopy. Animals with healthy gingiva served as controls. Venule diameter changes were compared to the baseline and to control groups (no ligature). Immunohistochemical and Western blot analysis for VEGFR2 were utilized. Results: After 15, 30 and 60 min of local application of ZM323881, there was a significant venoconstriction in the inflamed gingiva compared to the baseline, while no change was recorded in controls. Endothelium, smooth muscle cells and pericytes of the gingivitis group showed increased VEGFR2 expression. Conclusion: Our findings suggest that there is an increased VEGF production in gingivitis, which may play an important role in vasodilation of rat gingival venules. M. Gyurkovics 1 , Z. Lohinai 1 A. Gy } orfi 1 , C. Bodor 2 , A. D. Sze ´ kely 3 , E. Dinya 4 , L. Rosivall 2 1 Department of Conservative Dentistry, Faculty of Dentistry, Semmelweis University, Budapest, Hungary, 2 Institute of Pathophysiology, Faculty of Medicine, Hungarian Academy of Sciences and Semmelweis University Research Group for Pediatrics and Nephrology, Semmelweis University, Budapest, Hungary, 3 Department of Anatomy, Faculty of Medicine, Histology and Embryology, Semmelweis University, Budapest, Hungary and 4 Institute of Health Informatics, Faculty of Medicine, Semmelweis University, Budapest, Hungary Zsolt Lohinai DMD, PhD, Department of Conservative Dentistry, Faculty of Dentistry, Semmelweis University, 1088 Budapest, Szentkira ´lyi utca 47, Nr 732, Hungary Tel: 00363171598 Fax: 00363171122 e-mail: lohinai@elet2.sote.hu M. Gyurkovics and Z. Lohinai contributed equally to this work and should be considered co-first authors. Key words: experimental gingivitis; rats; VEGF receptor type 2; venule; ZM323881 Accepted for publication July 12, 2012 J Periodontal Res 2012 All rights reserved © 2012 John Wiley & Sons A/S JOURNAL OF PERIODONTAL RESEARCH doi:10.1111/j.1600-0765.2012.01520.x