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Volume 16 , Issue 3
May/June 2001

Pages 389-393

Vascular Endothelial Growth Factor and Microvessel Density Around Healthy and Failing Dental Implants

Roberto Cornelini, DDS, Luciano Artese, MD, Corrado Rubini, MD, Massimiliano Fioroni, DDS, Giuseppina Ferrero, MD, Alfredo Santinelli, MD, Adriano Piattelli, MD, DDS

PMID: 11432658

Inflammatory infiltrate may be important in the evolution of inflammatory processes involving peri-implant tissues. Angiogenesis is an important feature of inflammation and healing, but its role in the development and progression or in the healing of periodontal lesions has not been elucidated. Vascular endothelial growth factor (VEGF) is a potent inducer of endothelial cell proliferation. The aim of the present study was to conduct a comparative immunohistochemical evaluation of VEGF and microvessel density (MVD) in normal keratinized gingiva and in peri-implant soft tissues surrounding failing implants. Fifteen patients participated in this study. Ten biopsies were taken from healthy keratinized gingiva, and 10 were taken from peri-implant soft tissues surrounding failing non-submerged implants. In healthy sites, the endothelial lining cells of the vessels always tested positive for VEGF; also, VEGF intensity was high in most cases. Stromal cells were positive for VEGF in 70% to 90% of samples. The MVD was 60.250 5.123. In peri-implantitis samples, the cells of the inflammatory infiltrate were positive for VEGF in 80% to 100% of cases, and the VEGF intensity was low in all cases. The stromal cells were positive for VEGF in 90% to 100% of cases, and in most cases the intensity was low. The MVD was 101.800 11.256. The difference in MVD between healthy sites and peri-implantitis was statistically significant (P = .0158). Expression of VEGF was lower in peri-implantitis samples, and this difference was statistically significant (P = .0373). Because of its extensive presence, VEGF is probably a factor in both the maintenance of periodontal physiology and in the progression of peri-implant inflammatory disease. (INT J ORAL MAXILLOFAC IMPLANTS 2001;16:389-393)

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