Stomatološki glasnik Srbije (Jan 2023)

Vascular endothelial growth factor as a response of denture bearing tissues on mechanical stress in diabetes mellitus

  • Radović Katarina,
  • Brković Božidar,
  • Ilić Jugoslav,
  • Milić-Lemić Aleksandra,
  • Jovanović Tamara,
  • Jovanović Boris,
  • Roganović Jelena

Journal volume & issue
Vol. 70, no. 1
pp. 18 – 25

Abstract

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Introduction Vascular endothelial growth factor (VEGF) is signal molecule enrolled in diabetes mellitus type 2 (DM type 2) oral complications, but there are no studies showing the relation between VEGF and pressure caused by denture wearing in diabetic conditions. The aim of this study is to compare tissue VEGF levels in patients and animals with/without DM in conditions of chronic and acute pressure. Methods Research was conducted on DM type 2 and healthy partial denture wearers for more than 5 years (78), candidates for teeth extractions and experimental animals of the Wistar rats (40). For chronic conditions, VEGF was measured in 2 mucosal samples covered and not covered by denture in all denture wearers. Demonstrating acute conditions, after 3 days of wearing experimental plate VEGF was measured in 2 gingival samples of palatal mucosa of DM (20) and control rats (20). The concentrations of VEGF (pg/ml) in human and animal tissues were measured by commercially available ELISA kit. Results Tissue VEGF levels in control and diabetic partial denture wearers not covered by denture were without statistical difference. In comparison to noncovered tissue, VEGF decreased in samples covered by denture, being significantly lower in DM type 2, comparing to healthiest. VEGF levels in palatal mucosa without palatal base did not significantly differ in control and DM rats. VEGF levels under palatal base increased being significantly lower in DM rats comparing to controls. Conclusion Both, chronic and acute mechanical stress caused by wearing palatal denture (plate) decreased the VEGF levels in diabetic conditions comparing the health's suggesting the altered homeostasis.

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