Lymphangiogenesis and NOS Localization in Healing Process after Tooth Extraction in Akita Mouse.

摘要: Type I diabetes, an autoimmune disease, induces insulin deficiency, which then disrupts vascular endothelial cell function, affecting blood and lymphatic vessels. Nitric oxide (NO) is immune-induced destructive mediator in type inhibition of its production promotes arteriosclerosis. In this study, lymphangiogenesis expression NO synthase (NOS) during the healing process after tooth extraction were investigated immunohistochemically control (C57BL) Akita mice as a diabetes model. Between 1, 4, 10 days extraction, NOS, growth factor-C (VEGF-C), VEGF receptor-3 (VEGFR-3), von Willebrand factor was strongest granulation tissue phase. This suggests that severe inflammation triggers regulation NOS these other angiogenic lymphangiogenic factors. During callus phase, few induced osteoblasts positive for VEGF-C VEGFR-3 both mice, suggesting bone formation active period. Bone group exceeded controls. disrupted under hyperglycemic conditions, however, such activity would be insufficient to produce new bone.