IADR Abstract Archives
Antiangiogenesis and osseous wound healing
Objectives: Angiogenesis plays an important role in wound healing. During healing, blood clot formation first occurs and works as a scaffold for hard and soft tissue formation. Subsequently, invasion of new blood vessels takes place. It’s been thought that angiogenesis inhibitors which suppress new blood vessel formation hinder tooth extraction socket healing. However, there is no solid evidence that an antiangiogenic drug impairs osseous wound healing. In this study, the effect of angiogenesis inhibitors on tooth extraction socket healing was investigated.
Methods: Bortezomib (Vel) and Thalidomide (Thal) were administered to suppress angiogenesis. Zoledronic acid (ZA) was used to suppresses osteoclasts. Mice received either Vel/Thal/ZA , Vel/Thal/saline (VC), or VC. Tooth extractions were conducted at 3 weeks after the initiation of therapy. Healing was evaluated weekly with micro-computed tomography (µCT). Mice were euthanized at 4 weeks post-tooth extraction. To confirm the antiangiogenic effect of Thal/Vel, CD31(+)CD309(+) vascular endothelial cells were assessed in blood by Flow cytometry. Furthermore, B16F10 mouse melanoma cells were inoculated in the back of B6 mice and the antiangiogenic effect of Vel/Thal administration was assessed immunohistochemically using von Willebrand factor.
Results: Circulating CD31(+)CD309(+) cells decreased in mice on Vel/Thal regardless of ZA administration. In addition, Immunohistochemical analysis is of blood vessels revealed that vascular density in tumors was significantly suppressed by Vel/Thal/ZA and Vel/Thal/VC compared to VC. Thus, Vel/Thal therapy suppressed angiogenesis in mice. However, oral wound healing was uneventful in all groups. The µCT assessment revealed a significant decrease in the bone fill at 7-day post-extraction in Vel/Thal/ZA and Vel/Thal/VC compared to VC.
Conclusions: The suppression of angiogenesis and bone resorption was indued in the Vel/Thal/ZA group, but no significant alterations were observed in tooth extractions socket healing. Therefore, the use of antiangicgenic drug may not have a major negative impact on tooth extraction socket healing.
Methods: Bortezomib (Vel) and Thalidomide (Thal) were administered to suppress angiogenesis. Zoledronic acid (ZA) was used to suppresses osteoclasts. Mice received either Vel/Thal/ZA , Vel/Thal/saline (VC), or VC. Tooth extractions were conducted at 3 weeks after the initiation of therapy. Healing was evaluated weekly with micro-computed tomography (µCT). Mice were euthanized at 4 weeks post-tooth extraction. To confirm the antiangiogenic effect of Thal/Vel, CD31(+)CD309(+) vascular endothelial cells were assessed in blood by Flow cytometry. Furthermore, B16F10 mouse melanoma cells were inoculated in the back of B6 mice and the antiangiogenic effect of Vel/Thal administration was assessed immunohistochemically using von Willebrand factor.
Results: Circulating CD31(+)CD309(+) cells decreased in mice on Vel/Thal regardless of ZA administration. In addition, Immunohistochemical analysis is of blood vessels revealed that vascular density in tumors was significantly suppressed by Vel/Thal/ZA and Vel/Thal/VC compared to VC. Thus, Vel/Thal therapy suppressed angiogenesis in mice. However, oral wound healing was uneventful in all groups. The µCT assessment revealed a significant decrease in the bone fill at 7-day post-extraction in Vel/Thal/ZA and Vel/Thal/VC compared to VC.
Conclusions: The suppression of angiogenesis and bone resorption was indued in the Vel/Thal/ZA group, but no significant alterations were observed in tooth extractions socket healing. Therefore, the use of antiangicgenic drug may not have a major negative impact on tooth extraction socket healing.