Figure 2.

Factors responsible for the healing process of diabetic extraction sockets. Diabetes inhibits mitotic growth factor expression through epigenetic mechanisms; difficulty in wound healing after tooth extraction is associated with diminished osteogenic differentiation of mesenchymal stem cells, activation of matrix metalloproteinase-9, persistent imbalance of RANKL/OPG ratio, and reduced expression of neuropeptides. Hyperglycemia affects hormone receptor conversion as well as the formation of new blood vessels, and impaired angiogenesis not only hinders bone formation but also affects the rate of wound healing. Diabetic wounds are characterized by chronic inflammation due to high levels of reactive oxygen species, dysregulated M1/M2 macrophage polarization, and pro-inflammatory chemokines. High glucose levels have a negative impact on macrophage function, mainly in the form of dysregulated levels of cytokine secretion such as TNF-α, IL-6 and IL-1β, in addition to the inability of neutrophils to function in the inflammatory response phases of wound healing, migration, chemotaxis and adhesion. MicroRNAs also influence the different phases of diabetic wound healing.