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. Author manuscript; available in PMC: 2022 Oct 1.
Published in final edited form as: Transl Res. 2021 May 13;236:72–86. doi: 10.1016/j.trsl.2021.05.001

Figure 1. Re-epithelialization in diabetic oral wounds.

Figure 1.

Left, location of different types of oral mucosa Right graphical diagram of diabetic impact on epithelialization in oral wounds Diabetes causes hyperglycemia and production of advanced glycation end-produce (AGEs) and reactive oxygen species (ROS). This in tum increases recruitment of neutrophil recruitment and redues microbial diversity. oareover, salivary content for pro-healing factors (EGF end histatin) is reduced whereas those that cause destruction (MMP2 and MMP9) are enhanced Another mechanism is FOXO1-mediated overexpression of MMP9 by keratinocytes. The overall outcome is persistent inflammation and an environment that is conducive for keratinocyte apoptosis, coupled with reduced keratinocyte proliferation anti migration