Diabetic wound healing in soft and hard oral tissues.

There is significant interest in understanding the cellular mechanisms responsible for expedited healing response in various oral tissues and how they are impacted by systemic diseases. Depending upon the types of oral tissue, wound healing may occur by predominantly re-eptihelialization, by re-epithelialization with substantial new connective tissue formation, or by a a combination of both plus new bone formation. As a result, the cells involved differ and are impacted by systemic diaseses in various ways. Diabetes mellitus is a prevalent metabolic disorder that impairs barrier function and healing responses throughout the human body. In the oral cavity, diabetes is a known risk factor for exacerbated periodontal disease and delayed wound healing, which includes both soft and hard tissue components. Here, we review the mechanisms of diabetic oral wound healing, particularly on impaired keratinocyte proliferation and migration, altered level of inflammation, and reduced formation of new connective tissue and bone. In particular, diabetes inhibits the expression of mitogenic growth factors whereas that of pro-inflammatory cytokines is elevated through epigenetic mechanisms. Moreover, hyperglycemia and oxidative stress induced by diabetes prevents the expansion of mesengenic cells that are involved in both soft and hard tissue oral wounds. A better understanding of how diabetes influences the healing processes is crucial for the prevention and treatment of diabetes-associated oral complications.