Periodontitis is one of the most common diseases in humans, characterized by progressive destruction of the tooth-supporting tissues. Apart from tooth desorption, periodontitis has been linked to many systematic disorders, such as diabetes, coronary artery disease and stroke, as well as high risk of premature birth. Diabetes mellitus (DM) is a disorder that affects millions of people worldwide. The risk of the development of periodontitis is substantially greater in people with T2DM than in the general population. Periodontitis has been identified as a possible risk owing to poor metabolic control in patients with T2DM. During tooth extractions, there is a great risk of postoperative complications from impaired wound healing and thus the necessity to apply procedures that can accelerate and foster the healing process.
Wound healing is a complex process which involves the activation of extracellular matrix components, remodeling enzymes, cellular adhesion molecules, and growth factors, cytokines, and chemokines genes. The molecular mechanism underlying the healing process still remains unclear. The host response to irritant follows a cascade of events involved in wound healing including vascular and cellular inflammatory events, cellular migration, proliferation and differentiation, angiogenesis and epithelialization, fibroplasia, matrix deposition and remodeling. This process may be enhanced by the production of increased level of free radicals during the inflammatory phase, which leads to the inhibition of cell migration and proliferation, and thus damage the wound nearby tissue. Although the reactive oxygen species activities of healthy and diseased periodontal soft tissues have been documented, their activities during periodontal wound healing still need to be investigated. Hence, this review aims to highlight the new target and recent mechanisms involved in wound healing.