**1. Introduction**

Wound healing is a highly structured physiological process involving cells and signal molecules; it is known to run throughout inflammation, cell proliferation, angiogenesis,

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

collagen deposition, and re‐epithelization [1]. In the very first steps, natural immunity [2] plays an important role through aggregation of inflammasomes. The next step goes through inflammatory cell types, and messages from the first to this step together with monocyte responsivity are able to determine whether inflammation will prolong to a sort of a steady, chronically established state, which freezes the whole process transforming it into a chronic inflammation [2–6].

Monocyte/macrophage sequestration together with their lack of switch to type 2 [3, 4, 6] impairs angiogenesis and cell activities resulting in a delayed re‐epithelialization, reduced call for fibroblasts and diminishing collagen deposition, as well as a decreased cell proliferation.

The aim of this chapter is to report our experience on how to modify impaired wound healing, starting from our experimental studies and concluding with our recent clinical experiences.
