Wound Healing Disorders: Chronic Wounds and Keloids

Abstract

The normal wound healing response can be divided into (1) inflammatory, (2) proliferative, and (3) tissue remodeling (i.e., fibroplasia and maturation) phases that involve complex interactions between various cutaneous-derived and inflammatory cells, cytokines, and the extracellular matrix (ECM) [1–6]. Numerous studies continue to uncover the genetic, epigenetic (i.e., microRNA), cellular (including stem cells), molecular, and biochemical mechanisms underlying this process [1–9]. An in-depth review of normal wound healing principles is beyond the scope of this chapter. However, it is important to point out that a tightly regulated balance between ECM production and degradation is required for normal scar formation. Any disturbances in these opposing processes can lead to wound healing disorders, such as chronic nonhealing ulcers (i.e., ↓ production and ↑ degradation of ECM) or keloids (↑ production and ↓ degradation of ECM) [1–9]. It is envisioned that efforts to improve our current understanding of the mechanisms and pathways that underpin the pathobiology of these disorders may also lead to the development of predictive and/or diagnostic molecular tests that are clinically useful in the management of patients with these conditions, as well as to the discovery of novel therapeutic targets. In this regard, gene and stem-cell therapy is emerging as a promising approach to cutaneous wound treatment [5,8]