Skin Burns: Review of Molecular Mechanisms and Therapeutic Approaches

Ahad Ferdowsi Khosroshahi, PhD; Jafar Soleimani Rad, PhD; Raziyeh Kheirjou, PhD student; Mohammad Reza Ranjkesh, MD; Leila Roshangar, PhD

Disclosures

Wounds. 2019;31(12):308-315. 

In This Article

Pathophysiology of Burns

There are various models for burn wound evaluation. One of most commonly used is Jackson's model in which 3 concentric areas can be detected based on the severity of tissue damage and changes in blood flow of a burn wound (Figure).[2,7,8] Briefly, the first zone is the zone of coagulation; this is the point of maximum damage with irreversible tissue loss due to coagulation of the proteins and tissue necrosis. Surrounding the coagulation zone is the zone of stasis, which is characterized by decreased perfusion. This ischemic zone may progress to full necrosis unless the ischemia is reversed. Therefore, the main aim of burn resuscitation is to increase tissue perfusion here and prevent any further damage. The outermost layer is the zone of hyperemia. Tissue perfusion is increased and the tissue here invariably is recovered, unless there is severe sepsis or prolonged hypoperfusion.

Figure.

The pathophysiology mechanism of burn on skin according to the Jackson model.7 MØ: macrophage; NF-κβ: nuclear factor κβ; TNF-α: tumor necrosis factor alpha; VEGF: vascular endothelial growth factor; PDGF: platelet-derived growth factor; TGF-β: transforming growth factor beta; IL-1α: interleukin 1 alpha; IL-1β: interleukin 1 beta; IL-6: interleukin 6; ROS: reactive oxygen species

In burn injuries, released chemical factors from damaged cells are activated in a 2-phase proinflammatory and anti-inflammatory response. In the first phase, a transcriptional activator (protein), nuclear factor κB, is activated immediately after a severe burn injury to regulate the induction of several proinflammatory mediators, including tumor necrosis factor alpha (TNF-α) and intercellular adhesion molecule-1 (ICAM-1).[8] These mediators activate neutrophils and monocytes and trigger antimicrobial activity. In addition, TNF-α is responsible for the secretion of other proinflammatory mediators, including interleukins 1 and 6 (IL-1, IL-6), and inducing apoptosis of various cells in the wound area. Thermal injuries increase hypermetabolism, which leads to increased production of anti-inflammatory cytokines, reactive oxygen species (ROS), and reactive nitrogen species (RNS).[9] The anti-inflammatory phase of a burn injury are related to T helper (TH) 2 lymphocytes and the secretion of 3 cytokines: IL-4, IL-10, and TNF-α.[10]

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