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Page 12 of 18 Wilgus. Plast Aesthet Res 2020;7:54 I http://dx.doi.org/10.20517/2347-9264.2020.150

CONCLUSION
There is a large body of evidence suggesting that the magnitude of the inflammatory response influences
the amount of scar tissue that will result from the healing process [Figure 2]. This likely results, at least in
part, from the array of mediators released by inflammatory cells capable of stimulating fibroblast activity.
Studies examining human tissue and samples from animal models suggest that pro-inflammatory cytokines
and the number of inflammatory cells (e.g., mast cells and macrophages) are elevated in problematic scars
such as HTS and keloids whereas the inflammatory response is muted in scarless wounds. Functional data
support these correlative results as depleting inflammatory cells or reducing pro-inflammatory mediators
generally reduces scar formation. Collectively, these data support the idea that targeting inflammation
could be useful for limiting scar formation. Indeed, there are several studies, mainly using animal models,
that show anti-inflammatory compounds reduce scar formation, and several other potential anti-scar
treatment modalities have documented anti-inflammatory effects.

Despite the large number of studies on inflammation and scar formation, more research is needed to
fully understand this relationship. Conflicting data from some studies demonstrates the complexity of the
relationship between inflammation and scar formation and highlights the lack of standardized approaches
for studying this relationship experimentally. In particular, variability in experimental models can make it
difficult to draw broad conclusions; these models include the use of human tissue, large animal models (e.g.,
pigs, which have similar skin anatomy to human), and small animal models (e.g., mice, which have loose
skin, but can be used for advanced functional studies). More precise characterization of inflammation that
includes an expanded view of different inflammatory cell types as well as the specific subtypes of each cell
and how changes in these cells over time affect scar formation are needed, especially in human specimens.
In addition, further investigation is needed to determine how beneficial various anti-inflammatory
approaches could be for minimizing scar formation in human skin.

DECLARATIONS
Authors’ contributions
The author contributed solely to the article.

Availability of data and materials
Not applicable.

Financial support and sponsorship
The author has received research support from NIH (AR071115).

Conflicts of interest
The author declared that there are no conflicts of interest.

Ethical approval and consent to participate
Not applicable.

Consent for publication
Not applicable.

Copyright
© The Author(s) 2020.