One of the defining features of chronic wounds is their high levels of inflammation. Patients present with high levels of inflammation, around 80%, of cells at the wound margin being macrophages and with wound fluid laden with pro- inflammatory cytokines. The latter is in part responsible for preventing wound closure, along with the low levels of growth factors. In healthy acute wounds, two types of macrophages can be found: pro-inflammatory M1 macrophages and anti-inflammatory M2 macrophages, with more M1 cells present early post-injury and M2 appearing later to regulate repair and wound closure. This pro-repair M2 phenotype, that secrete a range of mediators including growth factors that regulate re-vascularisation and closure of a wound, is lacking in chronic wounds, leading to excessive inflammation, enhanced degradation within the wound, reduced matrix deposition and lack of closure. This review will discuss the alterations seen in chronic wound macrophages, how this might affect the repair process and some potential reasons for their dysregulation.
