In both animals and humans it is well accepted that chronic stress delays dermal wound healing. This occurs through activation of both the HPA and SNS pathways. It is mediated by the release of cortisol and norepinephrine into the periphery. Through these pathways stress dysregulates the early wound repair process, prolonging the inflammatory phase of healing. A prolonged inflammatory phase results in higher bacterial counts and an increased incidence of infection, which in itself delays wound closure and worsens healing outcomes (e.g., scarring). Negative effects on wound healing caused by other factors (e.g., aging, diabetes) are exacerbated by stress.
|Original language||English (US)|
|Title of host publication||Neuroimmunology of the Skin|
|Subtitle of host publication||Basic Science to Clinical Practice|
|Publisher||Springer Berlin Heidelberg|
|Number of pages||15|
|State||Published - 2009|
All Science Journal Classification (ASJC) codes