The Instable Scar

Abstract

There is increasing evidence that inguinal hernia formation is based on a disorder of the connective tissue biology [1]–[12]. Similarly, secondary herniations as incisional hernias or diverse recurrent hernias are supposed to be associated with biological factors that provoke an instable scar formation during the wound-healing process. Patients with congenital connective tissue disorders have a higher risk of developing of incisional or recurrent hernias [13,14]. Furthermore, aneurismal disease, as another collagen disorder, has repeatedly been shown to be associated with an increased risk for the development of incisional hernias [15]–[17]. Previous work was able to support the hypothesis of a dysregulation of the collagen metabolism in patients with incisional hernias. In patients with either primary or recurrent incisional hernias, a significantly decreased ratio of collagen type I to type III and alterations of collagen-interacting proteins were found [18]–[21]. An alteration of the collagen composition was further verified by a comparative immunhistochemical analysis of surgical mesh explants where patients operated for hernia recurrence had a lowered collagen I/III ratio as compared to patients operated due to mesh infection or mesh-related pain [22].