The biology of hernia formation

Abstract

Abdominal wall hernia is a multifactorial pathology involving both endogenous and exogenous factors. Male gender and familial history of inguinal hernia are important risk factors for primary inguinal hernia formation, whereas smoking and insufficient surgical technique is associated with recurrent inguinal hernia and incisional hernia formation. Moreover, alterations in collagen composition contribute to the formation of abdominal wall hernias. Apart from decreased levels of total collagen quantity in fascia, reduced collagen quality seems to be a key feature in many hernia patients. Especially, a decreased type I to III collagen ratio has been demonstrated in the fascia of patients with inguinal or incisional hernias, leading to thinner collagen fibers with less strength. These findings are also present in skin suggesting that abdominal wall hernia is a systemic disease. Increased collagen breakdown mediated by matrix metalloproteinase-2 (MMP-2) is suggested to be involved in inguinal hernia formation. Furthermore, systemically decreased type V collagen turnover leading to overall impaired collagen synthesis is present in patients with inguinal or incisional hernias. Published data point towards hernia disease as an inherited disease. The inheritance pattern and identification of gene defects for clinical use remain to be clarified.