The biology of hernias and the abdominal wall

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Abstract
The fundamental mechanism for hernia formation is loss of the mechanical integrity of abdominal wall structural tissue that results in the inability to offset and contain intra-abdominal forces during valsalva and loading of the torso. There is evidence that genetic or systemic extracellular matrix disorders may predispose patients to hernia formation. There is also evidence that acute laparotomy wound failure leads to hernia formation and increases the risk of recurrent hernia disease. It may be that hernia formation is a heterogeneous disease, not unlike cancer, where one population of patients express an extracellular matrix defect leading to primary hernia disease, while other subsets of patients acquire a defective, chronic wound phenotype following failed laparotomy and hernia repairs. It is evident that an improved understanding of structural tissue matrix biology will lead to improved results following abdominal wall reconstructions.