Our understanding of the pathobiology of hernia formation has grown tremendously in the past decade. Indeed, several well-designed, molecular-based studies have shown that many acquired hernias (e.g. direct inguinal hernia) as well as incisional hernias arise in the setting of measurable abnormalities in tissue healing - either in the production of the various types of collagen or in the remodeling and breakdown via matrix metalloproteinases [1, 2]. In addition, several well-conducted, long-term studies (>5 years follow-up) have shown that the rate of recurrences after primary autogenous repairs of incisional hernias is really much greater than we ever appreciated previously [3, 4].
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