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Abdominal Wall Reconstruction.

Hernias can result from genetically impaired collagen formation, deposition, organization, or degradation; from wound-healing deficiencies; and from injury, failed laparotomy closures, or failed hernia repairs. Decades ago, it was suggested that both primary and recurrent hernias resulted from abnormal collagen metabolism. Original proposed risk factors for the development of hernias included tobacco use and a strong family history of hernia, which suggests a genetic predisposition. Subsequently, ratios of type I and type III collagen and tissue metalloprotease expression in patients with inguinal and incisional hernias were studied in an attempt to isolate an etiology. Further studies suggested that mechanical strain on load-bearing tissues can induce secondary changes in tissue fibroblast function that in turn can result in failure of abdominal wall repairs. Although more studies are needed, it is evident that some primary hernias are the result of a genetic predisposition, whereas the rest may be due to acquired structural collagen abnormalities from mechanical strain, with or without associated predisposing risk factors, such as tobacco use, diabetes, and obesity.