The surgical mesh-free repair of incisional hernias has to face recurrence rates of up to 50%. Apart from technical faults this is probably due to collagen metabolic disorders, known to play an important role in the development of inguinal hernia. In particular an altered ratio of collagen types I and III with an increase in collagen type III has been claimed to reduce the mechanical strength of connective tissues. Therefore, we investigated the content of collagen types I and III in the skin of patients with incisional hernia (n = 7) and recurrent incisional hernia (n = 5) in comparison to controls with healthy skin (n = 7) and normal skin scar (n = 7) both by immunohistochemistry and Western blot analysis. Both immunohistochemistry and Western blot analysis revealed a decrease in the ratio of collagen I/III due to a concomitant increase in collagen III. The patients with incisional hernias and with recurrent incisional hernias showed a ratio of 1.0 ± 0.1 and 0.8 ± 0.1, respectively, whereas the controls exhibit a ratio of 2.1 ± 0.2 in healthy skin and of 1.2 ± 0.2 in normal skin scar, respectively. The decrease was highly significant (p < 0.01) between the patients with either primary or recurrent hernia and the controls or the normal scar, as well as between controls and normal scar, whereas there was not any significant difference between primary and recurrent hernia (p > 0.05). Our data for the first time confirmed that the presence of incisional hernia is accompanied by impaired collagen synthesis in the skin. The decreased tensile strength of collagen type III may play a key role in the development of incisional hernias. Furthermore, it might explain the high recurrence rates of hernia repair by simple closure, as a repetition of the primarily failing technique, and the improvement by the additional use of alloplastic material.

The late appearance ofincisional hernias several years after laparotomy and the high recurrence rates after operation strongly imply the presence of a disorder of the connective tissue, although a specific defect in patients with incisional hernias has not yet been identified. In the present study we used both immunohistochemistry and Western blot analysis to evaluate the ratio of collagen I and III and the expression of the metalloproteinases (MMP) 1 and 13 in the fascia of patients with incisional or recurrent incisional hernias. Samples of healthy skin or stable skin scar in patients without hernias served as controls. Altogether, our data indicated a significantly decreased ratio of collagen I/III in the fascia of patients with incisional hernias and recurrent incisional hernias. Furthermore, in these patients the expression of MMP-1 was decreased compared to the controls, whereas MMP-13 could not be detected in any fascia sample, with or without hernias present. For the first time, our results give evidence of the existence of a possible collagen disorder in these patients. The decreased ratio ofcollagen I/III is explainable due to a relative increase of collagen type III, which is known to be characterized by thin fibril diameters and lowered mechanical strength. The altered collagen ratio might be the result of the decreased activity of MMP-1, whereas the absent MMP-13 expression did not seem to modify the scar formation. Thus, our data indicate the presence of collagen metabolic disorders in patients with incisional hernias and recurrent incisional hernias. Furthermore, these results might explain the poor results of a mesh-free hernia repair, which again builds up scar tissue of inadequate collagen composition and strength.

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