Background: In recent years a disorder of the collagen metabolism has been suggested for the pathogenesis of abdominal wall hernias. Previous investigations of skin specimens revealed a reduction in the collagen I/III ratio and alterations in matrix metalloproteinases in patients with incisional hernias. We investigated known collagen-interacting proteins to further characterize connective tissue in these patients. Patients and methods: Skin scars from patients with either primary or recurrent incisional and recurrent inguinal hernias, as a subgroup of incisional hernias, were analyzed for overall collagen content and for the distribution of collagen types I and III by crosspolarization microscopy. The expression of collagen type V, collagen receptor discoidin domain receptor 2, matrix metalloproteinase 1, connective tissue-like growth factor, and tenascin was determined by immunohistochemistry. Mature abdominal skin scars from patients without evident hernia served as controls. Results: Patients with recurrent incisional hernia showed lowest ratios of collagen types I to III. Contents of overall collagen and of collagen type V did not differ between the groups. In patients with either primary or recurrent incisional hernias the proportion of collagen receptor discoidin domain receptor 2 positive cells was increased. Matrix metalloproteinase 1 expression was more pronounced in patients with recurrent incisional or inguinal hernias than in controls. Connective tissue-like growth factor was significantly increased in recurrent inguinal hernia patients. The expression of tenascin was notably decreased in all hernia groups. Conclusions: The observed alterations in the expression of collagen-interacting proteins again indicate the possibility of a fundamental connective tissue disease as the causal factor in the pathogenesis of (recurrent) incisional hernias.
With regard to the pathogenesis of recurrent incisional hernia, an impaired connective tissue quality leading to an aberrant scarring process has been proposed. For the matrix metalloproteinase (MMP-2) a pathogenetic involvement in direct inguinal hernia development is reported. With mesh implantation as the gold standard treatment for incisional hernias, the aim of the present study was to investigate the MMP-2 expression in patients with recurrent incisional hernias with and without mesh-materials. In primary fibroblast cultures obtained from skin scars in patients with and without recurrent incisional hernias, MMP-2 synthesis and gene expression were investigated. Furthermore, MMP-2 synthesis and gene expression of fibroblasts were compared after incubation with two different mesh materials: polypropylene and absorbable polyglactin filaments. MMP-2 enzyme activity was determined by semiquantitative zymography and mRNA synthesis by quantitative RT-PCR. Both MMP-2 enzyme activity and mRNA expression were similar in hernia and control fibroblasts in vitro. In control fibroblasts mesh incubation did not significantly affect MMP-2 expression, whereas polypropylene mesh contact of fibroblasts from patients with recurrent incisional hernias led to a major decrease of MMP-2 activity and of mRNA expression. In the absence of biomaterials fibroblasts from recurrent incisional hernia, patients have no alterations of their MMP-2 synthesis compared to control fibroblasts, whereas a specific response was found after biomaterial contact hereby indicating differences in fibroblast phenotype.
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