Analysis of collagen-interacting proteins in patients with incisional hernias

Abstract

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.

Hernias- Is it a primary defect or a systemic disorder? Role of collagen III in all hernias- A case control study

“…Collagen type I is characteristic for mature scars or fascial tissues while collagen type III represents the mechanically instable less cross linked collagen synthesized during the early days of wound healing [2], [3]. Its already proved that the presence of collagen in adequate amounts and its properties are essential to render the transversalis fascia functional and give it adequate strength [4], [5], [6].…”

Advanced glycation end products as a biomarker for incisional hernia

“…Also Matrix Metallo Proteinases (MMPs) 1, 2, 9 and 13 are up-regulated in incisional hernia patients. The balance between MMPs and their inhibitors, the tissue inhibitors of metalloproteinases (TIMPs), is one of the responsible factors for the remodeling of tissues [23, 25, 26]. …”

Complications and recurrence rates of patients with Ehlers-Danlos syndrome undergoing ventral hernioplasty: a case series

“…Collagen type I is mature, mechanically stable collagen, whereas collagen type III is immature, mechanically instable collagen [3]. Alongside the previously mentioned collagens, it has been hypothesized by Schumpelick et al that tenascin, a family of glycoproteins, could be linked to hernia formation [5]. Given this mechanism, patients with an underlying connective tissue disease, such as Ehlers-Danlos syndrome (EDS), can be at risk for a higher recurrence rate after both ventral and incisional hernia repair [5–7].…”

“…Alongside the previously mentioned collagens, it has been hypothesized by Schumpelick et al that tenascin, a family of glycoproteins, could be linked to hernia formation [5]. Given this mechanism, patients with an underlying connective tissue disease, such as Ehlers-Danlos syndrome (EDS), can be at risk for a higher recurrence rate after both ventral and incisional hernia repair [5–7]. EDS was first described in 1901 and the syndrome characterizes itself by a triad of skin hyperextensibility, joint hypermobility, and tissue fragility.…”

“…The hypermobility type is linked to tenascin X alterations. Although not all types of EDS have been linked to a specific protein disorder, many surgeons fear a high recurrence rate following hernia repair in EDS patients because of similar collagen disorders associated with both EDS and hernia recurrence [5–7]. …”