Analysis of collagen-interacting proteins in patients with incisional hernias

• Published in: Langenbeck's archives of surgery Vol. 387; no. 11-12; pp. 427 - 432
• Main Authors: Rosch, R, Junge, K, Knops, M, Lynen, P, Klinge, U, Schumpelick, V
• Format: Journal Article
• Language: English
• Published: Germany 01-02-2003
• Subjects: Aged; Analysis of Variance; Cicatrix - metabolism; Collagen - metabolism; Connective Tissue Growth Factor; Discoidin Domain Receptors; Female; Hernia, Ventral - metabolism; Humans; Immediate-Early Proteins - metabolism; Immunoenzyme Techniques; Intercellular Signaling Peptides and Proteins - metabolism; Male; Matrix Metalloproteinase 1 - metabolism; Middle Aged; Receptor Protein-Tyrosine Kinases - metabolism; Receptors, Mitogen - metabolism; Recurrence; Statistics, Nonparametric; Tenascin - metabolism
• ISSN: 1435-2443; 1435-2451
• DOI: 10.1007/s00423-002-0345-3

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.
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.
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.
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.