The biology of hernia formation.

The Biology of Hernia Formation

Abnormal collagen metabolism is suspected to play an important role in the pathogenesis of recurring inguinal and incisional hernias. Whereas alloplastic prostheses are nowadays routinely used, the quantity and quality of collagen formation after repair in humans has not been analysed in a large cohort. Seventy-eight prostheses (Prolene, Atrium, Marlex, Vypro, Mersilene, Gore-Tex) implanted for inguinal and incisional hernia repair were explanted because of recurrence, chronic pain or infection. The mean implantation period was 17.9±11.2 (range 0.5–48) months. Collagen formation was investigated quantitatively (collagen–protein ratio) and qualitatively (collagen type I/III ratio). Results were related to clinical data that included gender, age, implantation period, indication for implantation/explantation, type and location of prosthesis. Mean collagen–protein ratio was 45.3±8.5 μg/mg, with significant differences between male (43.8±9.1 μg/mg) and female tissue samples (48.1±6.8 μg/mg, P=0.033). The mean collagen type I/III ratio of all samples investigated was 2.1±1.4. Samples explanted for recurring hernias exhibited a significantly decreased ratio (1.3±0.7, P<0.05) compared to samples explanted because of pain (3.4±1.2) or infection (2.9±1.6). Multivariate analysis excluded independent effects of age, gender, indication for implantation of prostheses, location and implantation period on collagen type I/III ratio. The present study confirms the importance of a biological approach, next to technical aspects, to the understanding of the pathogenesis of recurrent hernia formation and underscores the presence of a disturbed scarring process. The composition of scar tissue with a lowered collagen type I/III ratio and, therefore, reduced tensile strength may be a major contribution to hernia recurrence.

Decreased collagen type I/III ratio in patients with recurring hernia after implantation of alloplastic prostheses

Incisional hernias represent one of the most frequent complications of abdominal surgery. The incidence is probably underestimated. The pathogenesis is complex and not fully understood, implying patient-related factors (i.e., collagen biochemistry, obesity, age) as well as technical factors, including, among others, wound infection, suture material, and types of incisions and closures. In this paper, the first of two, the authors review the literature emphasizing the current knowledge concerning the pathogenesis of incisional hernias. The second article is focused on the treatment.

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Incisional hernias. I. Related risk factors.

Background:

The aetiology and pathogenesis of abdominal wall hernia formation is complex. Optimal treatment of hernias depends on a full understanding of the pathophysiological mechanisms involved in their formation. The aim of this study was to review the literature on specific collagen alterations in abdominal wall hernia formation.



Methods:

A computer-assisted search of the medical databases PubMed and Embase was performed, together with a cross-reference search of eligible papers.



Results:

Fifty-two papers were included. Collagen alteration depended on the type of hernia; there were more pronounced changes in patients with a direct inguinal hernia than in those with an indirect inguinal hernia, recurrent inguinal hernia or incisional hernia. A consistent finding was a significant increase in immature type III collagen relative to the stronger type I collagen in patients with a hernia. This resulted in thinner collagen fibres with a correspondingly diminished biomechanical strength. It has been suggested that these alterations are due to variation in the synthesis, maturation or degradation of collagen by matrix metalloproteinases, in combination or alone.



Conclusion:

Hernia formation and recurrence is associated with altered collagen metabolism manifested by a decreased type I:III collagen ratio. Copyright © 2010 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.

Connective tissue alteration in abdominal wall hernia

Inguinal hernias are among the disorders that most frequently require surgery: their repair accounts for 10% to 15% of all general surgical procedures. 1 Although the cause remains unknown, it has been established that the integrity of the abdominal wall in the groin area is dependent on the transversalis fascia (TF), the oblique orientation of the inguinal canal, and a sphincterlike structure of the internal ring. 2

Despite numerous predisposing factors, including anatomical features (persistence of the peritoneal-vaginal conduit, high insertion point of the transverse arch) and those associated with other diseases (obesity, chronic obstructive pulmonary disease, constipation), the underlying cause of the development of the different types of hernias is of a biologic nature. Research aimed at evaluating the role played by biologic factors has centered on possible alterations in connective tissue metabolism. This idea is also supported by the fact that diseases such as Marfan and Ehlers-Danlos syndromes, cutis laxa, osteogenesis imperfecta, 3 and congenital hip dislocation 4 have been associated with hernial processes.

Tissue specimens from patients with hernias for this type of experimental study include the abdominal anterior rectus muscle sheath, 5 cremaster, hernial sac, 6 and even skin tissue. 7 The expression pattern of certain types of collagen 8 and certain enzyme dysfunctions 9 have also been the subject of several of these studies.

Concerned about the cause of hernias, we have conducted several investigations on TF biopsy specimens from patients with hernias. We correlated the ultrastructural features of the TF with collagen activity and degradation through the study of certain metalloproteinases (MMPs) and observed an increase in MMP-2 expression in TF specimens from patients with direct hernias. 10 This enzyme degrades and participates in the turnover of the extracellular matrix, acting on certain types of collagen and elastin. Its expression is enhanced in processes such as genitourinary prolapse 11 and aortic aneurysm. 12,13 Further, it has been reported that patients with this last pathology have an increased incidence of hernias. 14,15 These findings prompted us to propose a hypothesis for the behavior of MMP-2 in TF specimens of patients with hernias, based on the possibility of a similar mechanism that might explain why in some patients the posterior wall of the inguinal canal of the TF remains unaltered, and in others it presents defects that lead to hernial processes.

To this end, we designed an in vitro model using cultured fibroblasts from the TF to determine whether the modifications in MMP expression found in tissue are maintained in culture. If this were the case, it could point to a genetic predisposing factor for this pathology, and thus hernia types showing some alteration at the level of the TF could be candidates for primary repair with a prosthetic material in a effort to prevent future relapses.

Ana Guerrero

Papers

Fibroblasts from the transversalis fascia of young patients with direct inguinal hernias show constitutive MMP-2 overexpression.