Hernia recurrence as a problem of biology and collagen

Abstract

Usually an abdominal wall hernia is regarded as a mechanical problem with a local defect which has to be closed by technical means. Despite the introduction of several therapeutic improvements, recurrent hernias still appear in 10-15%. Therefore, reasons for a recurrence are discussed in a more fundamental way. It is assumed that a failure mainly depends on the quality of the repair. Correspondingly, in principle, the close causal relationship between the technical component and its failure during time is reflected by an s-shaped outcome curve. In contrast, the configuration of the outcome curve changes markedly if a breakdown is caused by numerous components. Then, the superposition of all incidence curves inevitably leads to a linear decline of the outcome curve without any s-shaped deformation. Regarding outcome curves after hernia repair, the cumulative incidences for recurrences of both incisional and inguinal hernia show a linear rise over years. Considering the configuration of outcome curves of patients with hernia disease, it may therefore be insufficient to explain a recurrence just by a failing technical repair. Rather, biological reasons should be suspected, such as a defective wound healing with impaired scarring process. Recent molecular-biological findings provide increasing evidence of underlying biochemical alterations in patients with recurrent hernia. Until predicting markers to identify patients with an impaired wound healing are available and considering the formation of insufficient scar as the underlying disease, the consequences for every surgical repair should be a supplementary reinforcement with nonabsorbable alloplastic nets as flat meshes with an extensive overlap.

Keywords: Biology; collagen; hernia; network; recurrence; wound healing.

Figure 1

Statistical data from the general automobile club of Germany ADAC, depicting a mono-causal failure of manual transmission. The sshaped black curve is representing the age-related number of nondefective cars, whereas the cross lined curve illustrates the yearly failure of cars caused by a defective manual transmission with a peak incidence after 5 years (with courtesy of H. Schmaler, ADAC Munich, Germany).

Figure 2

Statistical data from the general automobile club of Germany ADAC, representing a multi-causal failure. The black curve is representing the number of nondefective cars with regard to years of use. The cross-lined curve is illustrating the yearly failure of cars caused by various defects (with courtesy of H. Schmaler, ADAC Germany).

Figure 3

Cross polarization microscopical (CPM) and immunohistochemical features of human fascial tissue according to Junqueira.[12] CPM of Sirius red-stained section of normal fascia with a collagen type I/III ratio of 14 - (A); and specimen of recurrent incisional hernia fascia with a collagen type I/III ratio of 3.6 - (B). For the detection of MMP-2, we used rabbit polyclonal, 1:1000, from Biomol (Hamburg, Germany) as primary antibody; and goat anti-rabbit, 1:500, from Dako (Glostrup, Denmark) as secondary antibody. Positive cytoplasmatic expression of MMP-2 in granuloma adjacent to mesh filaments - (C, D) (positive stained cells marked with black arrows). (Magnification 400× in images IIIA - IIID).

Figure 4

Cumulative incidences of recurrences after incisional and inguinal hernia repair[1011]