Pathological Tissue Changes and Hernia Formation

Abstract

Classically, inguinal hernias are considered the result of a multifactorial process linking predisposing anatomical and dynamic factors: intra-abdominal pressure acting on a weak area, the myopectineal orifice, which is sealed by the transversalis fascia. All groin hernias are therefore characterized by the displacement of this fascia by a peritoneal sac. There are individual anatomical variations that aggravate the fragility of the inguinal region, enlarging the weak area and rendering less effective the physiological protective mechanisms of the inguinal region.1 To these are added histobiochemical factors, which are unquestionably the least known at present, but very likely play a key role in the genesis of inguinal hernias. In the light of the work of Peacock and Madden2 and Wagh, Read, and Cannon,3–6 it appeared that hernia formation was actually based on much more fundamental metabolic collagen anomalies. Hence, inguinal hernia could be considered a local manifestation of systemic collagen pathology. This aspect has, however, been studied very little up to now. This is why we undertook a detailed study of the transversalis fascia and the sheath of the rectus abdominis muscle in control groups and in patients with inguinal hernias. We first analyzed the macroscopic biomechanical properties of these structures, then proceeded to the microscopic level in an attempt to clarify them by means of their histologic characteristics.