ObjectiveTo determine the expression pattern of certain metalloproteinases (MMPs) known to be involved in the degradation of the extracellular matrix in cultured fibroblasts from the transversalis fascia (TF) of patients with inguinal hernia.
Summary Background DataInguinal hernia is a common pathology, the cause of which remains unknown. It is, however, clear that the TF is one of the anatomical structures that may impede the formation of hernias, and particularly the direct type of hernia. In previous studies the authors found enhanced MMP-2 expression in TF specimens in vivo. The persistence of increased expression in cultured fibroblasts might support the idea of a genetic defect as the cause for this pathology.
MethodsFibroblasts from the TF of patients with direct and indirect inguinal hernia were cultured and compared with those obtained from control TF in terms of MMP (MMP-2 and MMP-9) expression.
ResultsSignificant active MMP-2 expression was shown by TF fibroblasts from young patients with direct hernias. These findings were confirmed by immunosorbent assay, immunoblotting, and zymography of the fibroblast culture media. No MMP-9 expression was detected.
ConclusionThese results indicate that MMP-2 may be involved in the TF matrix degradative process in patients with direct hernia. The persistence of changes in MMP-2 levels in the cell cultures appears to suggest a genetic defect or irreversible change as the origin of this pathology rather than environmental factors, which may later participate in the development of the hernial process.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.
2Despite 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 tis-