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 hernia in the 21st century: an evidence-based review.

A variety of benign and malignant masses can be found in the inguinal canal (IC). Benign causes of masses in the IC include spermatic cord lipoma, hematoma, abscess, neurofibroma, varicocele, desmoid tumor, air, bowel contrast material, hydrocele, and prostheses. Primary neoplasms of the IC include liposarcoma, Burkitt lymphoma, testicular carcinoma, and sarcoma. Metastases to the IC can occur from alveolar rhabdomyosarcoma, monophasic sarcoma, prostate cancer, Wilms tumor, carcinoid tumor, melanoma, or pancreatic cancer. In patients with a known malignancy and peritoneal carcinomatosis, the diagnosis of metastases can be suggested when a mass is detected in the IC. When peritoneal disease is not evident, a mass in the IC is indicative of stage IV disease and may significantly alter clinical and surgical treatment of the patient. A combination of the clinical history, symptoms, laboratory values, and radiologic features aids the radiologist in accurately diagnosing mass lesions of the IC. Supplemental material available at radiographics.rsnajnls.org/cgi/content/full/28/3/819/DC1.

https://pubs.rsna.org/doi/pdf/10.1148/rg.283075110

The Inguinal Canal: Anatomy and Imaging Features of Common and Uncommon Masses

Background The etiology of inguinal hernias remains uncertain even though the lifetime risk of developing an inguinal hernia is 27% for men and 3% for women The aim was to summarize the evidence on hernia etiology, with focus on differences between lateral and medial hernias Results Lateral and medial hernias seem to have common as well as different etiologies A patent processus vaginalis and increased cumulative mechanical exposure are risk factors for lateral hernias Patients with medial hernias seem to have a more profoundly altered connective tissue architecture and homeostasis compared with patients with lateral hernias However, connective tissue alteration may play a role in development of both subtypes Inguinal hernias have a hereditary component with a complex inheritance pattern, and inguinal hernia susceptible genes have been identified that also are involved in connective tissue homeostasis Conclusion The etiology of lateral and medial hernias are at least partly different, but the final explanations are still lacking on certain areas Further investigations of inguinal hernia genes may explain the altered connective tissue observed in patients with inguinal hernias The precise mechanisms why processus vaginalis fails to obliterate in certain patients should also be clarified Not all patients with a patent processus vaginalis develop a lateral hernia, but increased intraabdominal pressure appears to be a contributing factor

/pdf/etiology-of-inguinal-hernias-a-comprehensive-review-1uof9hmrca.pdf

Etiology of Inguinal Hernias: A Comprehensive Review

Mutations in the two-handed zinc-finger homeodomain transcription factor gene (TCF8) have been associated with posterior polymorphous corneal dystrophy (PPCD) and extraocular developmental abnormalities. We performed screening of TCF8 in 32 affected, unrelated probands, affected and unaffected family members of probands identified with a TCF8 mutation, and in 100 control individuals. Eight different pathogenic mutations were identified in eight probands: four frameshift (c.953_954insA, c.1506dupA, c.1592delA, and c.3012_3013delAG); three nonsense (Gln12X, Gln214X, Arg325X); and one missense (Met1Arg). Screening of TCF8 in affected and unaffected family members in six families demonstrated that each identified mutation segregated with the disease phenotype in each family; two probands did not have additional family members available for analysis. None of the eight TCF8 mutations was identified in 200 control chromosomes. The prevalence of hernias of the abdominal region in affected individuals with PPCD associated with TCF8 mutations was significantly higher than the prevalence in both individuals with PPCD not associated with a TCF8 mutation and in unaffected individuals. Therefore, PPCD is associated with TCF8 mutations in one quarter of affected families in this study, or about one third of all PPCD families that have been screened thus far. In these families, the presence of apparently causative TCF8 mutations is associated with abdominal and inguinal hernias.

/pdf/posterior-polymorphous-corneal-dystrophy-is-associated-with-4atidhftg3.pdf

Posterior polymorphous corneal dystrophy is associated with TCF8 gene mutations and abdominal hernia

In the last decade, in the search for abdominal-wall hernia etiology, attention has been brought to alterations in the connective tissue ultrastructure as the probable etiological factor. These may cause weakening of connective tissue, which in turn may form ground for hernia formation. To investigate this hypothesis in depth, we compared the ultrastructure of the connective tissue in hernia patients and the control group. The study group consisted of five patients with primary inguinal hernia (Nyhus II = 4, Nyhus IIIa = 1). Another five patients posted for emergency appendectomy created the control group. Tissue specimens, harvested intraoperatively from the rectus muscle sheath (RAMS) and fixed in 4% glutaraldehyde, underwent staining by the Masson, H-E and methylene blue techniques and were assessed by microscopy (light and scanning electron). The examinations showed significant differences in the rectus sheath ultrastructure. They included altered architecture, placement and quantity of collagen and elastic fibers, differences in the caliber of individual fibers and disrupted ground matter-to-fiber ratio. In patients with hernias, chaotic arrangement of collagen fibers was seen, as well as their thinning and a decrease in the general amount of elastic fibers, replaced by ground matter. Our research has shown significant differences in the structure of the RAMS between patients with hernias and healthy individuals. This supports the theory linking connective tissue alterations with the etiology of hernia, and stating that these alterations include connective tissue at locations distant from the hernia site as well, as the rectus sheath itself does not form a hernial defect.

Karolina Cerkaska

Papers

Etiology of inguinal hernia: ultrastructure of rectus sheath revisited.