Systematic review Connective tissue alteration in abdominal wall hernia N. A. Henriksen 1 , D. H. Yadete 1 , L. T. Sorensen 1 , M. S. ˚ Agren 1,2 and L. N. Jorgensen 1 1 Department of Surgery K and 2 Copenhagen Wound Healing Centre, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark Correspondence to: Dr N. A. Henriksen, Department of Surgery K, Bispebjerg Hospital, Bispebjerg Bakke 23, DK-2400 Copenhagen NV, Denmark (e-mail: nadiahenriksen@gmail.com) 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. Paper accepted 1 October 2010 Published online 19 November 2010 in Wiley Online Library (www.bjs.co.uk). DOI: 10.1002/bjs.7339 Introduction The aetiology and pathogenesis of abdominal wall hernia formation is complex and multifactorial 1 . Evidence suggests that hernia formation and recurrence are linked to abnormal metabolism of connective tissue 2–4 , but the pathophysiological mechanisms have yet to be described fully. The prevalence of ventral hernia is similar in men and women, and increases with age 5 . In contrast, groin hernia is more common in men. A patent processus vaginalis is a well known congenital factor for the development of indirect inguinal hernia 6,7 . Despite this, fewer than 50 per cent of men with a patent processus vaginalis develop clinical herniation, suggesting that anatomical variation alone does not cause herniation 5,6 . Abdominal wall hernia formation and recurrence occur more frequently in patients with connective tissue disorders 8–10 and abdominal aortic aneurysms 11–13 , supporting the potential role of altered connective tissue metabolism. This study reviewed the literature on possible bio- chemical mechanisms involved in abdominal wall hernia formation and recurrence. The primary focus of the review was on the metabolism and structure of extracellular matrix (ECM) proteins in the formation of primary groin hernia, and also in the development of incisional and recurrent hernia. Methods A computer-assisted search of the medical databases PubMed and Embase was undertaken covering publi- cations from January 1966 to December 2009. The PubMed search included the medical subject heading (MeSH) term ‘hernia’ as major topic with the sub- headings ‘epidemiology’, ‘etiology’, ‘blood’, ‘surgery’ and ‘metabolism’, combined with the following MeSH terms as major topics using the explode function: ‘connec- tive tissue/abnormalities’, ‘connective tissue/metabolism’, ‘connective tissue/ultrastructure’, ‘collagen/metabolism’, ‘collagen/ultrastructure’, ‘metalloendopeptidases’ and ‘tis- sue inhibitor of metalloproteinases’. Embase was searched using the map term to subject heading and focus  2010 British Journal of Surgery Society Ltd British Journal of Surgery 2011; 98: 210–219 Published by John Wiley & Sons Ltd