A molecular perspective of obesity-mediated incisional hernia

Incisional hernia is a common complication following laparotomy. Obesity increases the incidence of incisional hernia by about three-fold. However, the pathophysiology behind the formation of incisional hernia is not well described. The current literature was reviewed, investigating the effect of the pro-inflammatory state of adipose tissue in obesity on post-operative wound healing and subsequent incisional hernia formation. The increase in leptin, M1 macrophages, and pro-inflammatory cytokines and concomitant decrease in adiponectin, M2 macrophages, and anti-inflammatory cytokines seen with the hypertrophy of adipocytes in obesity creates a chronic inflammatory state that impacts wound healing. Prolonged inflammation disrupts the interaction of endothelial tip cells and formation of vessel lumens during angiogenesis and decreases ratio of type I to type III collagen and number of cross-links, resulting in decreased tensile strength of the ECM and association with incisional hernia formation. Obesity has impacts on the inflammatory, fibroproliferative, and wound remodeling stages of wound healing that are suggested to contribute to incisional hernia formation. Further studies are needed to investigate the pathophysiology of incisional hernia formation in the setting of obesity to decrease the incidence of incisional hernias and identify possible treatments.