Molecular characterization of postoperative adhesions: the adhesion phenotype

Postoperative adhesion development remains a very frequent occurrence, which is often unrecognized by surgeons because of limited ability to conduct early second-look laparoscopies. The consequences include infertility, pelvic pain, bowel obstruction, and difficult reoperative procedures. To date, approaches to limit adhesions primarily have involved barriers to separate tissue during reepithelization. Future progress in regulating adhesion development and tissue fibrosis likely will require an improved understanding of the molecular processes involved in normal peritoneal repair and its aberrations leading to adhesion development. We hypothesize that tissue hypoxia (in part resulting from tissue incision, fulguration, suture ligation, etc.) is the major inciting event, which leads to a coordinated series of molecular events that promote an inflammatory response leading to enhanced tissue fibrosis. These events are reduced plasminogen activator activity, extracellular matrix deposition, increased cytokine production, increased angiogenesis, and reduced apoptosis (programmed cell death). Improved understanding of these events and their regulation will provide the opportunity to regulate better postoperative adhesion development and tissue fibrosis, thereby reducing the morbidity and mortality they cause.