Recent laboratory and clinical studies concerning the pathogenesis and prophylaxis of postoperative peritoneal adhesions are reviewed. Since the late 19th century there have been several clinical and experimental observations demonstrating that peritoneal defects usually fail to heal with adhesion formation. Instead, mesothelization takes place, producing a surface indistinguishable from the original. This occurs from the base of the defect, meaning large defects heal as quickly as smaller defects. In a study conducted in rats (Ellis), it was noted that areas reperitonealized under tension developed adhesions while similar peritoneal defects left unrepaired and suture controls placed loosely in peritoneum usually healed without adhesions. These findings were confirmed by Buckman and coworkers who discovered that plasminogen activator activity was normally present in the mesothelium and submesothelial blood vessels of peritoneum. 2 other peritoneal insults known to induce adhesion formation are infection and foreign body contamination. Theoretically, it seems possible to reduce adhesion formation by taking the following steps: 1) reducing the initial inflammatory reaction and subsequent exudate release; 2) inhibiting coagulation of this exudate; 3) promoting the removal of fibrin deposition; 4) mechanically separating fibrin-covered surfaces; and 5) inhibiting fibroplastic proliferation. Adhesions continue to be a frequent sequelae of pelvic surgery despite the use of meticulous surgical technique. Although dextran solutions appear promising, their clinical value is unconfirmed.