Chegini Nasser
Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, Institute for Wound Research, University of Florida, Gainesville, Florida 32610, USA.
Semin Reprod Med. 2008 Jul;26(4):298-312. doi: 10.1055/s-0028-1082388.
Whether induced by infection, inflammation, ischemia, and/or surgical injury, peritoneal adhesions are the leading cause of pelvic pain, bowel obstruction, and infertility. Although some patients develop limited scar tissues, others for unknown reasons develop severe adhesions from seemingly equal procedures. Additionally in the same patient, adhesions develop at one surgical site but not in another. The mechanisms underlying the predisposition to form scars as well as their site specificity are unknown. Because a large number of intraperitoneal surgical procedures are performed each day, many patients are at risk of developing postoperative adhesions. As such, understanding the nature of molecular events and their mechanisms of action is essential, and in the absence of such information, attempts to prevent patients from developing adhesions will remain an empirical process. An unprecedented advancement in surgical techniques have resulted in minimizing peritoneal tissue injury that cause adhesion formation. Increased understanding of the cellular and molecular events that lead to scar tissue formation has also led to the identification of many biologically active molecules with the potential of regulating inflammatory and immune responses, angiogenesis, and tissue remodeling, events that are central to normal peritoneal wound healing and adhesion formation. This article attempts to highlight some of the key molecules (i.e., the transforming growth factor family and its regulatory mechanisms) that are recognized to regulate peritoneal wound repair and adhesion formation. Such understanding of peritoneal biology not only will assist us to better manage patients with adhesions but also will assist those with endometriosis and malignant diseases that affect the peritoneal cavity.
无论是由感染、炎症、缺血和/或手术损伤引起，腹膜粘连都是盆腔疼痛、肠梗阻和不孕的主要原因。尽管一些患者形成的瘢痕组织有限，但其他患者在经历看似相同的手术时却会出于不明原因形成严重粘连。此外，在同一患者体内，粘连会在一个手术部位形成，而在另一个部位却不会。形成瘢痕的易感性及其部位特异性的潜在机制尚不清楚。由于每天都要进行大量的腹腔内手术，许多患者有发生术后粘连的风险。因此，了解分子事件的本质及其作用机制至关重要，在缺乏此类信息的情况下，试图防止患者发生粘连仍将是一个经验性过程。外科技术取得了前所未有的进步，已将导致粘连形成的腹膜组织损伤降至最低。对导致瘢痕组织形成的细胞和分子事件的深入了解，也促使人们识别出许多具有调节炎症和免疫反应、血管生成及组织重塑潜力的生物活性分子，而这些过程对于正常的腹膜伤口愈合和粘连形成至关重要。本文试图重点介绍一些已知的调节腹膜伤口修复和粘连形成的关键分子（即转化生长因子家族及其调节机制）。对腹膜生物学的这种理解不仅将有助于我们更好地治疗粘连患者，也将有助于治疗患有子宫内膜异位症和影响腹腔的恶性疾病的患者。
