In the present article, we describe the normal structure of the peritoneum and review the mechanisms of peritoneal
metastasis (PM) from
gastric cancer (GC). The structure of the peritoneum was studied by a double-
enzyme staining method using
alkaline-phosphatase and 5'-nucreotidase, scanning electron microscopy, and immunohistological methods. The fundamental structure consists of three layers, mesothelial cells and a basement membrane (layer 1), macula cribriformis (MC) (layer 2), and submesothelial connective tissue containing blood vessels and initial lymphatic vessels, attached to holes in the MC (layer 3). Macro molecules and macrophages migrate from mesothelial stomata to the initial lymphatic vessels through holes in the MC. These structures are characteristically found in the diaphragm, omentum, paracolic gutter, pelvic peritoneum, and falciform ligament. The first step of PM is spillage of
cancer cells (peritoneal free
cancer cells; PFCCs) into the peritoneal cavity from the serosal surface of the primary
tumor or
cancer cell contamination from lymphatic and blood vessels torn during
surgical procedures. After PFCCs adhere to the peritoneal surface, PMs form by three processes, i.e., (1) trans-mesothelial
metastasis, (2) trans-
lymphatic metastasis, and (3) superficial growing
metastasis. Because the intraperitoneal (IP) dose intensity is significantly higher when generated by IP
chemotherapy than by systemic
chemotherapy, IP
chemotherapy has a great role in the treatment of PFCCs, superficial growing
metastasis, trans-
lymphatic metastasis and in the early stages of trans-mesothelial
metastasis. However, an established trans-mesothelial
metastasis has its own interstitial tissue and vasculature which generate high interstitial pressure. Accordingly, it is reasonable to treat established trans-mesothelial
metastasis by bidirectional
chemotherapy from both IP and systemic
chemotherapy.