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Fetal topohistology of the mesocolon transversum with special reference to fusion with other mesenteries and fasciae
Author(s) -
Jeong Yeon Jun,
Cho Baik Hwan,
Kinugasa Yusuke,
Song Chang Ho,
Hirai Ichiro,
Kimura Wataru,
Fujimiya Mineko,
Murakami Gen
Publication year - 2009
Publication title -
clinical anatomy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.667
H-Index - 71
eISSN - 1098-2353
pISSN - 0897-3806
DOI - 10.1002/ca.20846
Subject(s) - mesenteries , medicine , anatomy
Abstract The developing mesocolon transversum was investigated using hematoxylin and eosin‐stained semiserial sections derived from 17 human fetuses between 12 and 30 weeks of gestation. The mesocolon was attached to the mesoduodenum and greater omentum until 12 weeks. However, the fetal duodenal attachment appeared not to correspond to the right colic flexure in adults. The greater omentum and mesocolon were likely to be irregularly folded at the attachment site possibly because the developing transverse colon “ran into” and pushed up the greater omentum and pancreatic head. Lymphatic vessels invaded the indistinct fusion plane to destroy the primary configuration. Moreover, the mesocolon seemed to “seize” or take‐over some parts of the splenic side of the greater omentum, but the thick gastric side containing the right gastroepiploic artery and vein remained along the greater curvature. Until 20 weeks, the left colic flexure was fixed to the pancreatic tail, and near the flexure the mesocolon also fused with the renal fascia. The left splenic end of the greater omentum was folded and fused together to form a thick ligament‐like structure, i.e., the gastrocolic ligament. In addition, near the duodenojejunal junction, a peritoneal bridge was often seen containing the inferior mesenteric artery or vein. Although surgeons generally believe that the mesocolon can be gently detached from the greater omentum, the fusion plane in adults appears to be the result of secondary modification and simplification by vascular development. Clin. Anat. 22:716–729, 2009. © 2009 Wiley‐Liss, Inc.