Introduction: There are many publications describing structure of full term umbilical vessels, however, few studies in early gestation.
Aim: To elucidate changes in microstructure of developing umbilical vessels in the second trimester of pregnancy.
Material and Methods: Twelve specimens of human umbilical cords were obtained from legal termination of uncomplicated pregnancies at gestational weeks 13, 16, and 20. Two centimeter segments of the cords were cut near the placenta. Specimens were processed for paraffin blocks, sectioned, and stained with haematoxylin & eosin, Masson Trichrome, Orcein, and Periodic Acid Schiff. Immunohistochemistry for alpha smooth muscle actin & laminin antibodies was performed. Morphometry and image analysis for vascular wall thickness & diameter of lumen, and diameter of umbilical cord were done.
Results: Umbilical cord sections revealed two arteries (UA) and one vein (UV) embedded in Wharton's jelly and covered with amniotic epithelium formed of flat then cuboidal epithelium. Umbilical vessels composed of inner intima and outer media. Endothelium demonstrated areas of damage and adhesion of inflammatory cells. Internal elastic lamina was thin, interrupted initially, double layered, and well-developed finally. Smooth muscle cells (SMCs) migrated from vascular lumen or from media by a process of mesenchymal-endothelial transition to replace injured endothelium. The media was composed of immature SMCs initially (thin (morphometry), non-contractile, non-secretory as proved by different stains and collagen content. Wharton's jelly spindle shaped mesenchymal cells close to vessels revealed positive staining for alpha smooth muscle actin and contributed to the media to compensate for SMC migration. UAs showed thicker wall, narrower lumen than veins and cord diameter increased significantly at the 20 week.
Conclusion: Development of umbilical vessels was the result of a continuous remodeling process initiated by secreted endothelial factors from damaged endothelium that influenced; SMCs of media, stem cells of cord blood and Wharton's jelly simulating early events of atherosclerosis.