Embryology of Extra‐ and Intrahepatic Bile Ducts, the Ductal plate

Abstract

In the human embryo, the first anlage of the bile ducts and the liver is the hepatic diverticulum or liver bud. For up to 8 weeks of gestation, the extrahepatic biliary tree develops through lengthening of the caudal part of the hepatic diverticulum. This structure is patent from the beginning and remains patent and in continuity with the developing liver at all stages. The hepatic duct (ductus hepaticus) develops from the cranial part (pars hepatica) of the hepatic diverticulum. The distal portions of the right and left hepatic ducts develop from the extrahepatic ducts and are clearly defined tubular structures by 12 weeks of gestation. The proximal portions of the main hilar ducts derive from the first intrahepatic ductal plates. The extrahepatic bile ducts and the developing intrahepatic biliary tree maintain luminal continuity from the very start of organogenesis throughout further development, contradicting a previous study in the mouse suggesting that the extrahepatic bile duct system develops independently from the intrahepatic biliary tree and that the systems are initially discontinuous but join up later. The normal development of intrahepatic bile ducts requires finely timed and precisely tuned epithelialmesenchymal interactions, which proceed from the hilum of the liver toward its periphery along the branches of the developing portal vein. Lack of remodeling of the ductal plate results in the persistence of an excess of embryonic bile duct structures remaining in their primitive ductal plate configuration. This abnormality has been termed the ductal plate malformation.

Biliary epithelial injury-induced regenerative response by IL-33 promotes cholangiocarcinogenesis from peribiliary glands

“…In the embryonic stage, the extrahepatic bile duct (EHBD) develops from the embryonic hepatic diverticulum, whereas the intrahepatic bile duct (IHBD) originates within the liver from the ductal plate (5). Therefore, the IHBD and EHBD may exhibit distinct properties and different carcinogenetic processes.…”

Repeated Minocycline Hydrochloride Injections for Symptomatic Polycystic Liver Disease

“…Symptomatic PLD was controlled by repeated MINO injections given over the course of 14.8 months on average. PLD is a collection of rare human disorders that result from structural changes in biliary tree development [48][49][50] . The biliary tree emerges from the endodermal hepatic diverticulum [48] .…”

Human ductal plate and its derivatives express antigens of cholangiocellular, hepatocellular, hepatic stellate/progenitor cell, stem cell, and neuroendocrine lineages, and proliferative antigens

“…They are abortions (spontaneous and artificial), intrauterine fetal death, and autopsies. The gestational ages (weeks) of the 32 fetal livers were as follows: 17,18,19,21,23,24,26,29,30,36,38, and 40. The sex was unclear.…”

“…Such structures are called DP malformations (DPM) or hepatobiliary fibropolycystic disease, which involves congenital hepatic fibrosis, polycystic diseases (adult and infantile) of the liver and kidneys, congenital biliary atresia, von-Meyenburg complex, and Caroli's disease. [18][19][20][21][38][39][40][41][42][43] DP is also seen in ductular reactions [44][45][46] and DPM in some liver hamartoma 45 and cholangiocarcinoma. 47 The DP in ductular reaction of focal nodular hyperplasia interestingly may express KIT, 46 a receptor of stem cell factor (SCF).…”