Gastrointestinal Tract - Gallbladder Development: Difference between revisions
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==Introduction== | ==Introduction== | ||
[[File:Stage_13_image_077.jpg|thumb|300px|Early embryonic | [[File:Stage_13_image_077.jpg|thumb|300px|Early embryonic gallbladder ([[Carnegie stage 13]], [[Week 4]])]] | ||
This section of notes gives an overview of {{gall bladder}} and | This section of notes gives an overview of {{gallbladder}} ({{gall bladder}}, {{gall-bladder}}) and billary tree development, histology and abnormalities associated with the biliary system. In the adult, the gallbladder is a site of bile salt storage and concentration, to then be released into the duodenum where they act to solubilize dietary lipids by their detergent effect. Bile salts are a cholesterol derivative (breakdown product). | ||
The transverse septum differentiates to form the hepatic diverticulum and the hepatic primordium, these two structures together will go on to form different components of the mature {{liver}} and {{ | The transverse septum differentiates to form the hepatic diverticulum and the hepatic primordium, these two structures together will go on to form different components of the mature {{liver}} and {{gallbladder}}. | ||
The hepatic diverticulum divides into two parts: pars hepatica (larger cranial part, primordium of the liver) and pars cystica (smaller ventral invagination, primordium of {{ | The hepatic diverticulum divides into two parts: pars hepatica (larger cranial part, primordium of the liver) and pars cystica (smaller ventral invagination, primordium of {{gallbladder}}). | ||
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See also: [[Gastrointestinal Tract - | See also: [[Gastrointestinal Tract - Gallbladder Histology|Gallbladder Histology]]. | ||
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* '''Anatomy of rodent and human livers: What are the differences?'''{{#pmid:29842921|PMID29842921}} "The size of the liver of terrestrial mammals obeys the allometric scaling law over a weight range of >3 ∗ 106. Since scaling reflects adaptive changes in size or scale among otherwise similar animals, we can expect to observe more similarities than differences between rodent and human livers. Obvious differences, such as the presence (rodents) or absence (humans) of lobation and the presence (mice, humans) or absence (rats) of a gallbladder, suggest qualitative differences between the livers of these species. After review, however, we conclude that these dissimilarities represent relatively small quantitative differences. The microarchitecture of the liver is very similar among mammalian species and best represented by the lobular concept, with the biggest difference present in the degree of connective tissue development in the portal tracts. Although larger mammals have larger lobules, increasing size of the liver is mainly accomplished by increasing the number of lobules. The increasing role of the hepatic artery in lobular perfusion of larger species is, perhaps, the most important and least known difference between small and large livers, because it profoundly affects not only interventions like liver transplantations, but also calculations of liver function." | |||
* '''The fate of the vitelline and umbilical veins during the development of the human liver'''{{#pmid:28786203|PMID28786203}} "Differentiation of endodermal cells into hepatoblasts is well studied, but the remodeling of the vitelline and umbilical veins during liver development is less well understood. We compared human embryos between 3 and 10 weeks of development with pig and mouse embryos at comparable stages, and used Amira 3D reconstruction and Cinema 4D remodeling software for visualization. The vitelline and umbilical veins enter the systemic venous sinus on each side via a common entrance, the hepatocardiac channel. During expansion into the transverse septum at Carnegie Stage (CS)12 the liver bud develops as two dorsolateral lobes or 'wings' and a single ventromedial lobe, with the liver hilum at the intersection of these lobes. The dorsolateral lobes each engulf a vitelline vein during CS13 and the ventromedial lobe both umbilical veins during CS14, but both venous systems remain temporarily identifiable inside the liver. The dominance of the left-sided umbilical vein and the rightward repositioning of the sinuatrial junction cause de novo development of left-to-right shunts between the left umbilical vein in the liver hilum and the right hepatocardiac channel (venous duct) and the right vitelline vein (portal sinus), respectively. Once these shunts have formed, portal branches develop from the intrahepatic portions of the portal vein on the right side and the umbilical vein on the left side. The gall bladder is a reliable marker for this hepatic vascular midline. We found no evidence for large-scale fragmentation of embryonic veins as claimed by the 'vestigial' theory. Instead and in agreement with the 'lineage' theory, the vitelline and umbilical veins remained temporally identifiable inside the liver after being engulfed by hepatoblasts. In agreement with the 'hemodynamic' theory, the left-right shunts develop de novo. | |||
* '''Fate mapping of gallbladder progenitors in posteroventral foregut endoderm of mouse early somite stage embryos'''{{#pmid:25648459|PMID25648459}} "In early embryogenesis, the posteroventral foregut endoderm gives rise to the budding endodermal organs including the liver, ventral pancreas and gallbladder during early somitogenesis. Despite the detailed fate maps of the liver and pancreatic progenitors in the mouse foregut endoderm, the exact location of the gallbladder progenitors remains unclear. In this study, we performed a DiI fate-mapping analysis using whole-embryo cultures of mouse early somite-stage embryos. Here, we show that the majority of gallbladder progenitors in 9-11-somite-stage embryos are located in the lateral-most domain of the foregut endoderm at the first intersomite junction level along the anteroposterior axis. This definition of their location highlights a novel entry point to understanding of the molecular mechanisms of initial specification of the gallbladder." | * '''Fate mapping of gallbladder progenitors in posteroventral foregut endoderm of mouse early somite stage embryos'''{{#pmid:25648459|PMID25648459}} "In early embryogenesis, the posteroventral foregut endoderm gives rise to the budding endodermal organs including the liver, ventral pancreas and gallbladder during early somitogenesis. Despite the detailed fate maps of the liver and pancreatic progenitors in the mouse foregut endoderm, the exact location of the gallbladder progenitors remains unclear. In this study, we performed a DiI fate-mapping analysis using whole-embryo cultures of mouse early somite-stage embryos. Here, we show that the majority of gallbladder progenitors in 9-11-somite-stage embryos are located in the lateral-most domain of the foregut endoderm at the first intersomite junction level along the anteroposterior axis. This definition of their location highlights a novel entry point to understanding of the molecular mechanisms of initial specification of the gallbladder." | ||
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| [[File:Mark_Hill.jpg|90px|left]] {{Most_Recent_Refs}} | | [[File:Mark_Hill.jpg|90px|left]] {{Most_Recent_Refs}} | ||
Search term: '' | Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Gallbladder+Embryology ''Gallbladder Embryology''] | [http://www.ncbi.nlm.nih.gov/pubmed/?term=Gallbladder+Development ''Gallbladder Development''] | [http://www.ncbi.nlm.nih.gov/pubmed/?term=Bile+Embryology ''Bile Embryology''] | ||
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| {{Older papers}} | | {{Older papers}} | ||
* '''Fate mapping of gallbladder progenitors in posteroventral foregut endoderm of mouse early somite stage embryos'''{{#pmid:25648459|PMID25648459}} "In early embryogenesis, the posteroventral foregut endoderm gives rise to the budding endodermal organs including the liver, ventral pancreas and gallbladder during early somitogenesis. Despite the detailed fate maps of the liver and pancreatic progenitors in the mouse foregut endoderm, the exact location of the gallbladder progenitors remains unclear. In this study, we performed a DiI fate-mapping analysis using whole-embryo cultures of mouse early somite-stage embryos. Here, we show that the majority of gallbladder progenitors in 9-11-somite-stage embryos are located in the lateral-most domain of the foregut endoderm at the first intersomite junction level along the anteroposterior axis. This definition of their location highlights a novel entry point to understanding of the molecular mechanisms of initial specification of the gallbladder." | |||
* '''Embryology of the biliary tract'''{{#pmid:20551648|PMID20551648}} "A hepatic diverticulum appears in the ventral wall of the primitive midgut early in the 4th week of intrauterine life in the development of the human embryo. This small diverticulum is the anlage for the development of the liver, extrahepatic biliary ducts, gallbladder, and ventral pancreas. By the 5th week, all elements of the biliary tree are recognizable. Marked elongation of the common duct occurs with plugging of the lumen by epithelial cells. Recanalization of the lumen of the common duct starts at the end of the 5th week and moves slowly distally. By the 6th week, the common duct and ventral pancreatic bud rotate 180 degrees clockwise around the duodenum. Early in the 7th week, the bile and pancreatic ducts end in closed cavities of the duodenum. Between the early 8th and 12th week, hepatopancreatic ducts have both superior and inferior orifices." | |||
* '''Muscularis mucosae versus muscularis propria in gallbladder, cystic duct, and common bile duct: smoothelin and desmin immunohistochemical study'''{{#pmid:21074688|PMID21074688}} "The muscle layer in the cystic duct and common bile duct is not well defined, and it is unresolved whether it represents muscularis mucosae or muscularis propria. ... Based on our findings, we conclude that, in the gallbladder wall, the muscle layer is muscularis propria and there is no muscularis mucosae present. In the cystic duct and common bile duct, only an attenuated and incomplete muscle layer of muscularis mucosae is present; because there is no muscularis propria, there probably is limited contractile function." | * '''Muscularis mucosae versus muscularis propria in gallbladder, cystic duct, and common bile duct: smoothelin and desmin immunohistochemical study'''{{#pmid:21074688|PMID21074688}} "The muscle layer in the cystic duct and common bile duct is not well defined, and it is unresolved whether it represents muscularis mucosae or muscularis propria. ... Based on our findings, we conclude that, in the gallbladder wall, the muscle layer is muscularis propria and there is no muscularis mucosae present. In the cystic duct and common bile duct, only an attenuated and incomplete muscle layer of muscularis mucosae is present; because there is no muscularis propria, there probably is limited contractile function." | ||
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[[File:Stage_13_image_077.jpg|600px]] | [[File:Stage_13_image_077.jpg|600px]] | ||
Early embryonic | Early embryonic gallbladder ([[Carnegie stage 13]], [[Week 4]]) | ||
===Stage 22=== | ===Stage 22=== | ||
[[File:Stage_22_image_084.jpg|600px]] | [[File:Stage_22_image_084.jpg|600px]] | ||
Late embryonic | Late embryonic gallbladder ([[Carnegie stage 22]], [[Week 8]]) | ||
==Historic== | ==Historic== | ||
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==Abnormalities== | ==Abnormalities== | ||
{{ICD11weblink}}1737370752 LB20.1 Structural developmental anomalies of gallbladder] | |||
===LB20.10 Agenesis, aplasia or hypoplasia of gallbladder=== | |||
{{ICD11weblink}}932947798 LB20.10 Agenesis, aplasia or hypoplasia of gallbladder] | |||
===Bile Ducts=== | |||
{{ICD11weblink}}252906655 LB20.2 Structural developmental anomalies of bile ducts] | |||
{{ICD11weblink}}819487805 LB20.20 Choledochal cyst] | |||
===LB20.21 Biliary atresia=== | |||
{{ICD11weblink}}645741117 LB20.21 Biliary atresia] - ''Biliary atresia is a rare disease characterised by an inflammatory biliary obstruction of unknown origin that presents in the neonatal period. It is the most frequent surgical cause of cholestatic jaundice in this age group. Untreated, this condition leads to cirrhosis and death within the first years of life.'' | |||
{{ICD11weblink}}1127675817 LB20.22 Congenital stenosis or stricture of bile ducts] (Congenital hypoplasia of bile ducts) | |||
{{ICD11weblink}}14483357 LB20.23 Structural developmental anomalies of cystic duct] | |||
{{ICD11weblink}}1259579536 LB20.24 Accessory bile duct] | |||
===Infections=== | ===Infections=== | ||
These mainly relate to postnatal infections. Recent studies in the mouse have identified that gastrointestinal tract listeria infections can relocate to the | These mainly relate to postnatal infections. Recent studies in the {{mouse}} have identified that gastrointestinal tract listeria infections can relocate to the gallbladder and reside there, leading to later reinfection of the gastrointestinal tract. | ||
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===Reviews=== | ===Reviews=== | ||
{{#pmid:29842921}} | |||
{{#pmid:21074731}} | {{#pmid:21074731}} | ||
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===Articles=== | ===Articles=== | ||
{{#pmid:30258310}} | |||
{{#pmid:25757833}} | |||
{{#pmid:21078254}} | {{#pmid:21078254}} | ||
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{{Footer}} | {{Footer}} | ||
[[Category: | [[Category:Gallbladder]][[Category:Liver]] |
Latest revision as of 14:39, 11 March 2019
Embryology - 29 Mar 2024 Expand to Translate |
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Introduction
This section of notes gives an overview of gallbladder (gall bladder, gall-bladder) and billary tree development, histology and abnormalities associated with the biliary system. In the adult, the gallbladder is a site of bile salt storage and concentration, to then be released into the duodenum where they act to solubilize dietary lipids by their detergent effect. Bile salts are a cholesterol derivative (breakdown product).
The transverse septum differentiates to form the hepatic diverticulum and the hepatic primordium, these two structures together will go on to form different components of the mature liver and gallbladder.
The hepatic diverticulum divides into two parts: pars hepatica (larger cranial part, primordium of the liver) and pars cystica (smaller ventral invagination, primordium of gallbladder).
The pars cystica vacuolates and expands, the stalk becoming the cystic duct. This structure is initially hollow, then solid (by proliferation of epithelial lining), and then recanalized occurs by vacuolation of this expanded epithelium. There are several opinions as to whether the duct has a solid phase or remains patent throughout development.[1][2]
Note that in some animals, for example horse and elephant, the gall bladder is normally absent.
See also: Gallbladder Histology.
Historic: Halpert B. and Lee H. The gall bladder and the extrahepatic biliary passages in late embryonic and early fetal life. (1932) Anat. Rec. 54(1): 29-42.
Some Recent Findings
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More recent papers |
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This table allows an automated computer search of the external PubMed database using the listed "Search term" text link.
More? References | Discussion Page | Journal Searches | 2019 References | 2020 References Search term: Gallbladder Embryology | Gallbladder Development | Bile Embryology |
Older papers |
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These papers originally appeared in the Some Recent Findings table, but as that list grew in length have now been shuffled down to this collapsible table.
See also the Discussion Page for other references listed by year and References on this current page.
|
Embryonic Development
Stage 13
Early embryonic gallbladder (Carnegie stage 13, Week 4)
Stage 22
Late embryonic gallbladder (Carnegie stage 22, Week 8)
Historic
Grosser O. Lewis FT. and McMurrich JP. The Development of the Digestive Tract and of the Organs of Respiration. (1912) chapter 17, vol. 2, in Keibel F. and Mall FP. Manual of Human Embryology II. (1912) J. B. Lippincott Company, Philadelphia.
Gall-bladder Human Embryo (CRL)
- 7.5 mm - epithelium is surrounded by a layer of mesenchyma, and the entire structure is so imbedded in the under surface of the liver that it causes only a slight swelling of the peritoneal surface. Above and on the sides the mesenchyma is in direct relation with the hepatic trabecular, and it receives a few prolongations of the venous capillaries. Below it is covered by the peritoneal epithelium except on the left, where that layer is reflected to the abdominal walls in connection with the falciform ligament. In later stages the gall-bladder is separated from the hepatic trabecular on either side, and is attached to the liver only along its upper surface.
- 16 mm mesenchyma surrounding the gall-bladder is still undifferentiated.
- 22.8 mm forms two broad concentric zones, of which the inner is darker and more compact than the outer.
- 29 mm certain cells in the peripheral part of the dark zone form a third layer, which is thin and somewhat interrupted. As seen in later stages these cells are myoblasts, so that at 29 mm all three layers of the adult gall-bladder are indicated. These are the mucosa, muscularis, and serosa. The layers become gradually less distinct toward the hepatic duct.
Abnormalities
LB20.1 Structural developmental anomalies of gallbladder
LB20.10 Agenesis, aplasia or hypoplasia of gallbladder
LB20.10 Agenesis, aplasia or hypoplasia of gallbladder
Bile Ducts
LB20.2 Structural developmental anomalies of bile ducts
LB20.21 Biliary atresia
LB20.21 Biliary atresia - Biliary atresia is a rare disease characterised by an inflammatory biliary obstruction of unknown origin that presents in the neonatal period. It is the most frequent surgical cause of cholestatic jaundice in this age group. Untreated, this condition leads to cirrhosis and death within the first years of life.
LB20.22 Congenital stenosis or stricture of bile ducts (Congenital hypoplasia of bile ducts)
LB20.23 Structural developmental anomalies of cystic duct
Infections
These mainly relate to postnatal infections. Recent studies in the mouse have identified that gastrointestinal tract listeria infections can relocate to the gallbladder and reside there, leading to later reinfection of the gastrointestinal tract.
- Links: Bacterial Infection
References
- ↑ Crawford JM. (2002). Development of the intrahepatic biliary tree. Semin. Liver Dis. , 22, 213-26. PMID: 12360416 DOI.
- ↑ 2.0 2.1 Ando H. (2010). Embryology of the biliary tract. Dig Surg , 27, 87-9. PMID: 20551648 DOI.
- ↑ Kruepunga N, Hakvoort TBM, Hikspoors JPJM, Köhler SE & Lamers WH. (2018). Anatomy of rodent and human livers: What are the differences?. Biochim Biophys Acta Mol Basis Dis , , . PMID: 29842921 DOI.
- ↑ Hikspoors JPJM, Peeters MMJP, Mekonen HK, Kruepunga N, Mommen GMC, Cornillie P, Köhler SE & Lamers WH. (2017). The fate of the vitelline and umbilical veins during the development of the human liver. J. Anat. , 231, 718-735. PMID: 28786203 DOI.
- ↑ 5.0 5.1 Uemura M, Igarashi H, Ozawa A, Tsunekawa N, Kurohmaru M, Kanai-Azuma M & Kanai Y. (2015). Fate mapping of gallbladder progenitors in posteroventral foregut endoderm of mouse early somite-stage embryos. J. Vet. Med. Sci. , 77, 587-91. PMID: 25648459 DOI.
- ↑ Raparia K, Zhai QJ, Schwartz MR, Shen SS, Ayala AG & Ro JY. (2010). Muscularis mucosae versus muscularis propria in gallbladder, cystic duct, and common bile duct: smoothelin and desmin immunohistochemical study. Ann Diagn Pathol , 14, 408-12. PMID: 21074688 DOI.
Reviews
Kruepunga N, Hakvoort TBM, Hikspoors JPJM, Köhler SE & Lamers WH. (2018). Anatomy of rodent and human livers: What are the differences?. Biochim Biophys Acta Mol Basis Dis , , . PMID: 29842921 DOI.
Lemaigre FP. (2010). Molecular mechanisms of biliary development. Prog Mol Biol Transl Sci , 97, 103-26. PMID: 21074731 DOI.
Causey MW, Miller S, Fernelius CA, Burgess JR, Brown TA & Newton C. (2010). Gallbladder duplication: evaluation, treatment, and classification. J. Pediatr. Surg. , 45, 443-6. PMID: 20152372 DOI.
Roskams T & Desmet V. (2008). Embryology of extra- and intrahepatic bile ducts, the ductal plate. Anat Rec (Hoboken) , 291, 628-35. PMID: 18484608 DOI.
Bani-Hani KE. (2005). Agenesis of the gallbladder: difficulties in management. J. Gastroenterol. Hepatol. , 20, 671-5. PMID: 15853977 DOI.
Delalande JM, Milla PJ & Burns AJ. (2004). Hepatic nervous system development. Anat Rec A Discov Mol Cell Evol Biol , 280, 848-53. PMID: 15382016 DOI.
Articles
Salazar MC, Brownson KE, Nadzam GS, Duffy A & Roberts KE. (2018). Gallbladder Agenesis: A Case Report. Yale J Biol Med , 91, 237-241. PMID: 30258310
Botsford A, McKay K, Hartery A & Hapgood C. (2015). MRCP imaging of duplicate gallbladder: a case report and review of the literature. Surg Radiol Anat , 37, 425-9. PMID: 25757833 DOI. Ahmed M & Aurangzeb. (2010). Triplication of gallbladder. J Coll Physicians Surg Pak , 20, 766-7. PMID: 21078254 DOI.
Blidaru D, Blidaru M, Pop C, Crivii C & Seceleanu A. (2010). The common bile duct: size, course, relations. Rom J Morphol Embryol , 51, 141-4. PMID: 20191134
Peloponissios N, Gillet M, Cavin R & Halkic N. (2005). Agenesis of the gallbladder: a dangerously misdiagnosed malformation. World J. Gastroenterol. , 11, 6228-31. PMID: 16273658
Search Pubmed
July 2010
Search Bookshelf Gall Bladder Development
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Additional Images
See also Gall Bladder Histology
Chapter XVIII. The Organs of Digestion Keith, A. (1902) Human Embryology and Morphology. London: Edward Arnold.
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Cite this page: Hill, M.A. (2024, March 29) Embryology Gastrointestinal Tract - Gallbladder Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Gastrointestinal_Tract_-_Gallbladder_Development
- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G