Talk:Colon Histology 2009

From Embryology



  • The development of large intestine during the fetal period. Malas MA, Aslankoç R, Ungör B, Sulak O, Candir O. Early Hum Dev. 2004 Jun;78(1):1-13. PMID: 15177668
"development of the haustra and tenia coli in the first trimester was quite slow, but later the development increased more and more, and during the full-term period, the haustra and tenia coli could be seen clearly. "
  • The development of jejunum and ileum during the fetal period. Malas MA, Aslankoç R, Ungör B, Sulak O, Candir O. Early Hum Dev. 2003 Nov;74(2):109-24. PMID: 14580751
  • Development of the vermiform appendix during the fetal period. Malas MA, Sulak O, Gökçimen A, Sari A. Surg Radiol Anat. 2004 Jun;26(3):202-7. Epub 2004 Apr 9. PMID: 15173960

  • Ontogeny and distribution of certain oendocrine cells in the human fetal large intestine. Histochemical and immunocytochemical studies. Lehy T, Cristina ML.

Cell Tissue Res. 1979;203(3):415-26. PMID: 519732

"In 9 fetuses, 9 to 24 weeks-old, the occurrence and relative distribution of argentaffin cells, as well as of cells immunoreactive to somatostatin (SRIF), glucagon-like polypeptide (GLI), pancreatic polypeptide (PP) and substance P (SP) were studied in five segments of the colon (appendix, cecum, ascending colon, descending colon, and rectosigmoid). For each colonic segment, data concerned with the occurrence of endocrine cells were expressed either as mean absolute numbers of specific cells per entire mucosal section, or as cell densities per mm3 of mucosa after calculation of the mucosal volume of the sections. Argentaffin, GLI, SRIF and PP immunoreactive cells are all present in relatively large numbers, scattered along the entire length of the colonic mucosa as early as the 9th-10th week of gestation, whereas substance P-containing cells occur sporadically and first appear during the 4th-17th week. Until the 20th week, with progressing embryonic development, an increase was determined in absolute numbers per section of all types of endocrine cells in all segments of the colon. This observation is clearly related to the general growth of the colonic mucosa, since cell densities per mm3 of mucosa do not greatly change or even decrease during gestation. However, it is possible that densities of argentaffin, GLI and BPP cells increase in the appendix around the 14th-17th week of gestation. Between 20th and 24th weeks, absolute numbers of cells per section remain stable or slightly increase, while cell densities tend rather to decrease in all segments. These data demonstrate that some endocrine cells are present very early in the human fetal colon, but their functional significance remains to be elucidated."
  • Timetable for intestinal rotation in staged human embryos and fetuses. Kim WK, Kim H, Ahn DH, Kim MH, Park HW. Birth Defects Res A Clin Mol Teratol. 2003 Nov;67(11):941-5. PMID: 14745932
"BACKGROUND: The existing data on intestinal rotation during human development are contradictory regarding the timing of major events, and as such an exact timetable for rotation of the intestine in humans is not yet available. METHODS: We studied the initial formation and rotation of the intestine by microdissection and histological observations in 72 human embryos and fetuses at two to 12 weeks postfertilization. The embryos were classified according to the Carnegie staging system. RESULTS: The primordium of the primitive gut was first observed as a yolk sac at stage 5. With the formation of the embryonic foldings, three divisions of the primitive gut (the foregut, midgut, and hindgut) were observed at stage 10. At stage 12, the primitive gut was located on the midline. At stage 15, a 90 degrees counterclockwise rotation of the intestine began. At stage 16, herniation of the intestine into the umbilical cord was not evident in observations of the external form or a transversely sectioned embryo, but was evident in a sagittally sectioned embryo. There was another 90 degrees counterclockwise rotation at stage 20. Reduction of the intestine was a rapid process, since it was still in the cord in fetuses of <40 mm crown-rump length (CRL), and was reduced above 40 mm in general during nine weeks of development. When the intestine returned to the abdominal cavity, the cecum was located in the right lower quadrant (the adult position). CONCLUSIONS: We have developed a standard timetable to describe the rotation of the intestine."


  • Morphology of myenteric plexuses in the human large intestine: comparison between large intestines with and without colonic diverticula. Iwase H, Sadahiro S, Mukoyama S, Makuuchi H, Yasuda M. J Clin Gastroenterol. 2005 Sep;39(8):674-8. PMID: 16082275
"The morphology of myenteric plexuses and the ganglion cells differs significantly among segments of the human large intestine. Large intestines with diverticula had significantly more plexuses but significantly fewer ganglion cells than large intestines without diverticula. The area of the nuclei of ganglion cells was also significantly smaller in large intestines with diverticula. Further studies are required to clarify how these changes are related to intestinal function and how they are involved in the etiology of diverticulosis."


antibody-secreting cells

(ASCs) mucosa-associated lymphoid tissue cells (nasopharynx-associated lymphoid tissues, isolated lymphoid follicles, and Peyer's patches) producing immunoglobulin A (IgA), the most abundant immunoglobulin in the body and the main class of antibody found in secretions.


"Now have a closer look at the components of the wall of the colon. Villi are absent and the crypts appear deeper than the ones you observed in the small intestine. Goblet cells are numerous. The lamina propria and muscularis mucosae may be difficult to distinguish. Note also that a thin layer of longitudinal muscle is found between the taenia coli on the outside of the inner circular muscle layer."

Colorectal polyps

Colon Cancer

"Several genes contributing to a susceptibility to two types of colon cancer:

FAP (familial adenomatous polyposis) So far, only one FAP gene has been discovered - the APC gene on chromosome 5. But over 300 different mutations of that gene have been identified. Individuals with this syndrome develop many polyps in their colon. People who inherit mutations in this gene have a nearly 100 percent chance of developing colon cancer by age 40.

HNPCC (hereditary nonpolyposis colorectal cancer) Individuals with an HNPCC gene mutation have an estimated 80 percent lifetime risk of developing colon or rectal cancer. However, these cancers account for only three to five percent of all colorectal cancers. So far, four HNPCC genes have been discovered:

hMSH2 on chromosome 2, which accounts for 60 percent of HNPCC colon cancer cases. hMLH1 on chromosome 3, which accounts for 30 percent of HNPCC colon cancer cases. hPMSI on chromosome 2, which accounts for 5 percent of HNPCC colon cancer cases. hPMS2 on chromosome 7, which accounts for 5 percent of HNPCC colon cancer cases. Together, FAP and HNPCC gene mutations account for approximately 5 percent of all colorectal cancers. These hereditary cancers typically occur at an earlier age than sporadic (non-inherited) cases of colon cancer. The risk of inheriting these mutated genes from an affected parent is 50 percent for both males and females. The genes that cause these two syndromes were relatively easy to discover because they exert strong effects. Other genes that cause susceptibility to colon cancer are harder to discover because the cancers are caused by an interplay among a number of genes, which individually exert a weak effect."

  • colon hemangiomas are rare, benign vascular lesions, with patients usually presenting with repetitive painless bleeding from the rectum
  • Fecal Occult Blood Screening Does Reduce Death From Colon Cancer George D. Lundberg Medscape J Med. 2008; 10(10): 244. Published online 2008 October 23. PMCID: PMC2605150
  • Survival from cancers of the colon and rectum in England and Wales up to 2001 A G Acheson and J H Scholefield Br J Cancer. 2008 September 23; 99(S1): S33–S34. Published online 2008 September 23. doi: 10.1038/sj.bjc.6604580. PMCID: PMC2557538
  • Lymph Node Evaluation as a Colon Cancer Quality Measure: A National Hospital Report Card Karl Y. Bilimoria, David J. Bentrem, Andrew K. Stewart, Mark S. Talamonti, David P. Winchester, Thomas R. Russell, and Clifford Y. Ko J Natl Cancer Inst. 2008 September 17; 100(18): 1310–1317. Published online 2008 September 17. doi: 10.1093/jnci/djn293. PMCID: PMC2720724

--Mark Hill 10:50, 1 November 2009 (EST) This page was last modified on October 30, 2009, at 17:22. This page has been accessed 65 times.