Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:
Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_699_Библиотеки_им_академика_М_И_Перельмана.pdf
Скачиваний:
0
Добавлен:
30.08.2026
Размер:
55 Мб
Скачать
48 Histology of the mesentery
operitoneal
(b)
Mesocolon and retroperitoneum
Mesocolon
Toldt’s fascia
(a)
Surface
mesothelium
Mesocolon
Toldt’s fascia
Mesentery
proper
Retroperitoneum
1 mm
Surface
mesothelium
Deep
mesothelium
Retr
mesothelium
Retroperitoneum
Toldt’s fascia
Retroperitoneum
(c)
Figure 4.1 (a) 2.5D snapshot of 3D digital sculpture depicting the histologic structure of the mesentery and underlying fascia. (b) Photomicrograph demonstrating the mesentery, underlying fascia, and retroperitoneum at the level of the left mesocolon. (c) Scanning electron micrograph demonstrating the mesentery, fascia, and retroperitoneum at the level of the right mesocolon.
Wherever mesentery attaches to retroperitoneum, a distinct fascial layer (Toldt’s fascia) occurs between both (Figure4.1b and c) [25–27]. Beneath Toldt’s fascia a fur­ther mesothelial layer covers the retroperitoneum itself. Variations occur in the composition of Toldt’s fascia [25,26].
e fascia will be discussed in detail in Chapter 5.
is arrangement of mesothelium and fascia is impor-
tant as it generates the plane that is exploited in good quality
colorectal surgery. A surgical plane is dened as the interface between two contiguous surfaces. Surgical planes provide an anatomic roadmap by which structures may be freed from their normal anatomic attachments to permit safe division and resection. e plane used most oen in colorectal sur­gery occurs at the interface between the mesothelium on the under surface of the mesentery and Toldt’s fascia, that is, the mesofascial plane. Components of this plane may
Sample
Small intestinal mesentery
20,000 µm
(a) (b)
tive tissue
Transverse mesocolon
(b)(a)
face
Nomenclature: The visceral andparietal peritoneum 49
Mesothelium
Adipocytes
origin
Small
intestinal
mesentery
Figure 4.2 (a) 2.5D snapshots from a 3D digital model of the mesentery demonstrating the location at which full thickness biopsies were taken through the small bowel mesentery. (b) Photomicrograph demonstrating the structure of the small intestinal mesentery.
Connective tissue
septation
Sample from
transverse colon
Adipocyte lobule
Connec
septation
Mesothelium
Upper sur mesothelium
Connective
tissue
Lower surface
mesothelium
Figure 4.3 (a) 2.5D snapshots from a 3D digital model of the mesentery demonstrating the location at which full thickness biopsies were taken through the transverse mesocolon. (b) Photomicrograph demonstrating the structure of the trans­verse mesocolon.
be separated surgically in a manner that allows complete separation of the mesentery from the posterior abdominal wall[24].
(including the mesentery) [1–3,27]. us, the mesothelial covering on either side of the human mesentery corre­sponds to “visceral peritoneum” (Figure 4.1). In keeping
20,000 µm
with the above, mesothelium overlying the retroperito-
NOMENCLATURE: THE VISCERAL ANDPARIETAL PERITONEUM
Mesenteric mesothelium is smooth surfaced, highly functional, and comprises a single layer of cuboidal­shaped cells [25]. It closely resembles pleural mesothelium and is similar to peritoneum elsewhere within the abdo­men. Manyanatomic texts subdivide the abdominal peri­toneum into “parietal” and “visceral” regions. Parietal peritoneum lines the inner aspect of the abdominal wall while visceral peritoneum covers the abdominal viscera
neum (i.e.,beneath Toldt’s fascia) corresponds to “pari­etal peritoneum” (Figure 4.1). It is not uncommon for these to be referred to as the visceral and parietal fascia, respectively [28–36]. As they are not anatomic fascia, this terminology is inaccurate. Moreover, it is also confusing as the only true fascia in this region is Toldt’s fascia, that is, the fascia interposed between the visceral and parietal peritoneum.
roughout this book, the terms “visceral” and “parietal”
peritoneum will be adopted and the term “fascia” will be reserved exclusively for Toldt’s fascia (Figure 4.3) [37].
50 Histology of the mesentery
(a) (b)
face mesothelium
Left mesocolon
100 µm
Sur
Adipocyte lobule
Left mesocolon
biopsy
Connective tissue
lattice
Left mesocolon
Toldt’s fascia
Retroperitoneum
Figure 4.4 (a) 2.5D snapshots from a 3D digital model of the mesentery demonstrating the location at which full thickness biopsies were taken through the left mesocolon. (b) Photomicrograph demonstrating the structure of the left mesocolon.
IMMUNOHISTOCHEMICAL ANALYSIS OFMESENTERIC MESOTHELIUM
Immunohistochemical evaluation of surface mesenteric meso­thelium demonstrates expression of markers including D2-40 (podoplanin) and CD-35 [26,38]. Few studies have directly focused on surface marker expression in mesenteric versus nonmesenteric mesothelium. Indeed, no studies have examined
Table 4.1 Immunohistochemical markers expressed in surface mesothelium
Study Year Journal Marker Reference
Satelli etal. 2015 Clin Cancer Res 84-1/vimentin [39] Yokobori etal. 2013 Cancer Res PLS3 [40] Yung etal. 2011 J Biomed Biotechnol Hyaluronan [41] Foroutan etal. 2010 J Biol Sci CD45 [42]
Rosellini etal. 2007 Folia Biol CKAE1-AE3 [43]
Yáñez-Mó etal. 2003 N Engl J Med Cytokeratins [44]
Yang etal. 1999 Perit Dial Int Cytokeratins [45]
Ho-dac-Pannekeet etal. 1997 Adv Perit Dial CA125 [46]
surface marker expression in mesocolic mesothelium (i.e., vis­ceral peritoneum), Toldt’s fascia, nor in mesothelium beneath Toldt’s fascia (i.e., parietal peritoneum). As surface marker expression relates to cellular functionality, this is a key area for future research. Table4.1 provides a summary of the surface markers associated with peritoneal mesothelium in general. Although it is feasible the properties listed can be extrapolated to the mesenteric context, this should be investigated.
CD34 HBME-1 Cytokeratin 18
CK19 p63 Ki-67 Vimentin CD34 HBME-1
ICAM-1
Vimentin
Mesenteric connective tissue lattice 51
tive tissue
Submesothelial connective tissue
connec
MESENTERIC CONNECTIVE TISSUE LAT TICE
A connective tissue layer occurs underneath mesenteric visceral peritoneum. is is the “submesothelial connec­tive tissue layer.” It is highly variable in thickness and composition. In some regions, it is well developed, while in others it is entirely absent (Figure 4.5). For example, it
Submesothelial
tive tissue
(a)
is well developed on the upper surface of the transverse mesocolon, where the latter is adherent to the greater omentum. It is also well developed on the lateral aspect of mesosigmoid. is distribution appears to correlate with the presence of congenital adhesions. For example, congenital adhesions are prominent at the lateral aspect of the mesosigmoid. ey also cause the greater omentum to adhere to the upper surface of the transverse mesocolon.
Surface
mesothelium
Septation
Surface
mesothelium
(b)
Submesothelial connective tissue
Connec
Undersurface
mesothelium
Avascular
interpedicular
mesentery
Ileocolic
adipovascular
pedicle
(c)
Figure 4.5 (a) Photomicrograph demonstrating the mesenteric surface. This is lined with mesothelium beneath which there is a connective tissue layer (arrows) and from which connective tissue septations arise. The latter separate adipocyte compartments. Adipocytes are packaged in a honeycomb-like conformation within compartments. (b)Histologic struc­ture in an avascular interpedicular region of mesentery. Adipocytes are minimal and both mesothelial surfaces are close. Thisgenerates a translucent macroscopic appearance (c).
52 Histology of the mesentery
Submesothelial
Mesenteric and intestinal connective tissue
Connective tissue branches, or septae, extend from the submesothelial connective tissue into the substance of the mesentery, separating the latter into adipocyte compart­ments. Adipocytes are packaged in a honeycomb-like con­formation (Figure 4.5) and together contribute the main bulk of the mesentery. In certain mesenteric regions, adipo­cytes are minimal and both mesenteric mesothelial surfaces come into close apposition (Figure 4.5b,c) [23,25,26]. Macroscopically, these regions are identiable as being near translucent. is property is of particular surgical relevance as it enables the surgeon to divide through the mesentery with minimal bleeding (Figure 4.5c).
Taken together, the connective tissue septae and subme­sothelial connective tissue layer generate a lattice, the “mes­enteric connective tissue lattice” (Figure 4.6a and b). is is present throughout the mesentery. At the gastrointestinal margin, it is continuous with connective tissue in outer lay­ers of the gastrointestinal tract (Figure 4.6b and c). Here, the lattice contributes directly to the formation of the intestinal
Mesenteric connective
tissue
connective
tissue
serosa. e serosa in turn contributes connective tissue to the longitudinal and circular smooth muscle layers. Within the mesentery, the lattice encases vessels contributing to the adventitia of these.
Where major vessels enter or leave the mesentery, the
connective tissue of the lattice coalesces with that of the underlying fascia to form a connective tissue cuor adven­titia. e perivascular connective tissue cuis also of surgi­cal relevance as it means that the mesentery can be readily cleared from vascular surfaces, with minimal disruption of either vessel or mesentery.
e submesothelial connective tissue layer is largely
acellular. However, cell clusters occur at points where septa­tions arise (Figure 4.7a). Analysis of serial sections demon­strates that on occasion, isolated cell clusters occur. e cells within these clusters have mesenchymal features, resem­bling broblast and myobroblasts. is is in keeping with earlier ndings suggesting that cells within the submeso­thelial connective tissue layer have surface markers that are
Intestinal
connective
tissue
Mesenteric connective
tissue
Intestinal
(a) (b)
Mesenteric connective
tissue
*
*
Surface
connective tissue
(c) (d)
Figure 4.6 (a) 2.5D image from 3D model demonstrating the mesenteric connective tissue lattice and its contiguity with that in the adjacent gastrointestinal tract. (b) All tissue with exception of the connective tissue has been conceptually removed from the model in (a) to depict the extent of the connective tissue lattice. (c) Photomicrograph showing connective tissue contiguity between the mesentery and the gastrointestinal tract. (d) Photomicrograph demonstrating connective tissue contiguity between deep and supercial muscle layers of the intestinal wall.
Connective tissue of
outer muscle layer
*
connective
tissue
Connective tissue of
outer muscle layer
Connective tissue of
inner muscle layer
Mesenteric connective tissue lattice and lymphatics
Mesenchymal
(b)
(c)
nodes and channels
cell cluster
Mesothelial cell plasticity 53
Surface
mesothelium
(a)
Surface
mesothelium
Connective
tissue lattice
Deep
mesothelium
Figure 4.7 (a) Photomicrograph showing the surface mesothelium of the right mesocolon. At certain points mesenchymal cells clustered as indicated. (b) 3D sculpture demonstrating the connective tissue of the lattice and contained lymphatic channels. (c) Same model as in (b) but with the connective tissue removed.
intermediate between mesothelial and mesenchymal cells [23,25,26]. Itisfeasible that mesenchymal cells within these clusters are derived from overlying mesenteric mesothelium.
e connective tissue lattice also houses a lymphatic net­work (Figure 4.7b and c). Lymphatic vessels are identiable in the submesothelial connective tissue monolayer as well as in septations. e frequency with which lymphatic ves­sels are identied varies (though not signicantly) between mesenteric regions. In submesothelial connective tissue, lymphatic vessels measure 10.2 ± 4.1µm in diameter and have an average radius of diusion of 174.72 ± 97.68µm. is means that a lymphatic vessel occurs every 0.17mm (Figure 4.7b and c). Lymphatic vessels also occur in Toldt’s fascia where they measure 4.3 ± 3.1µm in diameter and have a radius of diusion of 165.12 ± 66.26µm. Collectively, a rich lymphatic network occupies all levels of the mesen­teric connective tissue lattice and may be vulnerable during surgery [26].
suggest that mesenteric mesothelium may be plastic and capable of dierentiating into multiple mesenchymal cell types [42,50]. Foroutan etal. examined hematopoietic and mesenchymal stem markers in mesothelial cells in peri­toneal dialysate. ese were analyzed by cell culture, ow cytometry, and immunophenotyping for CD45 and CD34 (hematopoietic stem cell markers), HBME-1 (mesothe­lial cell marker), and cytokeratin 18 (epithelial marker). While mesothelial cells expressed classical mesothelial and epithelial surface markers, they also expressed CD34 (mesenchymal marker) and CD45 (hematopoietic marker) [42]. Both mesenteric mesothelia and lymphoepithelia are known to express podoplanin [38,51–53]. Mesothelia else­where (e.g., hepatic and pleural) can undergo mesothelial­to-mesenchymal transition [54–56]. Observations such as these support the intriguing suggestion that mesenteric mesothelial cells are not inert and could in fact contribute to the local mesenchymal cellular pool [57–62]. is sug-
Mesenteric lymph
with connective
tissue removed
gestion is supported by our recent observations related to
MESOTHELIAL CELL PLASTICITY
the culture of mesenteric mesothelia. If mesenteric meso­thelia are harvested, puried, and cultured, then follow-
A number of studies have demonstrated submesothelial connective tissue cells with surface markers normally observed in cells under transition from one state of dif­ferentiation to another (i.e., from mesothelial to mesen­chymal cell types) [39,40,47–49]. eseand other ndings
ing 2 weeks a mixture of mesenchymal cell types emerges. is property, when combined with the total surface area of the extensively plicated mesentery, means that mesen­teric mesothelium could represent a signicant stem cell reservoir [63].
54 Histology of the mesentery
Derangements of mesenteric mesothelial plasticity may contribute to multiple intraabdominal disease processes. e origin of the cells responsible for adhesion formation is not known. It is not unreasonable to suggest that surgical disruption of mesenteric mesothelium may lead to a local­ized or widespread mesenchymal response that results in adhesion formation [63,64].
All abdominal wall hernia (out with the acute setting) have a mesothelial component. is could be explained as follows. As mesothelium proliferates an invagination devel­ops. Given the secretery properties of mesothelium, the inner surface of this is highly lubricated and thus permits both entry and exit of abdominal contents. e cumulative eect of persistent mechanical pressures (including positive intraperitoneal pressure) leads to an increase in size of the mesothelial invagination and ultimately to clinical manifes­tation of the underlying pathology. Perhaps the best invivo model of this phenomenon is the parastomal hernia. Stoma creation requires formation of a defect in the abdominal wall. At formation, the local parietal mesothelium is disrupted. With time, a mesothelial invagination arises that carpets the subcutaneous tissue and is oen associated with herniation of adjacent bowel loops. is is the parastomal hernia.
Mesothelial-to-mesenchymal transformation may also contribute to the development of Crohn’s or diverticular dis­ease [65–69]. In Crohn’s disease, mesenteric lymphangiec­tasia occurs and correlates with the distribution of mucosal abnormalities [70–73]. In patients with mesenteric adeni­tis, a pronounced lymphadenopathy occurs at the ileocecal mesenteric conuence. Lymph nodes may also develop in appendices epiploicae [74–76]. is is surprising as classic descriptions indicate that lymph nodes are conned to major vessels. e identication of nodes in appendices epiploices (i.e., remote from major vessels) maybe further evidence of a cellular ux involving nearby mesenteric mesothelium.
FUTURE DIRECTIONS
e characterization of mesenteric histology has raised several suggestions that prompt investigation. ese could involve a characterization of the role of mesenteric mesothe­lium in several disease processes including adhesion forma­tion, hernia development, and Crohn’s disease. e concept of connective tissue contiguity should be explored in broader terms. As has been demonstrated to date, the mesenteric con­nective tissue lattice is contiguous with that of adjacent intes­tine. e mesenteric connective tissue lattice also contributes adventitia to contained vessels. ese ndings suggest that a systemic connective tissue platform occurs, which receives inputs from mesenteric and intestinal sources and which could provide a novel route of disease spread (Figure 4.6).
SUMMARY
e cellular and extracellular composition of the mesentery is similar from the root region to the anorectal junction. Multiple levels of continuity (including connective tissue,
vascular, neurologic, and lymphatic) occur between mesen­tery and adjacent intestinal tract and between mesentery and associated vessels. Characterization of mesenteric histology provides opportunities to refresh approaches to several disease processes including those involving systemic manifestations.
REFERENCES
1. Snell, R.S., Clinical Anatomy by Regions. Lippincott Williams & Wilkins, 2008, pp. 216, 226, 228, 233, 237,240.
2. Cunningham, D.J., Cunningham’s Textbook of Anatomy. W. Wood, 1818, pp. 1185, 1208, 1221, 1253, 1423.
3. Arnould-Taylor, W., A Textbook of Anatomy and Physiology. Stanley Thornes, Surrey, U.K., 1998, pp.60–68.
4. Hostmann, A. etal., Dendritic cells from human mesenteric lymph nodes in inammatory and non­inammatory bowel diseases: Subsets and function of plasmacytoid dendritic cells. Immunology, 2013. 139(1): 100–108.
5. Bell, S.J. etal., Migration and maturation of human colonic dendritic cells. J Immunol, 2001. 166(8): 4958–4967.
6. Silva, M.A., Intestinal dendritic cells and epithelial barrier dysfunction in Crohn’s disease. Inamm Bowel Dis, 2009. 15(3): 436–453.
7. Baumgart, D.C. etal., Patients with active inamma­tory bowel disease lack immature peripheral blood plasmacytoid and myeloid dendritic cells. Gut, 2005. 54(2): 228–236.
8. Kaser, A. etal., Increased expression of CCL20 in human inammatory bowel disease. J Clin Immunol,
2004. 24(1): 74 –85.
9. Exley, M.A. etal., Interplay between the immune system and adipose tissue in obesity. J Endocrinol,
2014. 223(2): R41–R48.
10. Fenzl, A. and F.W. Kiefer, Brown adipose tissue and thermogenesis. Horm Mol Biol Clin Investig, 2014. 19(1): 25 – 3 7.
11. Kloting, N. and M. Bluher, Adipocyte dysfunction, inammation and metabolic syndrome. Rev Endocr Metab Disord, 2014. 15(4): 277–287.
12. Porter, C., M. Chondronikola, and L.S. Sidossis, The therapeutic potential of brown adipocytes in humans. Front Endocrinol, 2015. 6: 156.
13. Ozen, G. etal., Human perivascular adipose tissue dysfunction as a cause of vascular disease: Focus on vascular tone and wall remodeling. Eur J Pharmacol,
2015. 766: 16–24.
14. Jeanson, Y., A. Carriere, and L. Casteilla, A new role for browning as a redox and stress adaptive mecha­nism? Front Endocrinol, 2015. 6: 158.
15. Grundy, S.M., Adipose tissue and metabolic syn­drome: Too much, too little or neither. Eur J Clin Invest, 2015. 45(11): 1209–1217.
References 55
16. Canfora, E.E., J.W. Jocken, and E.E. Blaak, Short­chain fatty acids in control of body weight and insulin sensitivity. Nat Rev Endocrinol, 2015. 11(10): 577–591.
17. Declercq, C. etal., Mapping of inammatory bowel disease in northern France: Spatial variations and relation to afuence. Inamm Bowel Dis, 2010. 16(5): 807–812.
18. Henriksen, M. etal., C-reactive protein: A predictive factor and marker of inammation in inammatory bowel disease. Results from a prospective popula­tion-based study. Gut, 2008. 57(11): 1518–1523.
19. Lu, X. etal., Decay-accelerating factor attenuates C-reactive protein-potentiated tissue injury after mesenteric ischemia/reperfusion. J Surg Res, 2011. 167(2): e103 –e115.
20. Magro, F., P. Sousa, and P. Ministro, C-reactive protein in Crohn’s disease: How informative is it? Expert Rev Gastroenterol Hepatol, 2014. 8(4): 393–408.
21. Peyrin-Biroulet, L. etal., Mesenteric fat in Crohn’s disease: A pathogenetic hallmark or an innocent bystander? Gut, 2007. 56(4): 577–583.
22. Peyrin-Biroulet, L. etal., Mesenteric fat as a source of C reactive protein and as a target for bacterial translocation in Crohn’s disease. Gut, 2012. 61(1): 78–85.
23. Culligan, K. etal., The mesocolon: A prospective observational study. Colorectal Dis, 2012. 14(4): 421–428; discussion 428–430.
24. Coffey, J.C. etal., Mesenteric-based surgery exploits gastrointestinal, peritoneal, mesenteric and fascial continuity from duodenojejunal exure to the anorectal junction—A review. Dig Surg, 2015. 32(4): 291–300.
25. Culligan, K. etal., The mesocolon: A histological and electron microscopic characterization of the mesen­teric attachment of the colon prior to and after surgi­cal mobilization. Ann Surg, 2014. 260(6): 1048–1056.
26. Culligan, K. etal., A detailed appraisal of mesocolic lymphangiology—An immunohistochemical and stereological analysis. J Anat, 2014. 225(4): 463 – 472.
27. Standring, S., Gray’s Anatomy: The Anatomical Basis of Clinical Practice. Churchill Livingstone/Elsevier, Edinburgh, Scotland, 2008, pp. 1085, 1099–1111, 1143.
28. Lin, M.B. etal., Understanding the planes of total mesorectal excision through surgical anatomy of pelvic fascia. Zhonghua Wei Chang Wai Ke Za Zhi,
2008. 11(4): 308 – 311.
29. Coffey, J.C. and P. Dockery, Colorectal cancer: Surgery for colorectal cancer—Standardization required. Nat Rev Gastroenterol Hepatol, 2016. 13(5): 256–257.
30. Thorek, P., C.T. Linden, and N. Swan, Anatomy in Surgery. Springer, New York, 2012, pp. 327–329, 458, 506, 511, 532.
31. Lin, M. etal., The anatomic basis of total mesorectal excision. Am J Surg, 201(4): 537–543.
32. Acar, H.I. etal., Dynamic article: Surgical anatomical planes for complete mesocolic excision and applied vascular anatomy of the right colon. Dis Colon Rectum, 2014. 57(10 ): 1169–1175.
33. Gao, Z. etal., An anatomical, histopathological, and molecular biological function study of the fascias posterior to the interperitoneal colon and its associ­ated mesocolon: Their relevance to colonic surgery. J Anat, 2013. 223(2): 123–132.
34. Sondenaa, K. etal., The rationale behind complete mesocolic excision (CME) and a central vascular ligation for colon cancer in open and laparoscopic surgery: Proceedings of a consensus conference. Int J Colorectal Dis, 2014. 29(4): 419–428.
35. Klingensmith, M.E. and W.U.D. Surgery, The Washington Manual of Surgery. Wolters Kluwer Health/Lippincott Williams & Wilkins, Philadelphia, PA, 2008, pp. 199, 207.
36. Roy, H., Short Textbook of Surgery. Jaypee Brothers, Medical Publishers Pvt. Limited, New Delhi, India, 2010, Chapter 41, p. 260.
37. Culligan, K. etal., Review of nomenclature in colonic surgery—Proposal of a standardised nomencla­ture based on mesocolic anatomy. Surgeon, 2013. 11(1):1–5.
38. Ordonez, N.G., D2-40 and podoplanin are highly specic and sensitive immunohistochemical markers of epithelioid malignant mesothelioma. Hum Pathol,
2005. 36(4): 372–380.
39. Satelli, A. etal., Epithelial-mesenchymal transitioned circulating tumor cells capture for detecting tumor progression. Clin Cancer Res, 2015. 21(4): 899–906.
40. Yokobori, T. etal., Plastin3 is a novel marker for circulating tumor cells undergoing the epithelial-mes­enchymal transition and is associated with colorectal cancer prognosis. Cancer Res, 2013. 73(7): 2059–2069.
41. Yung, S. and T.M. Chan, Pathophysiology of the perito­neal membrane during peritoneal dialysis: The role of hyaluronan. J Biomed Biotechnol, 2011. 2011: 180594.
42. Foroutan, T., A. Hosseini, A.A. Pourfatholah, M. Soleimani, K. Alimoghadam, and N. Mosaffa, Peritoneal mesothelial progenitor or stem cell. J Biol Sci, 2010. 10(5): 460.
43. Rosellini, A. etal., Expansion of human mesothelial progenitor cells in a longterm three-dimensional organotypic culture of Processus vaginalis peritonei. Folia Biol, 2007. 53(2): 50–57.
44. Yanez-Mo, M. etal., Peritoneal dialysis and epithelial-to-mesenchymal transition of mesothelial cells. NEngl J Med, 2003. 348(5): 403–413.
45. Yang, W.S. etal., Interleukin-1beta stimulates the production of extracellular matrix in cultured human peritoneal mesothelial cells. Perit Dial Int, 1999. 19(3): 211–220.
46. Ho-dac-Pannekeet, M.M. etal., Markers of peritoneal mesothelial cells during treatment with peritoneal dialysis. Adv Perit Dial, 1997. 13: 17–22.
56 Histology of the mesentery
47. Satelli, A. etal., Universal marker and detection tool for human sarcoma circulating tumor cells. Cancer Res, 2014. 74(6): 1645–1650.
48. Sieuwerts, A.M. etal., Anti-epithelial cell adhesion molecule antibodies and the detection of circulating normal-like breast tumor cells. J Natl Cancer Inst,
2009. 101(1): 61–66.
49. Yu, M. etal., Circulating breast tumor cells exhibit dynamic changes in epithelial and mesenchymal composition. Science, 2013. 339(6119): 580–584.
50. Gotloib, L., L.C. Gotloib, and V. Khrizman, The use of peritoneal mesothelium as a potential source of adult stem cells. Int J Artif Organs, 2007. 30(6): 501– 512.
51. Kalof, A.N. and K. Cooper, D2-40 immuno­histochemistry—So far! Adv Anat Pathol, 2009. 16(1):62–64.
52. Raftery, A.T., Regeneration of parietal and visceral peritoneum in the immature animal: A light and electron microscopical study. Br J Surg, 1973. 60(12): 969–975.
53. Raica, M., A.M. Cimpean, and D. Ribatti, The role of podoplanin in tumor progression and metastasis. Anticancer Res, 2008. 28(5b): 2997–3006.
54. Li, Y., J. Wang, and K. Asahina, Mesothelial cells give rise to hepatic stellate cells and myobroblasts via mesothelial-mesenchymal transition in liver injury. Proc Natl Acad Sci USA, 2013. 110(6): 2324–2329.
55. Okamoto, K. etal., Angiotensin II enhances epithelial­to-mesenchymal transition through the interaction between activated hepatic stellate cells and the stro­mal cell-derived factor-1/CXCR4 axis in intrahepatic cholangiocarcinoma. Int J Oncol, 2012. 41(2): 573–582.
56. Strippoli, R. etal., Epithelial-to-mesenchymal transition of peritoneal mesothelial cells is regulated by an ERK/NF-kappaB/Snail1 pathway. Dis Model Mech, 2008. 1(4–5): 264–274.
57. Balogh, P. etal., Estrogen receptor alpha is expressed in mesenteric mesothelial cells and is internalized in caveolae upon Freund’s adjuvant treatment. PLOS ONE, 2013. 8(11): e79508.
58. Kalluri, R. and R.A. Weinberg, The basics of epi­thelial-mesenchymal transition. J Clin Invest, 2009. 119(6): 1420–1428.
59. Lee, J.M. etal., The epithelial-mesenchymal transi­tion: New insights in signaling, development, and disease. J Cell Biol, 2006. 172(7): 973–981.
60. Planas-Silva, M.D. and P.K. Waltz, Estrogen pro­motes reversible epithelial-to-mesenchymal-like transition and collective motility in MCF-7 breast cancer cells. J Steroid Biochem Mol Biol, 2 007. 104(1–2): 11–21.
61. Sodek, K.L. etal., Cell-cell and cell-matrix dynamics in intraperitoneal cancer metastasis. Cancer Metastasis Rev, 2012. 31(1–2): 397–414.
62. Teng, R. etal., Morphological analysis of leucocyte transmigration in the pleural cavity. J Anat, 2003. 203(4): 391–404.
63. Lachaud, C.C. etal., Use of mesothelial cells and biological matrices for tissue engineering of simple epithelium surrogates. Front Bioeng Biotechnol,
2015. 3: 117.
64. diZerega, G., Peritoneal Surgery. Springer, New York, 1999, pp. 115–143, 215–295.
65. Liu, Z.J., Y. Zhuge, and O.C. Velazquez, Trafcking and differentiation of mesenchymal stem cells. J Cell Biochem, 2009. 106(6): 984 –991.
66. Miao, C.G. etal., Wnt signaling in liver brosis: Progress, challenges and potential directions. Biochimie, 2013. 95(12): 2326–2335.
67. Goncalves, P., F. Magro, and F. Martel, Metabolicinammation in inammatory boweldisease: Crosstalk between adipose tissueandbowel. Inamm Bowel Dis, 2015. 21(2): 453 – 467.
68. Olszanecka-Glinianowicz, M. etal., Adipokines in the pathogenesis of idiopathic inammatory bowel disease. Endokrynol Pol, 2013. 64(3): 226–231.
69. Shelley-Fraser, G. etal., The connective tissue changes of Crohn’s disease. Histopathology, 2012. 60(7): 1034–1044.
70. Ersoy, O. etal., Evaluation of primary intestinal lymphangiectasia by capsule endoscopy. Endoscopy,
2013. 45(Suppl. 2): E61–E62.
71. Freeman, H.J. and M. Nimmo, Intestinal lymphangiectasia in adults. World J Gastrointest Oncol, 2011. 3(2): 19–23.
72. Ingle, S.B. and C.R. Hinge Ingle, Primary intestinal lymphangiectasia: Minireview. World J Clin Cases,
2014. 2(10): 528–533.
73. Sura, R., J.F. Colombel, and H.J. Van Kruiningen, Lymphatics, tertiary lymphoid organs and the granulomas of Crohn’s disease: An immunohisto­chemical study. Aliment Pharmacol Ther, 2011. 33(8): 930–939.
74. Ghahremani, G.G. etal., Appendices epiploicae of the colon: Radiologic and pathologic features. Radiographics, 1992. 12(1): 59–77.
75. Medani, M. etal., An appraisal of lymph node ratio in colon and rectal cancer: Not one size ts all. Int JColorectal Dis, 2013. 28(10): 1377–1384.
76. Schnedl, W.J. etal., Insights into epiploic appendagitis. Nat Rev Gastroenterol Hepatol, 2 011. 8(1): 45 –49.

Toldt’s fascia

J. CALVIN COFFEY AND RAVI KIRAN
5
Aim 57 Introduction 57 Development 57 Composition 57 Demonstration of Toldt’s fascia 58 Toldt’s fascia: Regional anatomy 58
Mesorectal fascia 58 Mesosigmoidal fascia 59 Left mesocolic fascia and the white line ofToldt 59 Right mesocolic fascia and the white line ofToldt 61
The greater the ignorance the greater the dogma.
William Osler
AIM
e primary aim is to demonstrate the nature of Toldt’s fas­cia at all intestinal levels distal to the duodenojejunal ex­ure. Asecondary aim is to highlight the clinical relevance of the fascia.
INTRODUCTION
Toldt’s fascia is the connective tissue layer that occurs between attached regions of mesentery and retroperitoneum (or pelvis) (Figure5.1) [1–4]. Several terms have been used in reference to it. At the mesorectal level, the fascia is referred to as Waldeyer’s fascia, the retrorectal fascia, Denonvillier’s fascia, and the endo­pelvic fascia. Surrounding the kidney Toldt’s fascia is termed Gerota’s or the anterior pararenal fascia. Toldt’s characterization of the distribution of the fascia was remarkably accurate and closely mirrors current descriptions (Figure 5.2) [5]. Fortunately, Toldt worked with cadavers that had not been sub­jected to corrosive preservatives. As the fascia is exquisitely thin in particular regions, preservatives obliterate it, leading to the erroneous impression that it is absent in that region. In normal circumstances, the fascia is dicult to visualize unaided. ese properties explain why Toldt’s ndings have yet to be generally accepted[5,6]. Morerecently, the development of colorectal
Fascial continuity 62
Histology 62 Function of Toldt’s fascia 63 Surgical implications of Toldt’s fascia 66 Toldt’s fascia and radiologic implications 66 Adhesions and Toldt’s fascia 66 Future directions 67 Summary 67 References 67
surgery in general and of laparoscopic and robotic technolo­gies has shown that the fascia is universally present between the mesentery and retroperitoneum [7–17].
DEVELOPMENT
Toldt suggested that the fascia arose aer the visceral perito­neum of the mesentery fused with the parietal peritoneum of the retroperitoneum [4–6]. He suggested that during this process epithelial monolayers were lost and the underly­ing connective tissue fused to generate the fascia. It is now known that the visceral mesenteric and parietal peritoneal layers are retained into adulthood and that the fascia devel­ops between these. e resultant anatomic arrangement forms a cornerstone in mesenteric-based gastrointestinal surgery. Asa result, it is the focus of the current chapter.
COMPOSITION
e composition (and hence appearance) of Toldt’s fascia is variable. Beneath the right mesocolon, it is well developed com­prising multiple lamella of collagen [2,3,10]. Beneath the meso­sigmoid and mesorectum, it is areolar and exquisitely delicate, a property that has led to its comparison with angel hairs and candy oss. As a result, it can oen be quite dicult to identify in these regions. Variations in composition and appearance make its identication dicult. is represents a signicant challenge to both the novice and experienced surgeon. During colorectal surgery operating in a plane beneath the fascia threatens retro­peritoneal structures such as the ureters and gonadal vessels.
57