Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Esophagogastric  Junction

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Volume: The Esophagogastric Junction
Chapter: Esophageal columnar metaplasia (Barrett s esophagus)

What is the most frequent site of the stenosis?

J. Sarosiek, R.W. McCallum (Kansas City)

In this concise review we will focus only on strictures related to gastroesophageal reflux disease (GERD). Therefore, gastroesophageal reflux (GER) will remain as prerequisite for the formation of this type of esophageal stenosis. Endoscopically and radiologically stricture is a narrowing of the esophageal lumen resulting in inflammatory edema, scar formation, and secondarily induced esophageal spasm. Stricture represents, however, a spectrum of histological changes ranging from chronic mucosal damage (relentless reflux), restitution within the areas of epithelial damage (migration of epithelium), reconstitution of normal tissue architecture within some areas with adequately mobilized defensive regenerative capacity, and scar formation in the areas of excessive damage but inadequate protection. Therefore, in the late stage of stricture formation, edema, inflammatory cell infiltration, mucosal regeneration, destruction of muscularis mucosae (result of repeated dilatations), deposition of hyaline and fibrous tissue will be predominant.

It is still uncertain if the patients with stricture represent a selected GERD subpopulation with a unique pattern of motility disorders. Although some patients with esophageal stricture demonstrate an impairment in lower esophageal sphincter (LES) tone, abnormality in motility of the esophageal body, longer duration of gastroesophageal reflux symptomatology and older age, the pathomechanism of stricture formation is poorly understood [1-3]. In some patients with distally located stricture LES pressure and esophageal peristalsis could also be secondarily impaired promoting GER and delaying clearance of acid from the esophageal lumen but also making an assessment of the primary role of motility disorders in the development of stricture a formidable task, indeed. In general, stricture develops in patients with GER in the setting of Barrett's esophagus (BE) or within the esophageal mucosa not affected by intestinalization.

Although stricture may develop as a result of deep inflammatory changes accompanying esophageal ulcer, its frequency exceeds more than two times incidence of ulcers, therefore, in the majority of cases it seems to be related to chronic erosive inflammatory changes within the esophageal mucosa [4]. Stricture can be detected in approximately 10%-15% of patients with peptic esophagitis [1, 4]. Stricture most commonly is located within the transition region between the middle and distal thirds of the esophagus [4]. In the absence of BE esophageal strictures virtually always involve the distal esophagus [5]. If stricture develops in the setting of healed esophageal ulcer, its location and formation is strictly related to ulcer niche, narrowing the esophageal lumen, and represents clinical entity similar to gastric outlet obstruction in patients with chronic peptic ulcer.

When BE is present formation of the stricture is determined by the length of the intestinalized segment of the esophageal mucosa as stricture location exhibits predilection to the areas of squamocolumnar junction. Stricture accompanying BE almost always is located above the segment covered by columnar epithelium at squamocolumnar junction indicative of higher susceptibility to the damage of squamous epithelium than the columnar mucosa by GER [4]. In general, Barrett's mucosa can be found in up to 44% of patients with esophageal stricture [5]. If stricture is complicated by ulcer, its architecture is losing a symmetry, prevailing even after healing of ulcer. In patients with short segment of BE and in patients with incomplete BE stricture tends to be located distally with a still great preponderance to squamocolumnar junction [4]. Rarely stricture may be located within the segment of the esophageal body covered with columnar epithelium. This may indicate that stricture formed at an early stage of BE development when squamocolumnar junction with severe erosive inflammatory changes was located where currently stricture is existing. Of interest, in majority of cases the segment covered with columnar epithelium does not have tendency, for some unknown reason, to migrate further than the border of the esophageal stricture.

The most challenging question is why stricture develops in some patients with diminished LES tone and impaired motility and does not develop in others. Since erosive reflux esophagitis (RE) and BE in particular seem to represent a spectrum of GERD, multifactorial in pathogenetic origin, perhaps a unique combination of motility abnormalities leading to excessive GER, delayed clearance of refluxate (not only acid and pepsin but also other components of duodeno-gastroesophageal milieu) from the esophageal lumen and from the unstirred layer of mucus on the surface of epithelium, and impairment in response of defensive factors both within pre-epithelial, epithelial and postepithelial defense system leads to progressive damage to the squamous epithelium with inflammatory changes extending into deeper layer of the esophageal wall with subsequent repair and accompanying deposition of connective tissue [6-11].

Although in normal conditions early stage of healing should be accompanied by late phase resulting in reconstitution of architectural histological and anatomical characteristics of the mucosal and submucosal compartments, continuous damaging potential of relentless refluxate promotes palliative repair mechanisms dominated by activation of fibroblasts and deposition of fibrillous components of connective tissue.

Location of stricture may not only depend upon the extent of GER which may in majority of cases reach just one third of the lower part of the esophagus, but may also result from the lowest density of submucosal mucous glands within the lower third of the esophagus or may result from the strength of salivary protective tide which protects the most the upper third of the esophageal mucosa and to lesser extent the middle third of the esophagus [6-14]. In addition, development and location of stricture can potentially be influenced by the density and distribution of esophageal submucosal mucous glands which release and deposit their secretion through ducts onto the surface of the esophageal mucosa. A variation in the spatial distribution along the esophagus and the number of submucosal mucous glands in humans from as low as 62 to as high as 741 glandular lobules has been demonstrated in pioneering work by Goetsch [15].

In subjects with strongest salivary secretion and density of esophageal submucosal mucous glands GER has to be very severe to develop any mucosal damage, especially BE and or stricture. These are only however presumptions and extensive future research may shed some light on this intriguing phenomenon.


1. Marks RD, Richter JE. Peptic strictures of the esophagus. Am J Gastroenterol 1993;88:1160-1173.

2. Gillen P, Keeling P, Byrne PJ, Hennessy TPJ. Barrett's esophagus: pH profile. Br J Surg 1987;74:774-776.

3. Ahtaridis G, Snape W, Cohen SA. Clinical and manometric findings in benign peptic strictures of the esophagus. Dig Dis Sci 1979;24:858-861.

4. Savary M, Miller G. The esophagus. Handbook and atlas of endoscopy. Solothurn, Switzerland: Gassman AG, 1978:135-139.

5. Spechler SJ. Complications of gastroesophageal reflux disease. In: Castell DO, ed.The esophagus. Boston, Toronto, London: Little, Brown and Company, 1992:543-556.

6. Sarosiek J, McCallum RW. The evolving appreciation of the role of esophageal mucosal protection in the pathophysiology of gastroesophageal reflux disease. J Pract Gastroenterol 1994;18:20J-20Q.

7. Namiot Z, Sarosiek J, Rourk RM, McCallum RW. Human esophageal secretion: mucosal response to luminal acid and pepsin. Gastroenterology 1994;106:973-981.

8. Sarosiek J, Yu Z, Namiot Z, Rourk RM, Hetzel DP, McCallum RW. Impact of acid and pepsin on human esophageal prostaglandins. Am J Gastroenterol 1994;89:588-594.

9. Rourk RM, Namiot Z, Sarosiek J, Yu Z, McCallum RW. Diminished content of esophageal epidermal growth factor in patients with reflux esophagitis. Am J Gastroenterol 1994;89:1177-1184.

10. Li L, Yu Z, Piascik R, Hetzel DP, Rourk RM, Namiot Z, Sarosiek J, McCallum RW. Effect of esophageal intraluminal mechanical and chemical stressors on salivary epidermal growth factor in humans. Am J Gastroenterol 1993;88:1749-1755.

11. Rourk RM, Namiot Z, Sarosiek J, Yu Z, McCallum RW. Impairment of salivary epidermal growth factor secretory response to esophageal mechanical and chemical stimulation in patients with reflux esophagitis. Am J Gastroenterol 1994;89:237-244.

12. Hopwood D, Coghill G, Sanders DS. Human oesophageal submucosal glands. Their detection mucin, enzyme and secretory protein content. Histochemistry 1986;86:107-112.

13. Fenoglio-Preiser CM. The normal anatomy of the esophagus. In: Fenoglio-Preiser CM, Lantz PE, Listrom MB, Davis M Rilke FO, eds.Gastrointestinal pathology.New York: Raven Press, 1989:21-31.

14. Fawcett DW. The esophagus and stomach. In: Fawcet DW, ed. A textbook of histology, 11th ed. Philadelphia: W.B.Saunders Co. 1986:619-634.

15. Goetsch E. The structure of the mammalian esophagus. Am J Anat 1910;10:1-40.

Publication date: May 1998 OESO©2015