Sandbox: mahda20

# Overview
The exact pathogenesis of  is not fully understood.
OR
It is thought that esophageal stricture is the result of lower pressure of esophageal sphincter in gastroesophageal reflux disease,      esophageal motor disorder, inflammation and fibrosis and scar of esophagus  scarry esophagus and esophageal anastomosis strictures.
OR
 is usually transmitted via the  route to the human host.
OR
Following transmission/ingestion, the  uses the  to invade the  cell.
OR
 arises from s, which are  cells that are normally involved in .
OR
The progression to  usually involves the .
OR
The pathophysiology of  depends on the histological subtype.

# Pathophysiology

## Pathogenesis
- The exact pathogenesis of  is not fully understood.
OR
- It is thought that  esophageal stricture is the result of lower pressure of esophageal sphincter in gastroesophageal reflux disease, esophageal motor disorderor, . inflammation and fibrosis and scar of esophagus  scarry esophagus and esophageal anastomosis strictures.all possible variations of scarry esophageal strictures according their etiology, localization and the extension Histologically, the mucosal epithelium and lamina propria had regenerated as in the normal area. In the EBD group, the circumferential stricture site showed marked thickening, and there were hypertrophic scars associated with epithelial defects on the luminal surface. Histologically, defects of the mucosal epithelium and full-thickness proliferation of connective tissue were observed.
-  is usually transmitted via the  route to the human host.
- Following transmission/ingestion, the  uses the  to invade the  cell.
-  arises from s, which are  cells that are normally involved in .
- The progression to  usually involves the .
- The pathophysiology of  depends on the histological subtype.
Peptic strictures are the endstage result of chronic reflux esophagitis. They account for 90% of benign esophageal strictures and, by definition, imply a stricture arising as a result of exposure to the acid-peptic content of the stomach. The esophagus normally is exposed to frequent episodes of reflux of small amounts of gastric fluid which are limited by a competent lower esophageal sphincter and rapidly cleared by normal esophageal peristalsis. A defect in these and other esophageal protective mechanisms leads to inflammation due to prolonged esophageal exposure to acid, pepsin, and possibly bile and pancreatic enzymes. Stricture formation occurs in 723% of patients with reflux esophagitis. The process is progressive, beginning with mucosal edema and inflammatory cell infiltrates of the lamina propria. Chronic esophagitis progresses transmurally, even into periesophageal tissues, with subsequent fibrosis and scarring leading to luminal compromise and esophageal foreshortening (Kuo and Kalloo 1998,Mamazza et al 1998).
A stricture is an esophageal narrowing, usually 13 mm or less in diameter, that causes dysphagia. The normal esophagus measures up to 30 mm in diameter. Peptic strictures occur usually at the squamocolumnar junction and measure 14 cm in length. The typical patient with a peptic stricture is elderly with a long history of gastroesophageal reflux (GER). Significant predictors of stricture formation in patients with GER are lower esophageal sphincter (LES) tone of less than 8 mmHg, impaired esophageal motility, and duodenogastric reflux (Marks and Richter 1993,Stein et al 1992). Hiatus hernia is twice as prevalent in GER patients with stricture (85%) as compared to those with no esophagitis (42%) (Kuo and Kalloo 1998).

# Genetics
-  is transmitted in  pattern.
- Genes involved in the pathogenesis of  include , , and .
- The development of  is the result of multiple genetic mutations.

# Associated Conditions
- The most important conditions/diseases associated with esophageal stricture include:
gastroesophageal reflux disease
- gastroesophageal reflux disease

# Gross Pathology
- On gross pathology, , , and  are characteristic findings of .

# Microscopic Pathology
- On microscopic histopathological analysis, , , and  are characteristic findings of .

# Mahshid

### Normal physiology:
Gastric acid frequently get back as reflux to esophagus. Lower esophageal sphincter normally prevent large amount of gastric acid reflux.  The esophagus normally has the ability to clear gastric acid effect by normal esophageal peristalsis.