Classification and etiology
Depending on their origin, esophageal inflammations are divided into two large groups:
- Primary esophagitis develops upon direct contact of the mucosa with damaging agents. These include chemical burns from acid and alkali solutions, thermal injuries, the effects of pharmaceuticals, as well as components of gastric juice and bile.
- Secondary esophagitis acts as a manifestation or complication of other diseases. It accompanies specific infections (tuberculosis, diphtheria, measles, scarlet fever, typhus, mycoses) or systemic lesions such as Crohn's disease.
According to its clinical course, the process can be acute or chronic. Acute inflammation most commonly manifests as exudative reactions: serous, fibrinous, phlegmonous, hemorrhagic, or gangrenous inflammation. The chronic variant occurs with prolonged tissue alteration, for example, against the background of regular alcohol consumption, hot food, persistent infections, or constant reflux.
Pathogenesis of reflux esophagitis
Reflux esophagitis is a specific form of chronic inflammation serving as the morphological substrate of gastroesophageal reflux disease (GERD). It is based on dysfunction of the lower esophageal sphincter. This may be a consequence of vagotomy, peptic ulcer disease, various mechanical disorders, or systemic sclerosis (due to atrophy of the cardiac muscle fibers).
When gastric and duodenal contents are refluxed, bile acids act as the main aggressive factors. They cause intercellular edema in the spinous and functional layers of the epithelium, leading to the destruction of junctional complexes. The epithelial barrier loses its integrity, and the aggressive environment penetrates deeper, causing hyperstimulation of intraepithelial nerve receptors.
Clinically, this is expressed by retrosternal pain, heartburn, and sometimes vomiting and nocturnal cough. Notably, there is no direct clinicomorphological correlation: excruciating heartburn may occur without visible macroscopic mucosal changes, and 50% of patients with a severe morphological picture of inflammation experience no heartburn at all.
Microscopic picture and cellular dynamics
A histological diagnosis is made only on the basis of a combination of features, since none of them individually is strictly pathognomonic:
- Proliferative acanthosis: active division of committed cells of the basal layer (confirmed by DNA synthesis with tritium-labeled thymidine) and downward growth of the epithelium into the lamina propria in the form of characteristic cords.
- Papillary changes: connective tissue papillae elongate synchronously with epithelial growth, reaching 75% of the layer thickness. Venular ectasia is observed within them due to inflammatory hyperemia, stasis, and neoangiogenesis.
- Ballooning degeneration: hydropic changes in maturing cells in the upper parts of the epithelial layer.
- Inflammatory infiltration: eosinophilic infiltration is of key diagnostic importance. Under the influence of interleukin-5 (secreted by Th2 lymphocytes), eosinophils migrate intraepithelially and release major basic proteins from granules that damage cell membranes. Neutrophilic infiltration is less specific and usually reacts to necrosis products or complement system components.
In parallel, macrophages and degranulating platelets release growth factors, stimulating fibroblasts to intensively produce stromal collagen (types I and III) and fibronectin.
Macroscopy and complications
Initial macroscopic changes include focal hyperemia, edema, and mucus deposits. As the disease progresses, erosions and ulcers 5 mm or more in length appear. They are located on the apices of folds, can merge into chains, and form a ring encompassing 75% or more of the esophageal circumference. It is important to understand that an ulcer defect is not a manifestation, but rather a complication of esophagitis arising due to a drop in epithelial resistance.
Other severe outcomes and complications include:
- Bleeding: occurs when blood vessels in the submucosal layer are damaged.
- Perforation: disruption of the wall integrity due to a massive burn or secondary histolysis. It leads to the development of mediastinitis, pneumomediastinum, and subcutaneous emphysema.
- Inflammatory polyps: protrusion of granulation tissue covered by proliferating epithelium during ulcer scarring.
- Strictures: lumen narrowing due to intramural fibrosis. It develops when the muscular layer of the wall becomes the ulcer base.
- Barrett's esophagus and esophageal adenocarcinoma.
Briefly: answers to topical questions
What macroscopic forms are distinguished in chronic esophagitis?
In chronic reflux esophagitis, macroscopic changes depend on the severity of the process and include initial changes, erosive and ulcerative lesions, and strictures.
- Initial changes — focal hyperemia, edema, and mucus deposits.
- Erosive and ulcerative lesions — erosions and ulcers 5 mm or more in length, located on the apices of mucosal folds; they can merge or lie in a chain, forming a ring.
- Esophageal strictures — form as a result of chronic inflammation and ulcer repair.
What histological criteria are used to diagnose Barrett's esophagus?
For the histological diagnosis of Barrett's esophagus, signs of intestinal metaplasia of the mucosa are detected.
- Villous structures — formation of villous connective tissue structures.
- Intestinal epithelium — replacement of the stratified squamous epithelium of the distal esophagus with columnar epithelium of the intestinal type.
- Goblet cells — their presence is an obligatory morphological sign for establishing the diagnosis.
Histological triad of esophagitis: Acanthosis (downward epithelial growth), Papillae (upward stromal growth), Balloon cells (surface swelling).
Class and exam questions
Which inflammatory infiltrate is most specific for reflux esophagitis?
Eosinophilic infiltration. It is considered one of the earliest and most reliable signs, unlike neutrophilic infiltration, which can be a distant reaction to any necrosis.
Does severe heartburn always mean severe damage to the esophageal mucosa?
No, there is no direct clinicomorphological correlation. Patients with excruciating heartburn may lack macroscopic changes, and heartburn is often absent in severe esophagitis.
How does an esophageal stricture form in chronic esophagitis?
A stricture forms in the presence of a deep ulcer defect whose base becomes the muscular layer. During the healing process, pronounced intramural fibrosis develops, narrowing the organ's lumen.
What else to study on this topic
- Dynamics of basal cell renewal and apoptosis
- The role of macrophages and platelets in the remodeling of the esophageal stroma
- Differential diagnosis of eosinophilic infiltration
- Morphogenesis of inflammatory esophageal polyps
- Mechanisms of mediastinitis development in esophageal perforation
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