What are the pathological changes of reflux esophagitis

Reflux esophagitis is the inflammation of the esophageal mucosa caused by the reflux of acidic gastric juice. The degree of mucosal damage depends on: ① the ability of the esophagus to clear the reflux; Special role of mucous membranes.

Reflux esophagitis can be divided into three stages according to different stages of development, namely early, middle and late stages. Among them, the early lesions are the most characteristic, while the middle and late stages are difficult to distinguish from other types of esophagitis.

(1) In the early stage, that is, the stage of mild disease: in the early stage, the esophageal mucosa sometimes shows no abnormalities, or shows diffuse and plaque-like hyperemia, the thickness of the epithelial basal cells increases, and the lamina propria papilla extends to the epithelial layer. It is due to the stimulation of the esophageal mucosa by the reflux, which leads to the damage of the superficial cells, and the basal cells proliferate in order to repair the damaged superficial cells. The lamina propria papillae are elongated as a result of increased blood supply to this area.

Many scholars use Ismail-Beigi's early reflux esophagitis as pathological diagnostic criteria: ① basal cell hyperplasia, the thickness of which exceeds 15% of the thickness of the mucosal epithelium (about 10% of the normal thickness); 66% of epithelial thickness (less than 66% of normal thickness). The above changes alone can confirm the diagnosis even in the absence of other histological abnormalities.

In addition, Jessurun et al. believed that balloon-like cell changes occurred in esophageal squamous epithelial cells in reflux esophagitis. Among 10 cases of reflux esophagitis, balloon-like cells were seen in 7 cases. Among the 25 suspected patients with reflux esophagitis, balloon-like cells were found in 16 cases. Some authors have suggested that intraepithelial eosinophils in reflux esophagitis can be present in the absence of other tissue abnormalities and that their numbers are independent of the degree of endoscopic inflammation. Seefeld believes that the discovery of eosinophils and neutrophils in the lamina propria is decisive for the diagnosis of reflux esophagitis. It should be pointed out that the presence of eosinophils in the esophageal mucosa is not an inherent feature of reflux esophagitis, and obvious eosinophil infiltration can also be found in the esophageal mucosa of patients with hypereosinophilia and eosinophilic gastroenteritis. The presence of eosinophils in the epithelium can be considered a histological indicator of reflux esophagitis only when the above two conditions are excluded.

Geboes et al. believed that dilation of superficial telangiectasia of the lamina propria papillary, epithelial growth and red blood cell infiltration into the epithelium were reliable signs of early esophagitis. However, telangiectasia is meaningful only when it occurs together with other abnormal changes, and its presence alone is not enough to diagnose reflux esophagitis.

To sum up, reflux esophagitis, even in the early stage, is a dynamic process rather than a static state, showing slight differences in pathomorphological changes. Therefore, on the basis of the Ismail-Beigi criteria, the early lesions of reflux esophagitis are divided into 3 grades according to the degree of lesions:

Grade I: Growth of basal cells in the squamous epithelium, which is 15% of the thickness of the full-thickness epithelium. Superficial telangiectasia and hyperemia of the lamina propria. Eosinophils are occasionally seen in the epithelium.

Grade II: The squamous epithelial horn extends downward. The lamina propria papilla extends up to more than 60% of the epithelial thickness. Superficial telangiectasia and congestion, occasional oozing and neutrophils. Eosinophils and occasionally neutrophils are seen in the epithelium.

Grade III: On the basis of grade II, infiltration of neutrophils and chronic inflammatory cells can be seen in the lamina propria, and sometimes focal capillary and fibroblast proliferation can be seen, forming a granulation-like structure.

(2) Middle stage, that is, the stage of inflammation progression and erosion formation: endoscopically, striped erosion areas can be seen along the long axis of the esophagus. Covered by inflammatory cellulose membrane, infiltration of neutrophils, lymphocytes, and plasma cells can be seen underneath. The inflammatory changes are mainly above the muscularis mucosae, and the proliferation of capillaries and fibroblasts can be seen in the superficial parts, forming chronic inflammatory or healing granulation tissue.

(3) Late stage, that is, ulcer formation and inflammatory hyperplasia stage: the histological change is that the ulcer extends through the mucosa to the submucosa, and the ulcer appears confluent or solitary or circular. The lesion tissue in the ulcer has a layered structure, the surface is exudative cellulose, and the bottom is necrotic tissue. The granulation tissue composed of hyperplastic fibroblasts, new capillaries, chronic inflammatory cells or neutrophils is under the necrotic tissue. At the bottom is scar tissue formed from bud tissue.