GEJ

GEJ, an abbreviation for gastro‑esophageal junction, denotes the anatomical region where the distal esophagus meets the proximal stomach. Located at the level of the diaphragmatic hiatus, the junction comprises the lower esophageal sphincter (LES), the surrounding crural diaphragm fibers, and the mucosal transition from stratified squamous epithelium to columnar gastric epithelium. This complex structure establishes a pressure barrier that prevents gastric contents from refluxing into the esophagus while allowing the coordinated passage of ingested material during swallowing.

Functionally, the LES maintains basal tonicity of approximately 15–30 mm Hg, relaxing transiently in response to peristaltic waves and swallowing. The crural diaphragm augments LES pressure during inspiration, contributing to anti‑reflux competence. Neuro‑hormonal mechanisms, including vagal input and nitric oxide signaling, modulate sphincter relaxation and tone.

Pathologically, dysfunction of the GEJ is central to gastro‑esophageal reflux disease (GERD), Barrett’s esophagus, and hiatal hernia formation. In GERD, LES hypotonia or inappropriate transient relaxations permit acid exposure, leading to mucosal injury. Chronic reflux may induce metaplastic columnar epithelium—Barrett’s esophagus—which carries an elevated risk of adenocarcinoma. Hiatal hernias occur when the GEJ migrates above the diaphragm, compromising the anti‑reflux barrier.

Diagnostic evaluation of the GEJ includes endoscopy, esophageal manometry, and pH monitoring. Therapeutic strategies aim to restore barrier function via lifestyle modification, pharmacologic acid suppression, endoscopic procedures, or surgical fundoplication. Ongoing research explores endoscopic mucosal resection, radiofrequency treatment, and bio‑engineered sphincter augmentation to improve outcomes for patients with GEJ‑related disorders.