Clinical meaning
The gastroesophageal junction (GEJ) maintains a high-pressure zone through three complementary anti-reflux mechanisms: the intrinsic lower esophageal sphincter (LES, a 3-4 cm zone of tonically contracted smooth muscle generating 10-30 mmHg resting pressure), the extrinsic crural diaphragm (which augments LES pressure during inspiration and straining via a pinchcock mechanism), and the angle of His (the acute angle at which the esophagus enters the stomach, creating a flap-valve effect). Transient LES relaxations (TLESRs) are the primary mechanism of reflux in 70% of episodes: vagal afferents from the stomach sense gastric distension and trigger a reflexive LES relaxation lasting 10-60 seconds, independent of swallowing, allowing gastric contents to reflux. In hiatal hernia, the LES is displaced above the diaphragm, separating it from the crural reinforcement and creating an acid pocket — a layer of unbuffered acid floating on postprandial gastric contents that is positioned above the diaphragm and directly adjacent to the esophageal mucosa. Impaired esophageal body peristalsis reduces acid clearance time, prolonging mucosal contact. Obesity increases intra-abdominal pressure by 10-20 mmHg, mechanically promoting reflux and increasing TLESR frequency through gastric distension. When these protective mechanisms fail, gastric acid (pH 1-2) and activated pepsin damage the esophageal squamous epithelium, causing intercellular space dilation (the earliest histological change, detectable even in NERD), inflammatory cell infiltration, basal cell hyperplasia, and progressive mucosal erosion.