The relationship of hiatal hernia and gastroesophageal reflux symptoms—two-sphincter hypothesis: a review

Abstract

The gastroesophageal junction (GEJ) is an intricate and complicated part of the gastrointestinal tract. Abnormalities in the anatomy and physiology of this junction can result in debilitating reflux disease. For years, physicians and physiologists have debated the cause of reflux disease and how components of the GEJ prevent reflux while at the same time allowing for retrograde flow of gas and gastric contents when appropriate. The debate stems from whether this barrier is anatomical or physiological in origin. Does the position of the stomach and the angle of esophageal insertion prevent reflux or is there a physiologic sphincter similar to others found throughout the human body? Since before the 1950s a multitude of well-designed experiments involving animals, cadavers, asymptomatic volunteers, and patients suffering from reflux have been conducted to attempt to answer this question. There has been data supporting both arguments. During the late 1980s investigators began to piece together the evidence to form what is known today as the “two-sphincter hypothesis”. This review will present a current understanding of the two-sphincter hypothesis with a focus on the anatomy and physiology of the GEJ, how the components of the two sphincters interplay with one another to create a reflux barrier, what happens when there is a breakdown of the components, and how reconstructing the GEJ can improve defective parts of the two sphincters.