In eosinophilic esophagitis (EoE), activated eosinophils and mast cells in the esophagus degranulate and release pro-inflammatory, fibrogenic, and myoactive substances that cause esophageal remodeling and underlie EoE symptoms. Although EoE is diagnosed and managed primarily on the basis of eosinophil density found in endoscopic mucosal biopsies that frequently sample only the esophageal epithelium, EoE can involve all layers of the esophagus including the muscularis propria. Consequently, symptoms and esophageal dysfunction in EoE may not be caused solely by mucosal inflammation, but also by the effects of cytokines, inflammatory cells, and fibrosis in the deeper layers of the esophagus. Esophageal distensibility is an index of the stretchiness of the esophageal wall that can be measured using the functional lumen imaging probe (FLIP), which frequently reveals impaired esophageal distensibility in EoE patients. Although reduced esophageal distensibility in EoE frequently is attributed (without proof) exclusively to fibrosis, esophageal inflammation and muscle dysfunction also might contribute to impaired distensibility. In this review, we discuss the mechanisms regulating smooth muscle tone of the esophageal body, the impact of EoE on distensile properties of the esophageal wall including smooth muscle tension, and the current technologies available for evaluating esophageal wall distensibility in EoE, none of which can distinguish the relative contributions of inflammation, fibrosis, and muscle dysfunction to the decreased esophageal distensibility characteristic of the disease. Better techniques for assessing the depth and type of EoE disease activity may lead to more targeted and improved positioning of the options that are available for EoE treatment.