抄録
Objective : To clarify the pathological mechanism of LPRD by studying the histological changes of the pharynxes and the larynxes in rats with chronic acid reflux esophagitis.
Methods : An experimental rat model of chronic acid reflux esophagitis was surgically created. The pharynxes, larynxes, tracheas, lungs and esophagi of these rats were observed histologically every 2 weeks until 20 weeks after their operations.
Results : At 8 weeks after the operation, mucosal thickening and inflammatory cell infiltration was observed in the hypopharynx of the rat model. Moreover, chronic inflammation with proliferation of fibroblasts, deposition of collagen fibers and proliferation and dilatation of the capillaries was found as time progressed. However, little macroscopic change was observed in the hypopharyngeal mucosa. In addition, at 16 weeks post-operation, inflammatory cell infiltration was identified in the nerve cells around the thoracic esophagus, the arytenoid region, and the lungs.
Conclusions : The histological changes of the pharynx and the larynx associated with surgically induced chronic acid reflux esophagitis were observed in rats. Chronic inflammatory change due to gastric acid reflux was found in the pharynx and larynx microscopically. This finding indicated that inflammatory changes due to gastric acid reflux are associated with the pathogenesis of laryngopharyngeal reflux disease (LPRD).
