Posterior glottic stenosis is a disabling disease in which the vocal folds are fixed near the midline. This allows adequate vocal fold adduction for voicing, but does not permit useful abduction for ventilation. The most common cause is prolonged endotracheal intubation for mechanical ventilation, and the incidence is estimated at 4% for intubations between 5 and 10 days. Currently, our understanding and treatment modalities are based on retrospective reviews of small, nonrandomized clinical experiences. The purpose of this project was to develop an animal model that would improve our understanding of histologic changes and allow future prospective randomized trials for therapeutic intervention. Twelve dogs, 15 to 25 kg, were randomly divided into three groups. Animals in group I had a superficial injury produced in the tissue over the right cricoarytenoid joint; animals in group 2 had a deep soft tissue injury produced; and animals in group 3 underwent joint opening. The animals were allowed to recover for 2 months. Morphometric analysis of the harvested larynges demonstrated clinically significant limitation in motion in the animals with deep soft tissue injury and in animals with joint disruption. Histologic analysis revealed various degrees of injury, from loss of subepithelial soft tissue to cartilaginous resorption and fusion of the arytenoid to the cricoid. These findings were directly related to the depth of the initial injury. It is possible to produce posterior glottic stenosis in the canine species. This will serve as a reliable animal model for future study.