BACKGROUND : Dysphonia is a known consequence of premature birth, and is usually associated with endotracheal intubation in the neonatal period or surgical ligation of persistent patent ductus arteriosus. Recently, cases of dysphonia, in the absence of these causative factors, have been reported. OBJECTIVE : This review seeks to identify literature pertaining to those aspects of laryngeal development that may potentially be disrupted by premature birth. The purpose of the review is to determine whether there is any possible anatomical or physiological explanation for dysphonia to arose solely from premature birth. METHODS : This scoping review was conducted in accordance with the guidelines prescribed by Arskey and O'Malley (2005). Fifteen relevant papers were identified. Results were categorized into age-related categories, to identify changes in the developmental trajectory. Based on the results of the literature search, a further category of unphonated larynges was added. RESULTS : Potential differences in the laryngeal framework (e.g., the development of the cricoid cartilage and the shape of the glottis) and vocal fold histology, depending on gestational age and post-natal phonation were identified. Much literature focused on the macula flavae, however, the layers of the lamina propria were also discussed. CONCLUSIONS : It is unclear whether the process of differentiation of the layers of the lamina propria, which commences in the second to third months of life in term-born infants, is disrupted by prematurity. Further, development of the macula flavae continues until at least 28 weeks' gestation. Preterm children may not phonate immediately after birth, which may also affect laryngeal development.