Bronchopulmonary dysplasia (BPD) is among the most common and serious complications of prematurity. The pathobiology of BPD and BPD associated pulmonary arterial hypertension (BPD-PH) is multifactorial and not yet fully defined. Gastroesophageal reflux (GER), a physiologic process that occurs in most preterm infants and is typically benign, has been proposed as a potential contributor to the development or worsening of BPD and BPD-PH. Infants who develop BPD compared to those who do not are more frequently diagnosed with symptomatic GER and undergo therapeutic interventions to treat GER. However, current evidence does not support a direct causal relationship between GER and the onset or progression of BPD or BPD-PH in preterm infants. While GER may contribute to respiratory morbidity in individual cases, population-level data do not implicate it as a major driver of BPD pathogenesis. Moreover, the limited available data from clinical trials and observational studies does not consistently demonstrate improved outcomes in patients with BPD who are treated for GER. This narrative review summarizes the current literature evaluating the relationship between GER, BPD, and BPD-PH.