Purpose of review: Bronchopulmonary dysplasia (BPD) is a chronic lung disease of infancy affecting mostly premature infants with significant morbidity and mortality. Improved survival of very immature infants has led to increased numbers of infants with this disorder. Acute and chronic lung injury and impaired postnatal lung growth are thought to be responsible for the development of BPD. Whereas changes in clinical practice have improved the clinical course and outcomes for infants with BPD, over the past decade, the overall incidence of BPD has not changed. This review will describe the prenatal and postnatal factors that contribute to the pathogenesis of BPD as well as current and experimental therapies for treatment of BPD.
Recent findings: The factors that contribute to the pathogenesis of BPD are well described; however, recent studies have better defined how these factors modulate lung growth. Inflammation, proinflammatory cytokines and altered angiogenic gene signaling contribute to lung injury and impair prenatal and postnatal lung growth resulting in BPD; however, to date no therapy has been identified that potently and consistently prevents or reverses their effects on lung growth. We will discuss the cell signaling pathways affected in BPD and current therapies available for modulating these pathways.
Summary: Despite current advances in neonatal care, BPD remains a heavy burden on healthcare resources. New treatments directed at either reducing lung injury or improving lung growth are under study.