Send to

Choose Destination
Nat Rev Dis Primers. 2019 Nov 14;5(1):78. doi: 10.1038/s41572-019-0127-7.

Bronchopulmonary dysplasia.

Author information

Division of Neonatology, Department of Pediatrics, Children's Hospital of Eastern Ontario (CHEO) and CHEO Research Institute, Ottawa, Ontario, Canada.
Ottawa Hospital Research Institute, Sinclair Centre for Regenerative Medicine, Ottawa, Ontario, Canada.
Departments of Medicine and Pediatrics, University of Wisconsin-Madison, Madison, WI, USA.
The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Cincinnati Children's Hospital Medical Center, Division of Neonatology, Pulmonary Biology, University of Cincinnati, Cincinnati, OH, USA.
Pediatric Heart Lung Center, Section of Pulmonary Medicine, Department of Pediatrics, Children's Hospital Colorado and the University of Colorado Denver Anschutz Medical Center, Aurora, CO, USA.
Children's National Medical Center, Department of Pediatrics, Washington, DC, USA.
Joseph M. Sanzari Children's Hospital, Hackensack Meridian Health School of Medicine, Hackensack, NJ, USA.
Albert Einstein College of Medicine, Bronx, NY, USA.
The Royal Women's Hospital, University of Melbourne, Melbourne, Victoria, Australia.
Department of Pediatrics, Eudowood Division of Respiratory Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Department of Pediatrics, Larner School of Medicine, University of Vermont, Burlington, VT, USA.


In the absence of effective interventions to prevent preterm births, improved survival of infants who are born at the biological limits of viability has relied on advances in perinatal care over the past 50 years. Except for extremely preterm infants with suboptimal perinatal care or major antenatal events that cause severe respiratory failure at birth, most extremely preterm infants now survive, but they often develop chronic lung dysfunction termed bronchopulmonary dysplasia (BPD; also known as chronic lung disease). Despite major efforts to minimize injurious but often life-saving postnatal interventions (such as oxygen, mechanical ventilation and corticosteroids), BPD remains the most frequent complication of extreme preterm birth. BPD is now recognized as the result of an aberrant reparative response to both antenatal injury and repetitive postnatal injury to the developing lungs. Consequently, lung development is markedly impaired, which leads to persistent airway and pulmonary vascular disease that can affect adult lung function. Greater insights into the pathobiology of BPD will provide a better understanding of disease mechanisms and lung repair and regeneration, which will enable the discovery of novel therapeutic targets. In parallel, clinical and translational studies that improve the classification of disease phenotypes and enable early identification of at-risk preterm infants should improve trial design and individualized care to enhance outcomes in preterm infants.


Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center