The prenatal phase of retinopathy of prematurity.

AIM

To explore the current literature on prenatal inflammation-associated risk factors for retinopathy of prematurity (ROP).

METHODS

Subjective summary of selected experimental and epidemiological publications that support the authors' central hypothesis that the aetiology of ROP begins before birth.

RESULTS

Based on current evidence we suggest that, contrary to current aetiological models, the process of ROP development begins with a prephase in utero. This beginning is likely initiated by inflammatory responses that are associated with intrauterine infection.

CONCLUSION

We propose a novel aetio-pathogenetic model of ROP and suggest that the effects of postnatal exposure to inflammatory stressors (resulting from infection or hyperoxia or both) as well as those of other pre- and postnatal contributors to the complex pathogenesis of ROP might be modified by the prenatal phase of the disease.