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 etiology of ROP begins before birth.
Results: Based on current evidence we suggest that, contrary to current etiologic 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 etio-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.