Introduction: Proliferative Vitreoretinopathy (PVR) is a complication of rhegmatogenous retinal detachment (RRD). Epiretinal membranes (ERM) are thin, fibrous membranes formed by fibrotic scar tissue on the vitreal side of the retina and can lead to visual disturbances and loss and re-detachment. ERMs are shown to have contractile properties that contribute to the secondary retinal detachments. Most proposed mechanisms involving mouse models recreate PVR with traumatic methods. This project sought to induce the formation of retinal detachments (RD) and ERMs atraumatically.

Methods: Newborn C57BL/6J mice were placed in 65% oxygen for seven consecutive days. Eyes were observed with spectral-domain optical coherence tomography (OCT), sectioned and stained with either hematoxylin and eosin (H&E) or for alpha-smooth muscle actin (a-SMA).

Results: At four weeks, all eyes from hyperoxic mice had signs of retinal folding or blebs, 84.5% had ERMs (22/26), and 3.8% had RD (1/26). At five weeks, 100% of eyes had ERMs and 15.4% had RD (4/26). At week seven, 26.9% of eyes (7/26) had RD. The ERMs developed in proximity to the optic nerve head (ONH) and the RDs were visualized between the neurosensory retina and the RPE. Control mice did not develop ERMs or RD. There was co-localization of cells that stained for contractile proteins with some of these retinal abnormalities. SMA cells were found around the areas of retinopathy in hyperoxic mice, but not in control mice. Signs of PVR were detected in most of the experimental retinas that were examined.

Conclusion: The exposure of mice to 65% hyperoxia for seven days after birth created retinal pathology in the form of blebs, folds, ERMs, and detachment, similar to what is observed in PVR. Over the seven weeks retinal pathology progressed, indicating that this model seems to successfully create retinopathy in a nontraumatic, noninvasive manner.