Retinopathy of Prematurity: Clinic and Pathogenesis

Abstract

The structure of adult human vitreous condensations (tractus, membranelles) corresponds to the structure of obliterated embryonal vasa hyaloidea. Some embryonal hyaloidal vessels and structures extend from the tunica vasculosa lentis and attach to the retina between the equator and ora serrata. In normal fetal development, these hyaloidal vessels and structures successively disappear because of apoptosis. The lower the birth weight of a premature infant, the higher the risk of retinopathy of prematurity (ROP) due to the disproportion between the regression of vasa hyaloidea (hyaloideoretinal adherences) and the proliferation of retinal vessels. This may be caused by an enhanced growth of retinal vessels (or a delayed regression of vasa hyaloidea). The growth of retinal vessels stops at a barrier formed by the retina-attaching hyaloidal remnants (vessels), resulting in a demarcation line and ROP. The same retinal vessels may then, as a fibrovascular tissue, overgrow the remnants of retina-attaching hyaloidal structures (as guiding formations) through the vitreous cavity up to the tunica vasculosa lentis. The process may result in the progression from ROP stage 2 to ROP stage 5.