Early morphogenesis of persistent hyperplastic tunica vasculosa lentis and primary vitreous. The dog as an ontogenetic model.

Observations on (postnatal) persistent hyperplastic tunica vasculosa lentis/persistent hyperplastic primary vitreous (PHTVL/PHPV) in man and dog have been published previously. Up to the present, no evidence on the etiology of this entity was available. The hereditary occurrence of the disease in the Dobermann pinscher dog and the similarity of ocular development in mammals has provided a useful model in providing ontogenetic data. The present study deals with the early morphogenesis of PHTVL/PHPV, from day 25 to 44 post-coitum (D25-D44), in genetically affected dog fetuses. Normal beagle dog fetuses served as reference material, which has been described separately. At D30, the hyaloid system, including the tunica vasculosa lentis posterior, had developed further than in the reference fetuses. From that stage onward, a retrolental fibrovascular membrane developed. In some of the eyes of D37, posterior polar subcapsular cataracts and preretinal glial proliferations were observed. Capsular anomalies and distortions of the lens shape as seen in clinical PHTVL/PHPV were not observed, and are believed to be secondary entities. Extrapolation of some of the obtained data from dog to man is possible by the use of comparable gestational time scales. The anterior form of (PHTVL/PHPV) in man probably develops its main features in the period of approximately 43 to 66 days of pregnancy. Recently, anti-angiogenetic properties of normal vitreous have been described. This, and the fact that overdevelopment and subsequent incomplete regression of the hyaloid system plays a major role in the pathogenesis of PHTVL/PHPV, gives rise to the hypothesis that a changed amount or effectiveness of such (humoral) factors is an important factor in the etiology of this disease.