TY - JOUR
T1 - Pathogenetic mechanisms in anterior proliferative vitreoretinopathy
AU - Lopez, P. F.
AU - Grossniklaus, H. E.
AU - Aaberg, T. M.
AU - Sternberg, P.
AU - Capone, A.
AU - Lambert, H. M.
N1 - Funding Information:
From the Department of Ophthalmology (Drs. Lopez, Grossniklaus, Aaberg, Sternberg, Capone, and Lambert); and the L. F.Montgomery Ophthalmic Pathology Laboratory (Dr. Grossniklaus), Emory University, Atlanta, Georgia. This study was supported in part by an unrestricted department grant from Research to Prevent Blindness, Inc., New York, New York, and departmental core grant EY06360. Dr. Lopez was a 1990-1991 Heed-Knapp Ophthalmic Fellow and a 1991-1992 Heed-Knapp Ophthalmic Fellow.
PY - 1992
Y1 - 1992
N2 - A clinicopathologic study of ten consecutive patients (ten eyes) undergoing surgery for rhegmatogenous retinal detachment with anterior proliferative vitreoretinopathy and a subsequent histopathologic, immunohistochemical, and ultrastructural study of ten enucleated eyes with anterior proliferative vitreoretinopathy were performed in order to elucidate relevant pathogenetic mechanisms. Our findings suggest that the pathogenetic evolution of anterior proliferative vitreoretinopathy occurs in three consecutive stages: (1) traction on the ciliary body and peripheral retina induced by fibrocellular contraction of the vitreous base; (2) incorporation of tractionally denuded components of the ciliary body and peripheral retina into the fibrocellular membranes overlying the vitreous base; and (3) proliferation of the incorporated components and fibrovascular ingrowth from the uvea, the retina, or both, into the fibrocellular membranes. Tractional disruption of the epithelium of the ciliary body pars plicata and breakdown of the ciliary blood-aqueous barrier are the principal pathogenetic mechanisms of chronic intractable hypotony and the postvitrectomy fibrin syndrome in anterior proliferative vitreoretinopathy.
AB - A clinicopathologic study of ten consecutive patients (ten eyes) undergoing surgery for rhegmatogenous retinal detachment with anterior proliferative vitreoretinopathy and a subsequent histopathologic, immunohistochemical, and ultrastructural study of ten enucleated eyes with anterior proliferative vitreoretinopathy were performed in order to elucidate relevant pathogenetic mechanisms. Our findings suggest that the pathogenetic evolution of anterior proliferative vitreoretinopathy occurs in three consecutive stages: (1) traction on the ciliary body and peripheral retina induced by fibrocellular contraction of the vitreous base; (2) incorporation of tractionally denuded components of the ciliary body and peripheral retina into the fibrocellular membranes overlying the vitreous base; and (3) proliferation of the incorporated components and fibrovascular ingrowth from the uvea, the retina, or both, into the fibrocellular membranes. Tractional disruption of the epithelium of the ciliary body pars plicata and breakdown of the ciliary blood-aqueous barrier are the principal pathogenetic mechanisms of chronic intractable hypotony and the postvitrectomy fibrin syndrome in anterior proliferative vitreoretinopathy.
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U2 - 10.1016/S0002-9394(14)71790-8
DO - 10.1016/S0002-9394(14)71790-8
M3 - Article
C2 - 1524114
AN - SCOPUS:0026646527
SN - 0002-9394
VL - 114
SP - 257
EP - 279
JO - American Journal of Ophthalmology
JF - American Journal of Ophthalmology
IS - 3
ER -