Retinal detachment is a condition in which fluid exists in the subretinal space and causes separation of the neural retina from the underlying retinal pigment epithelium. Proliferative vitreoretinopathy is the proliferation of avascular fibrocellular retinal membranes associated with rhegmatogenous retinal detachment, a retina detached as a result of a retinal break or tear, which causes severe damage to the neural retina and retinal pigment epithelium. Contact between the retinal pigment epithelium and the vitreous fluid through retinal breakage may change the content of glycosaminoglycans in the fluid.
The glycosaminoglycans in the subretinal fluid of rhegmatogenous retinal detachment were characterized (52). The results revealed that hyaluronan alone (HA type) was present in 50% of the eyes. A combination of chondroitin sulfate (chSA) and hyaluronan (chSA type) was present in 15% of the eyes. A combination of dermatan sulfate (DS) and hyaluronan (DS type) was present in 35% of the eyes. Retinal detachment with a demarcation line resulted in subretinal strand formation in the DS-type eyes, while no such formation was seen in the chSA type. Vitreous haze was observed in one eye of the DS type. All eyes with grade C proliferative vitreoretinopathy were the DS type. The eyes with reoperated surgeries were the DS type. The presence of DS may indicate an advanced condition of retinal detachment.
The glycosaminoglycans in normal vitreous were identified as hyaluronan (92%) and chondroitin sulfate (8%). In contrast, up to 18% of the total glycosami-noglycans in pathological samples were identified as chondroitin sulfate (53). In pathological vitreous, two fractions of glycosaminoglycans representing about 10% were identified as undersulfated chondroitin and heparan sulfate. The hydro-dynamic size of hyaluronan differed between normal and pathological samples, and the hyaluronan in samples from patients with detached retinas showed a small hydrodynamic size.
Subretinal fluid from patients with rhegmatogenous retinal detachment showed hyaluronan in 70% of the eyes examined (54). Other samples showed no hyaluronan but hyaluronidase activity. The hyaluronidase activity in the subretinal fluid increased with the duration of the retinal detachment.
Part of the mechanism of the above vitreous glycosaminoglycan transformation in retinal detachment may be explained by modification of blood components.
Hyaluronan represented 91% of the total glycosaminoglycans synthesized by normal vitreous. Vitreous fibrosis was induced by intravitreal injection of monocytes and lymphocytes (55). In the fibrotic vitreous, the synthesis of hyaluronan was decreased to 30%, whereas the synthesis of chondroitin sulfate was increased to 47% of the total newly synthesized glycosaminoglycans. Similarly, vitreous fibrosis was induced by intravitreal injection of erythrocytes (56). In the fibrotic vitreous, the synthesis of hyaluronan was decreased to 26%, whereas the synthesis of chondroitin sulfate increased to 59% of the total newly synthesized glycosamino-glycans. These results suggest that blood cells may alter the synthesis of glycosami-noglycans in induced fibrotic vitreous.
The carbohydrates of the posterior vitreoretinal juncture were examined by electron microscopy (57). Globular material of intermediate electron density was found in the basement membrane of the retina and on collagen fibrils in the vitreous cortex after cetylpyridinium chloride fixation and disappeared after Streptomyces hyaluronidase digestion. These observations suggest that the globular material is hyaluronan that is more labile along the basement membrane than toward the inner vitreous cortex. A fine filamentous network may be formed by the oligosaccharide chains associated with vitreous proteins as part of the vitreoretinal juncture layer.
Vidaurri-Leal et al. reported the following implications for retinal pigment epithelial cells in the pathogenesis of proliferative vitreoretinopathy (58). Normal human retinal pigment epithelial cells in confluent monolayers maintained a hexagonal to oval shape. However, when these monolayers were overlaid with autol-ogous vitreous, the retinal pigment epithelial cells became elongated and migrated into the vitreous gel as bipolar fibrocyte-like cells. Retinal pigment epithelial cells overlaid with hyaluronate did not change their morphological features. When retinal pigment epithelial monolayers were overlaid with a collagen gel, the cells changed from their normal epithelial shape to bipolar fibrocyte-like cells that later migrated into the collagen gel. Thus, exposure of retinal pigment epithelial cells to vitreous in the presence of collagen may play a role in the pathogenesis of prolif-erative vitreoretinopathy.
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