PURPOSE: To test the hypothesis that glaucoma in eyes with pseudoexfoliation (PEX) syndrome results from blockage of the outflow channels by PEX material, melanin granules from the iris pigment epithelium, or both, and to determine the origin of intratrabecular PEX material. METHODS: Trabecular meshwork tissue was obtained from five surgically enucleated eyes with PEX glaucoma, ten autopsy eyes with PEX syndrome without evidence of glaucoma, and six age-matched control eyes. Morphometric methods were used to measure the percentage area occupied by open spaces, cells, plaque material, PEX material, and melanin granules on electron micrograph montages of the entire filtration area and the juxtacanalicular tissue (JCT) area. RESULTS: Independent of the presence of glaucoma, most PEX deposits were located in the JCT adjacent to the inner and outer walls of Schlemm's canal, as well as in the uveal meshwork. Although ultrastructural evidence indicates the local production of PEX fibers in the JCT by endothelial and connective tissue cells, PEX material in the uveal meshwork is derived partly from the aqueous humor. A significant correlation could be established between the presence of glaucoma and the amount of PEX material in both the filtration area and the JCT, the average thickness of the JCT, and the mean cross-sectional area of Schlemm's canal. No significant correlation existed, however, between glaucoma status and the concentration of melanin granules or plaque material, and the cellularity. CONCLUSION: In addition to a mechanical obstruction by PEX material of exotrabecular origin, the apparent production of PEX material by trabecular cells may be principally responsible for glaucoma development. Accumulation of locally produced PEX material in the JCT, followed by dysfunction of endothelial cells and disorganization of JCT and Schlemm's canal, appear to be causative factors in the development of a special type of secondary open-angle glaucoma in PEX syndrome.
PURPOSE: To test the hypothesis that glaucoma in eyes with pseudoexfoliation (PEX) syndrome results from blockage of the outflow channels by PEX material, melanin granules from the iris pigment epithelium, or both, and to determine the origin of intratrabecular PEX material. METHODS: Trabecular meshwork tissue was obtained from five surgically enucleated eyes with PEX glaucoma, ten autopsy eyes with PEX syndrome without evidence of glaucoma, and six age-matched control eyes. Morphometric methods were used to measure the percentage area occupied by open spaces, cells, plaque material, PEX material, and melanin granules on electron micrograph montages of the entire filtration area and the juxtacanalicular tissue (JCT) area. RESULTS: Independent of the presence of glaucoma, most PEX deposits were located in the JCT adjacent to the inner and outer walls of Schlemm's canal, as well as in the uveal meshwork. Although ultrastructural evidence indicates the local production of PEX fibers in the JCT by endothelial and connective tissue cells, PEX material in the uveal meshwork is derived partly from the aqueous humor. A significant correlation could be established between the presence of glaucoma and the amount of PEX material in both the filtration area and the JCT, the average thickness of the JCT, and the mean cross-sectional area of Schlemm's canal. No significant correlation existed, however, between glaucoma status and the concentration of melanin granules or plaque material, and the cellularity. CONCLUSION: In addition to a mechanical obstruction by PEX material of exotrabecular origin, the apparent production of PEX material by trabecular cells may be principally responsible for glaucoma development. Accumulation of locally produced PEX material in the JCT, followed by dysfunction of endothelial cells and disorganization of JCT and Schlemm's canal, appear to be causative factors in the development of a special type of secondary open-angle glaucoma in PEX syndrome.