TGF-beta2 reduces outflow facility when perfused into cultured human anterior segments. Furthermore, TGF-beta2 affects the extracellular matrix of the trabecular meshwork in a manner that is consistent with the observed reduction in outflow facility. Although the distribution of accumulated fibrillar material was different in these perfused eyes than that in POAG, the difference could be due to variation in biomechanical environment for TM cells in cultured anterior segments compared with the living eye. Overall, these results support the hypothesis that elevated TGF-beta2 levels in the aqueous humor play a role in the pathogenesis of the ocular hypertension in POAG.
Loss of trabecular cells, fusion of trabecular lamellae with collapse of intertrabecular spaces, increase in extracellular material, and obliteration of the canal were found in various amounts around the circumference of eyes with pigment dispersion syndrome and elevated intraocular pressure, and pigmentary glaucoma. These probably all contribute to the development of increased intraocular pressure. Meshworks from trabeculectomy specimens showed these findings and also showed artifactual damage of cells and loss of intertrabecular spaces. This suggests that handling during surgery may cause single trabeculectomy specimens to give only an incomplete picture of the pathophysiology of pigmentary glaucoma.
The difference in morphology of the optic nerves between POAG and PEXG indicates that in eyes with POAG, elevated IOP cannot be the only pathogenetic factor in glaucomatous optic neuropathy. Additional factors, inducing fibrosis and loss of capillaries, seem to be involved. Such additional factors may also contribute to the clinical finding in POAG that nerves can become damaged without elevation of intraocular pressure.
The decline in Fu in very old rhesus monkeys with normal IOP parallels that seen in normotensive aging humans. This may be correlated with thickening of the elastic fiber sheath in the CM tips in addition to other morphologic changes. The TM findings are analogous to those in the aging human eye and are consistent with the age-related decrease in outflow facility reported in both humans and monkeys.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.