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Editors Selection IGR 17-4

Clinical forms of glaucoma: Histology of POAG and pseudoexfoliation

Comment by John Morrison on:

13012 Pathophysiologic changes in the optic nerves of eyes with primary open angle and pseudoexfoliation glaucoma, Gottanka J; Kuhlmann A; Scholz M et al., Investigative Ophthalmology and Visual Science, 2005; 46: 4170-4181

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Histologic evaluation of glaucomatous eyes holds promise for providing pertinent clues to disease mechanisms. In this tradition, Gottanka et al. (789) have performed a careful study of optic nerves from eyes with well-documented primary open angle glaucoma (POAG) and pseudoexfoliation glaucoma (PEXG), considered here a form of secondary glaucoma. By specifically analyzing the retrobulbar optic nerve, where the tissue is more regular and less likely to be affected by physical alterations due to cupping and remodeling, the authors were able to perform quantitative comparisons between these two forms of glaucoma and age-matched control eyes. Cross sections of the retrobulbar optic nerves were analyzed for number of axons, neural area, septal and perivascular connective tissue, as well as compositional changes in connective tissue using immunohistochemistry. Capillary numbers and evidence of atherosclerosis were also studied.

Histologic studies suggest that vascular factors may also contribute to the pathogenesis of glaucoma

Both forms of glaucoma demonstrated a loss in total axons compared to controls. The absolute connective tissue area was increased only in the POAG eyes. Immunohistochemistry showed that this was associated with increases in collagen type IV and VI in POAG nerves only, located primarily in the perivascular and septal regions and confirmed by electron microscopy. Capillaries were decreased in both forms of glaucoma, but the density of capillaries was decreased only in the POAG eyes. Arteriosclerotic changes were more commonly seen in glaucomatous eyes as compared to controls, with a suggestion of greater changes in POAG than PEXG, which was not statistically significant.

Evaluation of optic nerve heads, the presumed site of glaucomatous optic nerve damage, might be expected to provide more direct information on mechanisms of optic nerve injury. However, the quantitative data provided by this study reveals conditions that co-exist with the damage process, and indirectly shed light on potential differences in mechanisms between primary and secondary forms of glaucomatous damage. The differences noted here suggest that pressure-induced mechanisms are not the sole pathogenic factor in damage to POAG eyes. Vascular factors, such as arteriosclerosis and loss of capillaries, may also contribute, as well as increased connective tissue fibrosis, which may interfere with nutrient delivery to axon bundles.

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