Morphology of age-related cuneiform cortical cataracts: The case for mechanical stress

Abstract

We evaluated the gross morphology, location, and fiber cell architecture of equatorial cortical opacities in the aging human lens. Using dark-field stereomicroscopy, we photographed donor lenses in toto and as thick slices. In addition, we investigated the details of the fiber cell architecture using fluorescent staining for membranes and by scanning electron microscopy. We then combined our data with data from recent studies on lens viscoelasticity. We found that small cortical and cuneiform opacities are accompanied by changes in fiber structure and architecture mainly in the equatorial border zone between the lens nucleus and cortex. Because the lens cortex and nucleus have different viscoelastic properties in young and old lenses, we hypothesize that external forces during accommodation cause shear stress predominantly in this border zone. The location of the described changes suggests that these mechanical forces may cause fiber disorganization, small cortical opacities, and ultimately, cuneiform cataracts.

The ageing lens and cataract: a model of normal and pathological ageing

“…The extent affected increases with age. In the equatorial plane, they lie consistently at around 500 mm deep to the lens surface and extend centrally to a depth of about 200 mm [64]. The cortex superficial to these opacities is always clear.…”

“…They originate in relation to equatorial fractures, perpendicular to the course of large groups of cortical fibres. Fractured ends are slightly swollen and membranes are folded, remotely from the break [74], but the membranes on either side of the fractures are normal, as is the architecture of fibres superficial and deep to the opacities [64]. Their formation involves a repair mechanism that anneals ruptured membranes and seals off the damaged from undamaged parts of the fibres [62].…”

“…With the onset of presbyopia, the elasticity of the lens centre decreases and the lens no longer changes shape, although the ciliary muscle continues to act, by way of its zonular insertion into the lens equator. It has been suggested by a number of authors, partly on the basis of experiments on the excised human lens, that mechanical stress at the C3 -C2 border zone creates a shearing force that initiates fibre fractures [64,81,82].…”

Oxidative Damage and the Prevention of Age-Related Cataracts

“…Since cortical fiber cells extend from the posterior to the anterior of the lens, this means that opacification begins in the center of a group of fiber cells; the anterior and posterior ends of the same cells remain transparent. Morphological studies found evidence of physical damage early in cortical cataract formation, involving the scission and fragmentation of the cortical fiber cells [8,9] . Cortical cataracts progress in severity by the involvement of increasing numbers of adjacent fiber cells and by the extension of the damage from the center of the cells to their anterior and posterior ends.…”

Homeostasis in the vertebrate lens: mechanisms of solute exchange

“…MRI studies on isolated human lenses [64,65] and preliminary in situ observations in bovine lenses (electronic supplementary material, figure S1) support a restricted entry of water and ions into the deep cortex and nucleus of the lens. Two recent studies [104,105] have shown that early age-related opacities and cortical cataracts have their origin in and stay restricted to the lens cortex, while the lens nucleus remains unaffected, supporting the independence of the lens nucleus behind the barrier compared with the more peripheral regions beyond the barrier. This also suggests that the cortical -nuclear interface forms a barrier preventing or delaying noxious substances from entering the nuclear region and thus postponing occurrence of nuclear lens opacities early in life.…”