The human lens grows by a process of epithelial cell division at its equator and the formation of generations of differentiated fibre cells. Despite the process of continuous remodelling necessary to achieve growth within a closed system, the lens can retain a high level of light transmission throughout the lifetime of the individual, with the ability to form sharp images on the retina. Continuous growth of the lens solves the problem imposed by terminal differentiation within a closed, avascular system, from which cells cannot be shed. The lens fibre tips arch over the equator to meet anteriorly and posteriorly and form branching sutures of increasing complexity. The stages of branching may create the optical zones of discontinuity seen on biomicroscopy. The lens is exposed to the cumulative effects of radiation, oxidation and postranslational modification. These later proteins and other lens molecules in such a way as to impair membrane functions and perturb protein (particularly crystallin) organisation, so that light transmission and image formation may be compromised. Damage is minimised by the presence of powerful scavenger and chaperone molecules. Progressive insolublisation of the crystallins of the lens nucleus in the first five decades of life, and the formation of higher molecular weight aggregates, may account for the decreased deformability of the lens nucleus which characterises presbyopia. Additional factors include: the progressive increase in lens mass with age, changes in the point of insertion of the lens zonules, and a shortening of the radius of curvature of the anterior surface of the lens. Also with age, there is a fall in light transmission by the lens, associated with increased light scatter, increased spectral absorption, particularly at the blue end of the spectrum, and increased lens fluorescence. A major factor responsible for the increased yellowing of the lens is the accumulation of a novel fluorogen, glutathione-3-hydroxy kynurenine glycoside, which makes a major contribution to the increasing fluorescence of the lens nucleus which occurs with age. Since this compound may also cross-link with the lens crystallins, it may contribute to the formation of high-molecular-weight aggregates and the increases in light scattering which occur with age. Focal changes of microscopic size are observed in apparently transparent, aged lenses and may be regarded as precursors of cortical cataract formation.
The human eye is programmed to achieve emmetropia in youth and to maintain emmetropia with advancing years. This is despite the changes in all eye dimensions during the period of growth and the continuing growth of the lens throughout life. The process of emmetropisation in the child's eye is indicated by a shift from the Gaussian distribution of refractive errors around a hypermetropic mean value at birth to the non-Gaussian leptokurtosis around an emmetropic mean value in the adult. Emmetropisation is the result of both passive and active processes. The passive process is that of proportional enlargement of the eye in the child. The proportional enlargement of the eye reduces the power of the dioptric system in proportion to the increasing axial length. The power of the cornea is reduced by lengthening of the radius of curvature. The power of the lens is reduced by lengthening radii of curvature and the effectivity of the lens is reduced by deepening of the anterior chamber. Ametropia results when these changes are not proportional. The active mechanism involves the feedback of image focus information from the retina and consequent adjustment of the axial length. Defective image formation interferes with this feedback and ametropia then results. Heredity determines the tendency to certain globe proportions and environment plays a part in influencing the action of active emmetropisation. The maintenance of emmetropia in the adult in spite of continuing lens growth with increasing lens thickness and increasing lens curvature, which is known as the lens paradox, is due to the refractive index changes balancing the effect of the increased curvature. These changes may be due to the differences between nucleus and cortex or to gradient changes within the cortex.
High-resolution imaging with a camera system built on the Scheimpflug principle has been used to characterize the geometry of the anterior segment of the adult human eye as a function of aging and accommodative state but is critically dependent on algorithms for correction of distortion. High-resolution magnetic resonance imaging (MRI), in contrast, provides lower-resolution information about the adult eye but is undistorted. To test the accuracy of the Scheimpflug correction methods used by Cook and Koretz [J. Opt. Soc. Am. A 15, 1473 (1998)]; [Appl. Opt. 30, 2088 (1991)], data on anterior chamber and segment lengths, as well as lens thickness and anterior and posterior curvatures, were compared with corresponding MRI data for adults aged 18-50 at 0 diopter accommodation. Excellent statistical agreement was found between the MRI and the Scheimpflug data sets with the exception of the posterior lens radius of curvature, which is less well defined than the other measurements in the Scheimpflug images. The considerable agreement between data obtained with MR and Scheimpflug imaging, two different yet complementary in vivo imaging techniques, validates the Scheimpflug correction algorithms of Cook and Koretz and suggests the capability of directly integrating information from both. A third, equivalent, data set obtained with a Scheimpflug-style camera system differs considerably from both Scheimpflug and MRI results in magnitude and age dependence, with negative implications for this alternative method and its correction procedures.
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