Mohamed Morgan

Age-related changes occur in all structures of the eye, with variable effects on vision, tear production, and cosmesis. These changes are largely physiological but may predispose individuals to ocular pathology. Below, we outline the key ways ageing affects the eye and its associated structures.

Eyelid & lacrimal system

With advancing age, the skin becomes thinner and more lax due to tissue atrophy, reduced synthesis and increased collagen cross-linking. These changes result in redundant skin folds and wrinkles around the eyelids. Eyelid laxity may lead to entropion (in-turning of the lower eyelid) or ectropion (out-turning of the lower eyelid). Eversion of the puncta on the lower lid can impair tear draining and result in excessive tearing (1).

Age-related fat and muscular atrophy, along with laxity of the canthal ligaments and tendons, contributes to orbital fat prolapse, lid ptosis, blepharoptosis and brow prolapse (1). In addition, atrophy of the lacrimal gland can reduce tear production, contributing to dry eye disease (2).

Cornea

Ageing results in changes to corneal curvature, with the vertical meridian becoming flatter and the horizontal meridian steepening. Additionally, loss of corneal lustre is commonly observed reflecting tear film instability (3). Corneal sensitivity declines due to reduced corneal nerve density, leading to diminished blink reflexes and increased susceptibility to dry eye disease (4).

The most common age-related corneal finding is arcus senilis, characterised by peripheral lipid deposits within the corneal stroma (5). It appears as a yellow-white ring separated from the limbus by a clear zone and is generally a benign finding.

Other age-related changes include Hassall-Henle bodies, which are localised thickenings at the periphery of the endothelium often seen on slit lamp examination and Krukenberg’s spindle which represents deposition of uveal pigment on the corneal endothelium (5). These changes do not interfere with vision.

Corneal endothelial cells do not regenerate, meaning endothelial cell density reduces with age. The remaining endothelial cells enlarge to compensate for the cell loss. Additional endothelium damage through surgery or disease may impair corneal deturgescence, resulting in corneal oedema, thickening and loss of transparency (1).

Trabecular meshwork and uvea

With age, pigmentation of the trabecular meshwork increases due to accumulation of melanin granules and cellular debris shed from adjacent uveal tissue, leading to increased aqueous outflow resistance (1). Concurrently, extracellular matrix accumulates within the trabecular meshwork and ciliary muscles, and trabecular meshwork cell loss occurs (6). Together, these changes reduce aqueous humour outflow. These changes can result in increased intraocular pressure and predisposing to glaucoma.

The uvea also undergoes notable changes. The pupil decreases in size and pupillary reactivity diminishes due to atrophy of the dilator muscles and increased rigidity of the iris stroma. This results in reduced light entry and impaired night vision (1). Additionally, fibrosis of the ciliary muscle impairs accommodation, contributing to presbyopia (7).

Lens

The lens continues grow throughout life through division of cells in the germinative zone. Newly formed fibres are added layer by layer, leading to gradual lens thickening and increased weight. Progressive cross-linking of lens crystallin occurs with age, leading to increasing lens stiffness and reduces deformability (8). This limits the accommodative power of the lens, resulting in presbyopia.

Lens crystallin cross-linking also promotes formation of high molecular weight aggregates, post-translational protein modifications, and lens pigmentation (8). These changes lead to reduced lens transparency which can result in cataract formation.

Vitreous

Age-related aggregation of collagen fibrils and hyaluronic acid within the vitreous leads to formation of benign floaters (9). Progressive condensation and liquefaction of the vitreous gel produce optically empty spaces known as lacunae (9). These cavities expand and coalesce over time, reducing vitreous volume and exerting traction on the retina, which can result in posterior vitreous detachment (9).

Retina and Retinal pigment epithelium

Ageing is associated with a reduction in retinal ganglion cells, optic nerve axons, and photoreceptors, particularly rods. These changes contribute to a decline in visual acuity, contrast sensitivity and night vision (1).

Thickening of basement membranes, especially Bruch’s membrane is another important age-related change (1). Bruch’s membrane serves as a conduit for metabolic waste transport from the Retinal Pigment Epithelium (RPE) to the choroid. With age, this clearance system may become overwhelmed, leading to accumulation of extracellular deposits between Bruch’s membrane and the RPE, known as drusen (10). Drusen alone does not impair vision.

The RPE itself also undergoes progressive atrophy and loss of melanin, reducing protection against oxidative stress. Concurrently, lipofuscin accumulates within RPE lysosomes. Lipofuscin is phototoxic and promotes oxidative damage, further impairing cellular function. The combined effects of drusen accumulation, RPE atrophy, and neuronal degeneration ultimately contributes to the development of age-related macular degeneration (11).

Conclusion

The cumulative effects of ageing on the eye and orbit can affect a person’s quality of life and lead to pathology. These complex changes can be subtle and develop gradually, but their combined impact can compromise visual acuity and increase susceptibility to conditions such as dry eye disease, glaucoma, cataracts and age-related macular degeneration. Early recognition of these processes is essential for clinicians to distinguish normal ageing from pathology and to guide appropriate management.

References

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