The ocular surfaceJun 11, 2026

Dry Eye Disease Caused by Aging: Defining a Unique Age-Related Type

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Jun 12, 2026

Abstract

Aging contributes to a distinct, aging-driven dry eye disease (DED) phenotype characterized by multiple structural changes in ocular surface tissues.

Age-related changes in the lacrimal gland include secretory cell exhaustion and lipid dysregulation.
Meibomian gland function declines, leading to impaired lipid production.
Corneal and conjunctival tissues exhibit epithelial barrier impairment and goblet cell loss.
These structural changes are associated with core aging mechanisms such as cellular senescence and oxidative stress.
The interplay of these processes creates a cycle of tear film instability and chronic inflammation, differentiating it from other DED forms.
Targeting oxidative stress and immune dysregulation may provide new therapeutic approaches for elderly patients with DED.

Simplified

Dry eye disease (DED) is highly prevalent in older adults and represents a growing public health burden in aging societies. Although age is a well-recognized risk factor for DED, it is still often treated as a background variable rather than an active biological driver of disease. Emerging evidence indicates that aging itself promotes progressive structural remodeling and functional decline across multiple ocular surface tissues, giving rise to a distinct, aging-driven DED phenotype. In this review, we synthesize current knowledge on how biological aging disrupts ocular surface homeostasis at tissue, cellular, and molecular levels. We describe age-associated changes in the lacrimal gland (LG), meibomian gland (MG), cornea, and conjunctiva, including secretory cell exhaustion, lipid dysregulation, epithelial barrier impairment, neural degeneration, and goblet cell (GC) loss. These structural changes are tightly linked to core aging mechanisms such as cellular senescence, oxidative stress, mitochondrial dysfunction, inflammaging, neuroendocrine imbalance, and stem/progenitor cell decline. Importantly, these processes interact as an integrated network, creating a self-reinforcing cycle of tear film instability, chronic low-grade inflammation, and impaired tissue repair that differs mechanistically from environmentally induced or autoimmune forms of DED. By reframing aging as a central pathogenic driver and considering age-related DED as a distinct subtype, this perspective highlights the need for mechanism-informed therapeutic strategies. Beyond conventional lubrication and anti-inflammatory therapy, interventions targeting oxidative stress, cellular senescence, inflammaging, neurosensory dysfunction, and hormonal alterations may offer more fundamental disease modification in elderly patients.

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Dry Eye Disease Caused by Aging: Defining a Unique Age-Related Type

Abstract

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