Meibomian Gland Atrophy: Causes, Symptoms, and More

Meibomian gland atrophy occurs when the tiny oil-producing glands in the eyelids shrink or deteriorate, disrupting tear stability. These glands help maintain eye moisture by preventing rapid tear evaporation. Their atrophy can lead to chronic discomfort and visual disturbances.

Key Anatomy Of Meibomian Glands

The meibomian glands are sebaceous glands embedded in the tarsal plates of the upper and lower eyelids. Each eyelid contains approximately 20 to 40 of these elongated glands, which secrete meibum—a lipid-rich substance forming the outermost layer of the tear film. This lipid layer reduces tear evaporation, ensuring ocular hydration and visual clarity. The glands’ function is regulated by hormones, neural control, and blinking.

These glands consist of acini, clusters of secretory cells that produce meibum, and a central duct that delivers the secretion to the eyelid margin. Meibum is released through holocrine secretion, where entire cells disintegrate to release their contents. This ensures a continuous supply but makes the glands vulnerable to dysfunction if cellular turnover is disrupted. The ducts are lined with keratinized epithelium, and obstructions can cause stagnation, leading to gland atrophy.

Blinking plays a crucial role in meibomian gland function, as mechanical pressure expels meibum onto the ocular surface. Reduced blink rates—common with prolonged screen use—are linked to higher gland dropout. Hormonal regulation, particularly androgens, also influences meibum production, with androgen deficiency associated with gland shrinkage and altered lipid composition.

Common Signs Of Gland Atrophy

Early signs of meibomian gland atrophy are often subtle. A gradual reduction in lipid secretion destabilizes the tear film, leading to intermittent dryness or mild burning. Patients frequently report fluctuating vision, especially after prolonged reading or screen use, due to inadequate lipid coverage and increased tear evaporation.

As atrophy progresses, discomfort becomes more persistent. Many individuals experience grittiness or a foreign body sensation due to insufficient lubrication between the eyelids and ocular surface. Clinical examinations often reveal reduced meibum expressibility, with secretions becoming turbid or absent upon manual compression of the eyelid margins. Meibography shows gland dropout as darkened, structurally compromised regions within the tarsal plate, correlating with symptom severity.

In advanced cases, compensatory reflex lacrimation may occur, where the compromised tear film triggers excessive aqueous tear production. However, these reflex tears lack the lipid component necessary for stability, providing only temporary relief and often worsening symptoms. This paradoxical tearing is particularly common in windy or air-conditioned environments.

Contributing Factors

Meibomian gland atrophy results from physiological changes, environmental exposures, and behavioral habits. Aging is a major factor, as studies show a decline in gland density and meibum secretion over time. Structural changes such as gland truncation further reduce function. While aging cannot be stopped, lifestyle factors can accelerate deterioration.

Chronic exposure to low-humidity environments, such as air-conditioned offices, places excessive demands on the tear film, leading to gland exhaustion. Prolonged screen use reduces blink rates, impairing meibum expression. Incomplete blinking, where the eyelids fail to fully close, worsens this issue by preventing uniform lipid distribution. This is particularly common among office workers and students.

Certain medications also contribute to gland atrophy, particularly those affecting lipid metabolism or androgen levels. Isotretinoin, used for acne treatment, has been linked to gland shrinkage and decreased meibum production, with some effects persisting after discontinuation. Antihistamines, antidepressants, and beta-blockers can also reduce tear secretion and alter meibum composition. Individuals using these medications should be monitored for early signs of gland dysfunction.

Tear Film Distribution Changes

Meibomian gland dysfunction directly affects tear film stability. The tear film consists of three layers: the innermost mucin layer, the middle aqueous layer, and the outermost lipid layer, which is derived from meibum. When lipid secretion decreases, the protective barrier weakens, allowing rapid tear evaporation. This instability causes ocular discomfort and intermittent visual disturbances.

A compromised lipid layer also leads to irregular tear distribution. High-resolution interferometry shows that individuals with gland dysfunction experience increased tear film breakup variability, with some areas of the cornea losing coverage faster than others. This uneven distribution creates dry spots, triggering reflex blinking. However, frequent blinking does not fully compensate for lipid deficiency, perpetuating tear instability.

Diagnostic Techniques

Diagnosing meibomian gland atrophy requires clinical examination and imaging to assess gland structure and function. Early detection is crucial to prevent irreversible damage. Ophthalmologists and optometrists use various diagnostic tools to evaluate gland loss, meibum quality, and tear film stability.

Meibography is a key imaging technique that uses infrared light to visualize gland structure. Healthy glands appear elongated and uniform, while atrophic glands appear shortened, irregular, or absent. Greater gland dropout correlates with more severe dry eye symptoms. Interferometry assesses lipid layer thickness, revealing whether the tear film contains enough meibum to prevent evaporation. Patients with atrophy typically exhibit a thinner, less stable lipid layer, leading to increased tear film breakup and discomfort.

Functional assessments complement imaging by evaluating meibum expressibility. Clinicians apply gentle pressure to the eyelid margins to observe secretion quality. In healthy individuals, meibum appears clear and fluid, whereas in atrophy, it becomes thickened, cloudy, or absent. Tear osmolarity testing further helps diagnose instability, as elevated osmolarity is a marker of evaporative stress. Combining structural imaging with functional assessments allows for accurate diagnosis and targeted management strategies.