Meibomian gland dysfunction (MGD) is the most common cause of dry eye disease (DED). The Tear Film & Ocular Surface Society’s Dry Eye Workshop II identified MGD as a prevalent and chronic disorder. It is often characterized by increased epithelial cell growth, blockages, meibum accumulation, gland dilation, and, ultimately, gland loss due to atrophy.¹ The theory of epithelial hyperkeratinization remains a subject of debate,^2,3 but the essential role of functional meibomian glands in secreting the tear film’s lipid layer—and thereby preventing rapid tear evaporation and preserving ocular surface health—is universally acknowledged.^4-7

MGD reduces or alters oil production, resulting in tear film instability and a host of ocular symptoms that can severely affect ocular health. These range in severity from dryness, blurred vision, and irritation to gland atrophy, contact lens intolerance, and an increased risk of infection.

This article provides tips on accurately diagnosing and effectively managing MGD.

Diagnosis

Meibography. As a pivotal technique in diagnosing MGD, meibography has revolutionized our ability to educate patients, identify gland dropout, and assess atrophy. Historically, it stood as the sole method for analyzing meibomian gland morphology. Obtaining accurate images can be challenging, however, due to factors such as inadequate lid eversion and variability in image clarity. These issues complicate the interpretation of gland dropout, making it difficult at times to distinguish between actual tissue loss and proximal tarsal tissue appearances. Traditional meibography also falls short in detailing the anatomic structure of acini and ducts, limiting its comprehensive assessment of glandular architecture.

Despite these challenges, meibography’s ability to reveal the extent of gland dropout or atrophy—a direct marker of MGD severity—remains indispensable. It facilitates the early detection and accurate assessment of the condition, where a higher degree of gland dropout indicates more advanced disease. Recognizing gland dilation and the consequent secretion accumulation helps in diagnosing obstruction early, crucial for managing end-stage MGD characterized by significant gland atrophy.

(Editors’ note: To explore the latest advances in meibography devices that address these challenges, see the sidebar.)

OCT imaging. The high-resolution cross-sectional images of ocular structures provided by OCT address some of meibography’s limitations. OCT enables clinicians to assess the thickness and structure of the tear film, evaluate meibomian gland morphology, and quantify changes in glandular volume. These insights are invaluable to elucidating the pathophysiology of MGD, including the alterations in glandular architecture that contribute to tear film instability. By providing a deeper understanding of these mechanisms, OCT imaging enhances the diagnostic process and permits a more targeted approach to treatment.

In vivo confocal microscopy. By enabling real-time imaging of tissue at a cellular level, in vivo confocal microscopy represents another leap forward in the diagnosis of MGD. This technology opens a window into the cellular world of the meibomian glands—specifically, the acini, epithelial cells, and inflammatory cells within the eyelids. The detailed imagery provided is critical for identifying cellular changes associated with MGD, such as inflammatory infiltrates, epithelial metaplasia, and glandular atrophy. Perhaps most importantly, in vivo confocal microscopy can help practitioners distinguish MGD from other conditions with similar clinical presentations.

Comprehensive Treatment Strategies

The first step of MGD treatment is a thorough assessment of the patient, including their symptoms and contributing factors. The latter include environmental influences, such as prolonged use of digital devices and contact lens wear, and dietary habits, including the balance between omega-6 and omega-3 fatty acid intake. Based on this comprehensive evaluation, a personalized treatment plan is devised to address the specific needs of the patient.

Traditional first-line treatments. These include lid hygiene measures such as warm compresses, which help liquefy meibum, making it easier to express. Antiinflammatory agents and antibiotics—both topical and systemic—play critical roles in controlling inflammation and microbial colonization of the lid margin. Topical azithromycin offers specific antiinflammatory benefits beyond its antimicrobial properties and has been prescribed off-label for the treatment of lid margin disease owing to the drug’s long duration of action and deep penetration into the ocular tissues.

Additional strategies include microblepharoexfoliation with BlephEx (BlephEx), debridement, and the use of tea tree oil or hypochlorous acid. These interventions are often most effective after the underlying gland obstruction has been addressed.^8,9

Adjunctive therapies. Preservative-free, lipid-containing artificial tears can supplement the tear film’s lipid layer, addressing the evaporative component of MGD-induced DED. Cyclosporine (CsA) ophthalmic emulsion 0.05% (Restasis, Allergan), CsA ophthalmic solution 0.1% (Vevye, Harrow), CsA ophthalmic solution 0.09% (Cequa, Sun Ophthalmics), and lifitegrast (Xiidra, Novartis) have proven efficacy for improving lipid layer thickness and managing tear film instability.^10-14

High-quality reesterified omega-3 supplements have been shown to reduce DED symptoms, decrease inflammation, and improve the quality of the tear film.¹⁵

In-office procedures. If traditional and adjunctive therapies are insufficient, in-office procedures may be considered. Thermal pulsation systems such as LipiFlow (Johnson & Johnson Vision), iLux (Alcon), and TearCare (Sight Sciences) facilitate the expression of meibum, improving gland function. Intense pulsed light therapy targets telangiectatic vessels on the lid margin, reducing inflammation and improving meibomian gland function. OptiLight (Lumenis) is an intense pulsed light device that is FDA approved for treating the signs of DED associated with MGD.

Addressing Coexisting Conditions

It is essential to treat coexisting eyelid conditions, such as blepharitis, to ensure comprehensive management of MGD. Lotilaner ophthalmic solution 0.25% (Xdemvy, Tarsus Pharmaceuticals) is FDA approved for the treatment of Demodex infestation. Systemic medications, such as oral tetracyclines or immunomodulators, may be prescribed to control inflammation and modulate the immune response, particularly in patients with rosacea or severe MGD.

Emerging Treatments

Innovative treatments are in development. Reproxalap (Aldeyra Therapeutics) is a reactive aldehyde species inhibitor that reduces ocular inflammation by binding free aldehydes. Other examples include keratolytic formulations, such as AZR-MD-001 (Azura Ophthalmics), aimed at reducing keratin production and stimulating meibum production; transient receptor potential melastatin 8 agonists, such as IVW-1001 (iView Therapeutics); and topical spironolactone for its antiandrogenic properties.

Recent research suggests it may be possible for atrophied meibomian glands to regenerate or become reactivated.¹⁶ This would open up new avenues for treating MGD and DED and could facilitate patients’ recovery following refractive and cataract surgery.

Patient Education and Long-Term Management

Educating patients about the chronic nature of MGD and the importance of adherence to treatment plans is crucial to long-term management success. Regular follow-up visits are vital for monitoring treatment efficacy, making necessary adjustments, and addressing any new concerns that may arise.

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15. Epitropoulos AT, Donnenfeld ED, Shah ZA, et al. Effect of oral re-esterified omega-3 nutritional supplementation on dry eyes. Cornea. 2016;35(9):1185-1191.

16. Hura AS, Epitropoulos AT, Czyz CN, Rosenberg ED. Visible meibomian gland structure increases after vectored thermal pulsation treatment in dry eye disease patients with meibomian gland dysfunction. Clin Ophthalmol. 2020:14:4287-4296.