Meibomian Gland Dysfunction And Dry Eye Disease: Mechanisms, Diagnostics, And Evidence Based Therapies
Özet
Dry eye disease (DED) is a multifactorial disorder characterized by disruption of tear film and ocular surface homeostasis, involving tear film instability, hyperosmolarity, inflammation, tissue damage, and neurosensory abnormalities. In this condition, meibomian gland dysfunction (MGD) is the primary cause of evaporative DED: obstruction and/or changes in meibum quality disrupt the tear lipid layer, accelerating evaporation and destabilizing the optical surface. The modern diagnostic approach, ranging from TFOS DEWS II to DEWS III, integrates symptoms with non-invasive homeostasis markers such as breakpoint time, osmolarity, and staining, while enabling mechanism-based subclassification through eyelid-blink assessment, meibography, interferometry, and meibum expressibility. Treatment is tiered and personalized: conservative care (warm compresses, eyelid hygiene, lipid-supported artificial tears), pharmacological options (anti-inflammatory drugs; sub-antimicrobial tetracyclines or azithromycin), and device-based interventions (thermal pulsation, intense pulsed light); probe application is considered in fibrotic obstruction. Significant improvements in symptoms and signs and generally favorable safety have been reported with thermal pulsation and IPL; persistence and cost-effectiveness are being investigated. In the future, factor-matched algorithms, biomarker-based endpoints, and AI-assisted imaging will improve phenotyping, response prediction, and treatment sequencing in mixed evaporative-aqueous phenotypes.
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