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Lipid layer thickness (LLT) is a clinical measurement of the outermost layer of the pre-ocular tear film, which is primarily composed of lipids (meibum) secreted by the meibomian glands of the eyelids [2, 6, 12]. In a healthy human eye, the LLT typically ranges from approximately 40 to 100 nm and performs the vital biological function of stabilizing the tear film and retarding the evaporation of the underlying aqueous-mucin layer [2, 13, 17]. A significant reduction in LLT is a diagnostic hallmark of evaporative dry eye disease (DED) and meibomian gland dysfunction (MGD), conditions where a thin or deficient lipid layer leads to rapid tear film instability, hyperosmolarity, and ocular surface damage [1, 5, 10]. While LLT is a physiological parameter rather than a specific protein or receptor, it serves as a primary clinical endpoint and therapeutic target for various ophthalmic interventions [4, 18]. Pharmacological treatments, such as perfluorohexyloctane (Miebo) or lipid-containing artificial tears, aim to increase or stabilize the LLT to restore ocular surface homeostasis and alleviate symptoms of dryness [9, 10, 14]. Thus, LLT is a critical biomarker for assessing disease severity and monitoring the efficacy of therapies targeting meibomian gland health and tear film integrity [4, 6].
Exogenous supplementation or stabilization of the precorneal lipid layer to increase its physical thickness, reduce aqueous evaporation, and restore tear film stability.
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