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The lipid–aqueous interface of the tear film is the critical boundary between the outermost lipid layer and the underlying aqueous-mucin phase of the precorneal tear film (Willcox et al., 2017, PubMed). This interface is primarily stabilized by polar lipids, such as phospholipids and O-acyl-omega-hydroxy fatty acids (OAHFAs), which act as surfactants to bridge the hydrophobic non-polar lipids and the hydrophilic aqueous layer (Stahl et al., 2012, PubMed). When therapeutic emulsions are applied, the interface of the formulation droplets must interact and integrate with the natural tear film interface to be effective (Craig et al., 2017, TFOS DEWS II). The primary biological function of this boundary is to lower the surface tension of the tear film, ensuring a stable optical surface and reducing aqueous evaporation. In diseases such as Meibomian Gland Dysfunction (MGD) and Evaporative Dry Eye, the interface becomes unstable, leading to rapid tear film breakup and ocular surface inflammation (Bron et al., 2017, PubMed). Therapeutic strategies, such as perfluorohexyloctane or lipid-based artificial tears, aim to reinforce this interface, thereby restoring the tear film's barrier properties and protecting the corneal epithelium (Sheppard et al., 2023, Ophthalmology).
Stabilization of the tear film by reducing surface tension and replenishing the lipid layer to prevent aqueous evaporation (Craig et al., 2017, TFOS DEWS II).
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