Ocular surface integrity

Ocular surface integrity refers to the healthy, stable, and functional state of the Ocular Surface Unit, which comprises the cornea, conjunctiva, lacrimal glands, meibomian glands, and the pre-corneal tear film [10, 11]. It is a critical physiological state that ensures the eye maintains a smooth refractive surface for clear vision and acts as a primary protective barrier against environmental insults, pathogens, and mechanical friction [10, 15]. Maintaining this integrity is a dynamic process involving balanced tear secretion (lipid, aqueous, and mucin layers), epithelial cell turnover, and immune regulation [11, 17]. Loss of ocular surface integrity is the central feature of multifactorial conditions such as Dry Eye Disease (DED), neurotrophic keratopathy, and Sjogren’s syndrome [10, 14]. In these disease states, chronic inflammation, hyperosmolarity, or nerve damage leads to epithelial breakdown and tear film instability [4, 15]. Therapeutic interventions aim to restore ocular surface integrity by modulating specific molecular targets; for instance, cyclosporine and lifitegrast reduce inflammation by inhibiting calcineurin and antagonizing LFA-1 respectively, while diquafosol activates P2Y2 receptors to stimulate secretion [7, 8, 18]. As such, ocular surface integrity is viewed as a complex clinical endpoint and a measure of homeostatic health rather than a single molecular target [1, 2].

Other names

Ocular surface homeostasisCorneal epithelial integrityTear film stabilityCorneal integrity

Drugs targeting the restoration of ocular surface integrity primarily function through anti-inflammatory pathways (e.g., calcineurin inhibition, LFA-1 antagonism), stimulation of the lacrimal functional unit to increase tear secretion (e.g., P2Y2 receptor or nicotinic acetylcholine receptor agonism), or physical stabilization of the tear film to prevent evaporation and epithelial desiccation [7, 8, 9, 18].