Abnormal Blinking Disruption of Ocular Surface Homeostasis: A Phenotype-Driven Murine Model by Mechanical Intervention

Purpose To establish an abnormal blinking murine model to serve as a reproducible platform for investigating mechanical force-induced ocular surface damage.Methods Abnormal blinking was induced in female C57BL/6J mice using a mini-reciprocating device at 10 or 40 blinks/min for 20 min/day over 3 days (AB-10 and AB-40 groups). Normal-blinking mice (BC group) and lacrimal gland ConA-injected mice served as controls. Tear film stability, tear secretion, and corneal fluorescein staining were evaluated longitudinally on days 7, 14, and 21. Subbasal nerve plexus (SNP) alterations, epithelial remodeling, and corneal ultrastructure were evaluated longitudinally up to day 21 via IVCM, histological, and TEM/SEM analyses.Results Both AB groups exhibited comprehensive disruptions of ocular surface homeostasis. These changes were by significantly increased corneal fluorescein staining (p < 0.001) and reduced TUBT and tear secretion from day 7 through day 21. IVCM and TEM/SEM revealed that subbasal nerve fibers largely disappeared by day 7, accompanied by prominent corneal stromal cell activation, acute corneal edema, and severe epithelial ultrastructural degradation (loss of microvilli, cell apoptosis, and shedding). Most of these acute alterations gradually resolved by day 21, with the AB-40 group exhibiting the most severe, prolonged damage and delayed homeostatic recovery.Conclusions Abnormal blinking mice model establishes a stable, reproducible model of mechanical force-induced ocular surface homeostasis damage, the model may be a mixed effect of blinking-induced acute mechanical microtrauma and secondary tear film function impairment. This research provides a valuable in vivo tool for investigating the mechanisms of biomechanical action in ocular surface diseases.