Divergent interfacial mineralization pathways on hydrophilic intraocular lenses driven by pathological microenvironments.

Late-onset optical opacification caused by calcium phosphate deposition is the primary failure mode of hydrophilic acrylic intraocular lenses (IOLs). Clinical evidence suggests that the extent and pattern of calcification vary significantly among patients, particularly those with different systemic diseases. However, the mechanistic role of systemic pathologies in driving heterogeneous calcification remains unclear. Herein, we investigate the interfacial mineralization mechanisms of opacified IOLs using multiscale physicochemical characterization, focusing on patients with hypertension (HTN), diabetes mellitus (DM), and no comorbidities (Control), as well as pristine IOLs as a baseline. Our findings reveal that late-onset IOL opacification is a surface-confined ectopic mineralization process without bulk material degradation. Specifically, continuous, highly crystalline mineral precipitates were detected in the HTN group. This observation is consistent with a protein-modulated interfacial microenvironment, in which leaked plasma proteins may serve as organic templates on the IOL surface, reduce the nucleation energy barrier, and accelerate the formation of HA-type calcium phosphate. By comparison, AGE accumulation is hypothesized to generate steric hindrance and competitive adsorption at the solid-liquid interface in diabetic conditions, thereby kinetically stabilizing TCP-type calcium phosphate and producing scattered, discontinuous mineral deposits. Patients without comorbidities show only mild nascent mineralization. This work clarifies the pathological mechanisms linking systemic diseases to IOL calcification, providing a theoretical basis for interfacial engineering of anti-calcification IOLs and guiding clinical practice to protect visual function.