A drug-eluting contact lens combining a regenerative compound with a tear film lipid could offer a two-pronged approach to ocular surface disease, according to new preclinical research published in Scientific Reports. The experimental lens accelerated corneal epithelial healing while also improving tear film stability in rabbit models of corneal injury and meibomian gland dysfunction (MGD)-induced dry eye.
The lens co-delivers polydeoxyribonucleotide (PDRN), a salmon-derived DNA compound with regenerative and anti-inflammatory properties, and 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC), a phospholipid designed to mimic components of the natural tear film lipid layer. The researchers reasoned that combining the two could simultaneously promote epithelial repair, suppress inflammation, and reduce tear evaporation.
To test the concept, the investigators used two rabbit models: a corneal epithelial wound model and an MGD-induced dry eye model. In each animal, one eye wore a control lens and the fellow eye received the PDRN+DMPC lens for six hours per day. Outcomes included epithelial defect area, tear break-up time (TBUT), tear osmolarity, histology, and expression of inflammatory, epithelial, tight junction, and mucin-related genes.
In the wound-healing model, epithelial defects closed more rapidly with the combination lens. By the afternoon of day two, mean residual defect area was 0.37% with PDRN+DMPC versus 4.46% with the control lens. Both groups were close to complete re-epithelialization by the following morning. The regenerated epithelium was also significantly thicker in treated eyes at day three: 28.33 μm versus 14.82 μm.
The treatment was accompanied by reductions in inflammatory and matrix-remodeling gene expression. The study authors suggest that this anti-inflammatory effect, alongside PDRN-mediated tissue regeneration, may help create a more favorable environment for corneal repair.
Results were similarly encouraging in the dry eye model. TBUT improved from approximately 3.5 seconds at baseline to 15.1 seconds by day 7 with PDRN+DMPC, compared with 8.0 seconds with the control lens. Tear osmolarity was also significantly lower at several time points, while histology showed fewer desquamated epithelial cells in treated eyes.
The treatment appeared to preserve epithelial differentiation and tight junction-related gene expression in the dry eye model. Although membrane-associated mucins MUC1 and MUC16 were reduced, the researchers found preserved MUC5AC expression and conjunctival goblet cells, interpreting the changes as possible normalization of inflammation-associated mucin signaling rather than loss of the protective mucin layer.
The study authors do caution that the study was short, conducted in animals, and did not separate the individual contributions of PDRN, DMPC, and the lens itself. Eye allocation was also nonrandomized. The findings nonetheless provide proof of concept for a contact lens designed to address epithelial damage, inflammation, and tear film instability simultaneously – a combination that could be attractive for future ocular surface therapies if the effects can be translated to humans.
