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Background and Objectives: The aim of this study is to evaluate and compare changes in corneal densitometry after standard (30 min exposure time of 3 mW/cm2 UVA) and accelerated (10 min exposure time of 9 mW/cm2 UVA) protocols of corneal cross-linking (CXL) in patients with progressive keratoconus. Materials and Methods: This study included a total of 38 eyes of 38 patients divided into two equal-sized subgroups. CXL was performed in one group according to the standard epithelium-off protocol (30 min, 3 mW/cm2 UVA) and in the other group according to an accelerated epithelium-off protocol (10 min, 9 mW/cm2 UVA). Scheimpflug imaging was used to evaluate corneal densitometry in the anterior, central, and posterior corneal layers in three concentric zones (0–2 mm, 2–6 mm, and 6–10 mm) at baseline and 1, 3, and 9 months after surgery. Results: This study included 38 patients divided into two subgroups of 19. One group of patients underwent standard and the other accelerated CXL protocol. Participants in the accelerated group were significantly older (p < 0.001). 9 months after CXL treatment, the accelerated group showed higher central and posterior corneal densitometry values, but, after adjusting for age and baseline values, ANCOVA analysis revealed no significant intergroup differences. Both protocols led to overall reductions in corneal densitometry over time. Conclusions: Both the standard and accelerated CXL protocols induce transient corneal haze, which can be objectified by increased corneal densitometry values in first three months post-CXL. The dynamics of the onset and recovery of postoperative corneal haze are comparable and similar in both protocols.

To better address the challenge of corneal ulcer healing, with already available standard agents, and those recently introduced, such as stable gastric pentadecapeptide BPC 157, we introduced a novel conceptual framework-the \"triad\" of corneal ulcer healing↔corneal neovascularization↔intraocular pressure-and extended it to avascular tissues such as tendon. Within this framework, cytoprotection serves as the unifying principle, underscoring that therapeutic effects are not isolated but interconnected. Preclinical studies with BPC 157 therapy, as a cytoprotection agent, illustrate this integration. BPC 157 rapidly normalizes elevated intraocular pressure in glaucomatous rats, preserves retinal integrity, restores pupil function, maintains corneal transparency during ulcer or abrasion healing, and counteracts both corneal neovascularization and dry eye. In parallel, its consistent efficacy in tendon injury models highlights a cytoprotective specificity across avascular tissues. The cornea's \"angiogenic privilege,\" preserved during healing and tendon recovery together, provides strong proof of concept. Furthermore, mapping standard therapeutic agents used for corneal ulcers, neovascularization, or glaucoma onto this triad, and linking them with tendon healing, reveals both shared pathways and inconsistencies across existing drug classes. Analyzed were the ascorbate, fibronectin, hyaluronic acid, metalloproteinase inhibitors, EGF, FGF, NGF, insulin, and IGF-1 (corneal ulcer healing), the antiangiogenic agents (endostatin, PAI-1, PEDF, angiostatin, TSP-1, TSP-2, IFN-α), corticosteroids, NSAIDs, cyclosporine A, anti-VEGF drops (treatment of corneal neovascularization), and alpha 2-agonists, beta-blockers, carboanhydrase inhibitors, muscarinic agonists, Rho-kinase inhibitors, and prostaglandin analogs (glaucoma). Taken together, these findings advance cytoprotection as a unifying therapeutic paradigm, with BPC 157 emerging as its first exemplar, and encourage further translational research toward clinical application.