Experimental corneal alkali burn models: Methodological standards, biological outcomes, and translational gaps.

Corneal chemical burns represent a severe category of ocular trauma, particularly when caused by alkaline agents whose hydroxyl ions penetrate successive tissue planes through membrane saponification, ultimately depleting limbal epithelial stem cells and triggering irreversible conjunctivalisation. Experimental animal models have been central to decoding the cellular and molecular events governing this cascade and to evaluating candidate therapies under controlled conditions. This review synthesises the principal methodological frameworks used to establish corneal alkali burn models and critically examines how protocol variables, alkali concentration, exposure duration, and disc preparation technique, shape injury severity and inter-animal consistency. A temporally organised account of the pathophysiological cascade is provided, from the initial oxidative burst through neovascularisation, fibrosis, and epithelial reconstitution. The comparative strengths and limitations of murine, rabbit, and rat platforms are assessed alongside contemporary outcome measurement strategies. Preclinical therapeutic evidence encompassing amniotic membrane derivatives, anti-angiogenic agents, cultivated epithelial transplantation, regenerative biologics, and novel drug delivery systems is reviewed with attention to cross-cutting methodological themes. Persistent translational gaps are identified, including the predominance of immediate post-injury intervention designs, incomplete histopathological severity relative to human disease, and protocol heterogeneity across laboratories, alongside priorities for future investigation.