Background: The corneal epithelium serves as a barrier and contributes to the maintenance of corneal transparency and rigidity. Ulcers and erosions of the corneal epithelium as well as delays in resurfacing of the cornea after wounding are major causes of ocular morbidity and visual loss. Corneal ulceration is very frequent and represents one of the most important eye diseases. Chemical burns of eye presents a major therapeutic challenge to the ophthalmologist. Corneal alkali burns represent between 7% and 10% of eye injuries. Aim: To investigate the structure and organization of corneal epithelium during the healing process of rabbit corneal wounds with monitoring of the corneal electrolyte contents with energy dispersive X-ray analyzer (EDAX) and to screen through immunohistochemistry corneal cellular changes for apoptosis and proliferation during healing process using Proliferating cell nuclear antigen (PCNA) and Tunnel Apoptosis Assay. Material and methods: 30 New Zealand rabbits weighing 2.5 kg were used. An alkali wound of the cornea was performed in the right eye of with round filter paper, 5.5 mm in diameter which were soaked in 0.5 mol/L NaOH for 5 seconds and then were placed centrally on the cornea for 60 seconds. The left eyes will serve as controls. The corneas (normal ulcerated and healed (epithelialized) were harvested at various time points (0, day one, 3 days, 7 days, 14 days of corneal injury and processed for examination with light and scanning electron microscopy with monitoring of the corneal electrolyte contents C, N, O, Na, P, Mo, Ag, Ca, K, Silica with an EDAX. Results: Inflammatory response with massive inflammatory cell infiltrates mainly leukocytes (PML) are the first cells that migrate into the tissues in response to injury insult in the first 24 hours cells were mainly neutrophils. Steadily other mononuclear cells begin to appear along with signs of new capillaries formation. Moreover, progressive increase in basal corneal epithelial cell proliferative activity both in limbal region and leading corneal ulcer edge, stromal keratocytes and endothelial capillaries cells. Labeling for apoptosis was found only on the epithelial surface of normal cornea and not in deeper layers. After alkali injury few positive deeper epithelial cell were seen. In addition, stromal cells apoptosis was present in all the alkali-burned corneas; Observable alterations of mineral concentrations in the rabbit cornea after alkali injury burns. Conclusion: Basal corneal epithelial cell proliferative activity starts earlier after 24 hour of alkali injury and was headed by massive leukocytes infiltrate in the stroma and within epithelial cells. PCNA was expressed in the vascular endothelium. The PCNA expression starts later in the keratocytes but lasts somewhat longer. In present investigations, we found alterations of mineral concentrations in the rabbit cornea both in epithelial and collagen contents after alkali injury burns Mo is an essential trace element was found to decline during the healing process of corneal wound injury. Medical intervention with appropriate solutions containing element such as Mo may require with other mineral deficient in restoring and maintaining the normal mineral composition of the denuded corneal stroma.