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The number and distribution of mitotic epithelial cells in the ocular surface during homeostasis and in response to abrasion of the mammalian cornea were determined. Normal rats and those receiving a 3 mm diameter centrally located epithelial defect, received an intraperitoneal injection of colchicine 6 h prior to sacrifice. Mitosis in the basal epithelium during homeostasis was comparable in magnitude across the ocular surface epithelium, with the exception of a few mitotic figures in the midline. Thirty percent of the mitotic figures were in the basal layer (layer 1), and 70% were in layer 2; the cells in layer 2 were often noted to retain connection to the basal lamina by cytoplasmic stalks. Mitosis was rarely noted in the regenerating epithelium. However, summation of M phase cells in both the basal and suprabasal epithelium adjacent to the wound showed increases of 3- and 5-fold at 30 and 36 h after abrasion, respectively, from levels at homeostasis and the time of injury. In striking contrast to homeostatic epithelium, 80% of the mitotic cells were located in layer 1 of the corneal epithelium, with normal distribution observed by 72 h. Mitosis in the limbus and conjunctiva was increased 3-fold at 30 h and 24 h, respectively, from values at homeostasis and the time of debridement. These results, using rigorous statistical analysis and precise topographic assessment, showed that mitosis is not impeded - but rather often accelerated - following denuding of the corneal epithelium and that the spatial distribution of mitotic cells is correlated with wounding. The data revealed that re-epithelialization of the corneal epithelium is not dependent on mitosis in the regenerating epithelium, but rather in the adjacent unwounded epithelium of the cornea, with most cells being located in the basal layer until re-epithelialization is completed. Mitotic cells in the limbus and conjunctiva may be related to replenishment of ocular surface epithelial cells used in the repair process rather than directly supplying the abraded surface.

To determine the fate of ocular surface epithelial cells in response to corneal injury, epithelial cells undergoing DNA synthesis were labeled at discrete time points following abrasion. A 3-mm diameter epithelial defect was made in the center of the rat cornea. One hour prior to sacrifice, animals received an intraperitoneal injection of [3H]-thymidine. DNA synthesis in the regenerating epithelium was of low abundance (2%). The undamaged corneal epithelium had a labeling index (LI) that was markedly elevated from unwounded specimens in the first 48 h after abrasion. The LIs of suprabasal cells were increased at 24 h and 36 h; these cells were believed to be displaced basal epithelial cells. Basal and suprabasal cells of the limbus and conjunctiva exhibited increases in LIs from unwounded subjects at singular timepoints (within 24 h of injury). These results, using rigorous statistical analysis, show that DNA synthesis is not impeded--but rather often accelerated--following denuding of the corneal epithelium. Re-epithelialization is not dependent on DNA synthesis in the regenerating region, but appears to be related to an increase in DNA synthesis (along with centripetal migration) in the adjacent, undamaged epithelium. The increase in DNA synthesis occurring in the limbus and conjunctiva does not directly supply cells to the regenerating region within the 72 h required for epithelial restitution, but is conjectured to serve in replenishing ocular surface epithelial cells used in the repair process.

The fate of ocular surface epithelial cells in response to injury of the cornea was examined. Corneal epithelial cells were labeled during DNA synthesis with [3H]thymidine 1 h prior to wounding. A 3-mm diameter epithelial defect was made in the center of the rat cornea, with the basement membrane remaining intact. Within 12 h of abrasion, labeled cells were detected in the regenerating surface. At 18 h, there was a 2.7- and 17-fold increase of labeled basal and suprabasal cells, respectively, in the epithelium adjacent to the wound, and at 24 and 30 h there was an excessive number of cell layers (up to 7) at the margin of the abrasion. Re-epithelialization progressed as a gradient of cell layers that became diminished towards the center of the wound. Completion of layers 1, 2, 3, and 4 were recorded at 24, 30, 36, and 72 h, respectively. No changes in the labeling index of the limbus or conjunctiva were noted. These results suggest that processes of centripetal and vertical migration, as well as events related to cell division, in the uninjured corneal surface are not impeded by wounding of the corneal epithelium. However, wound healing appears to require cells with a basal phenotype, presumably because of this cell type's migratory capability.

A 90-year-old woman was referred to us with a 1-month history of progressively worsening blepharoconjunctivitis. She had a complete acquired ankyloblepharon of the right lids, which resulted in the appearance of a right upper lid abscess on computed tomography.Blepharotomy with separation and debridement of the lid margins was performed.Cultures were positive only for herpes simplex virus, type II.Herpes simplex blepharoconjunctivitis may take many clinical forms. Our patient's severe manifestations led to the clinical and radiologic appearance of preseptal cellulitis with a right upper lid abscess.