Intracorneal bacterial colonization in a crystalline pattern

We report the case of a 78-year-old woman who developed an intrastromal bacterial colonization 22 months after penetrating keratoplasty. Slit-lamp examination revealed discrete, finely branched, fernlike stromal opacities, which were histopathologically found to be large intrastromal aggregates of gram-positive cocci with almost no inflammatory cell response.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47391/1/417_2005_Article_BF02143065.pd

EGF does not enhance corneal epithelial cell motility

Although it is well known that epidermal growth factor (EGF) accelerates corneal epithelial wound healing by stimulating mitosis, it is also believed that EGF may directly stimulate the motility of individual corneal epithelial cells. We employed three different experimental methods to determine if EGF does indeed enhance the motility of corneal epithelial cells (independent of mitotic effects). First, the effects of EGF on the motility of tissue-cultured rat and rabbit corneal epithelial cells were investigated by a Boyden chamber assay. In rat corneal epithelium, these effects were further investigated by a second method, the agarose drop assay. Both assay techniques demonstrated no increase in corneal epithelial cell motility in the presence of EGF. These findings were corroborated by a third method which consisted of measuring the closure rate of epithelial wounds in organ-cultured rat corneas in the presence and absence of EGF, while concurrently arresting mitosis with colchicine. The wound closure rate before addition of any drug was 0.46 ± 0.03 mm 2 /hr. The wound closure rate with EGF (50 ng/ml) was 0.55 ± 0.03 mm 2 /hr, significantly {P < 0.005) more rapid than the drug-free controls. However, when EGF (50 ng/ml) and colchicine (40 fig/m\) were used simultaneously, the acceleration of wound closure by EGF was completely negated by the presence of colchicine, resulting in a wound closure rate (0.46 ± 0.06 mm 2 /hr) that did not differ significantly (P > 0.50) from that of the drug-free control. These results, together with the Boyden chamber and agarose drop assay results, suggest that the acceleration of corneal epithelial wound healing by EGF is due primarily to increased cell proliferation (with the increase in cell population causing the cells to spill over into the epithelial defect). It appears that individual cell motility, independent of mitosis, is not primarily responsible for accelerated wound healing in the presence of EGF. Invest Ophthalmol Vis Sci 30:1808-1812,198

Finite-element modeling of posterior lamellar keratoplasty: construction of theoretical nomograms for induced refractive errors

To estimate the theoretical corneal refractive error induced by mechanical weakening effects from posterior lamellar keratoplasty (PLKP) in the human cornea. The refractive effects of PLKP are simulated by finite-element modeling (FEM) as a mathematical function of the thickness of the excised posterior lamellar corneal button, with a nonlinear formulation of stress-strain relation for the corneal material. A theoretical nomogram was developed to correlate the refractive changes to button thickness. The predicted refractive change after PLKP is less than 1 dpt for a 170-microm thickness posterior corneal button over a broad range of Young's modulus. Thicker buttons result in greater surgically induced refractive errors. According to FEM analysis, the excision of a posterior lamellar button of less than 170 microm thickness produces a minimal predicted refractive change (< 1 dpt) in the cornea after PLKP