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Recovery of Corneal Endothelial Cells from Periphery after Injury.

Choi SO, Jeon HS, Hyon JY, Oh YJ, Wee WR, Chung TY, Shin YJ, Kim JW - PLoS ONE (2015)

Bottom Line: Corneal edema subsided from the periphery to the center, CEC density increased, and central corneal thickness decreased over time.In the animal study, corneal edema was greater in the NaOH group compared to the control at both day 1 and day 7.The peripheral corneal endothelium may act as a cell resource for the recovery of corneal endothelium.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Hallym University College of Medicine, Seoul, Republic of Korea.

ABSTRACT

Background: Wound healing of the endothelium occurs through cell enlargement and migration. However, the peripheral corneal endothelium may act as a cell resource for the recovery of corneal endothelium in endothelial injury.

Aim: To investigate the recovery process of corneal endothelial cells (CECs) from corneal endothelial injury.

Methods: Three patients with unilateral chemical eye injuries, and 15 rabbit eyes with corneal endothelial chemical injuries were studied. Slit lamp examination, specular microscopy, and ultrasound pachymetry were performed immediately after chemical injury and 1, 3, 6, and 9 months later. The anterior chambers of eyes from New Zealand white rabbits were injected with 0.1 mL of 0.05 N NaOH for 10 min (NaOH group). Corneal edema was evaluated at day 1, 7, and 14. Vital staining was performed using alizarin red and trypan blue.

Results: Specular microscopy did not reveal any corneal endothelial cells immediately after injury. Corneal edema subsided from the periphery to the center, CEC density increased, and central corneal thickness decreased over time. In the animal study, corneal edema was greater in the NaOH group compared to the control at both day 1 and day 7. At day 1, no CECs were detected at the center and periphery of the corneas in the NaOH group. Two weeks after injury, small, hexagonal CECs were detected in peripheral cornea, while CECs in mid-periphery were large and non-hexagonal.

Conclusions: CECs migrated from the periphery to the center of the cornea after endothelial injury. The peripheral corneal endothelium may act as a cell resource for the recovery of corneal endothelium.

No MeSH data available.


Related in: MedlinePlus

Photographs of anterior segments (A) and central corneal thickness data (CCT; B).A. Chemical injury of the cornea causes severe corneal edema and endothelial damage immediately after chemical injury. Slit lamp examination shows severe edematous and opaque cornea, and Descemet’s membrane folds. Endothelial cells are absent under specular microscopy. Corneal edema is reduced from the periphery to the center over time. Case 1 shows severe corneal edema and Descemet’s membrane fold immediately after injury, central edema and peripheral transparency 1 month after injury, and a clear cornea 6 months after injury. Case 2 shows severe corneal edema and Descemet’s membrane folds immediately after injury; the cornea becomes more transparent from periphery 1 month after injury. Case 3 shows severe corneal edema and Descemet’s membrane folds immediately after injury and the cornea becoming clear from the periphery 1 month after injury. This case also shows transparency of the central edema and periphery 6 months after injury. B. CCT is greater immediately after injury but decreases significantly 6 and 9 months later (p = 0.014 and 0.012, respectively, paired t-test) * Statistically significant by paired t-test
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pone.0138076.g001: Photographs of anterior segments (A) and central corneal thickness data (CCT; B).A. Chemical injury of the cornea causes severe corneal edema and endothelial damage immediately after chemical injury. Slit lamp examination shows severe edematous and opaque cornea, and Descemet’s membrane folds. Endothelial cells are absent under specular microscopy. Corneal edema is reduced from the periphery to the center over time. Case 1 shows severe corneal edema and Descemet’s membrane fold immediately after injury, central edema and peripheral transparency 1 month after injury, and a clear cornea 6 months after injury. Case 2 shows severe corneal edema and Descemet’s membrane folds immediately after injury; the cornea becomes more transparent from periphery 1 month after injury. Case 3 shows severe corneal edema and Descemet’s membrane folds immediately after injury and the cornea becoming clear from the periphery 1 month after injury. This case also shows transparency of the central edema and periphery 6 months after injury. B. CCT is greater immediately after injury but decreases significantly 6 and 9 months later (p = 0.014 and 0.012, respectively, paired t-test) * Statistically significant by paired t-test

Mentions: Chemical injury of the cornea caused severe corneal edema and endothelial damage immediately after chemical injury (Fig 1A). Slit lamp examination showed severe edematous, opaque corneas, Descemet’s membrane folds, and more than 1/2 limbal ischemia while specular microscopy revealed an absence of endothelial cells. Corneal edema reduced from the periphery to the center over time. Case 1 showed severe corneal edema, Descemet’s membrane folds and more than 1/2 limbal ischemia immediately after injury, and central edema and peripheral transparency 1 month later. Partial limbal deficiency (1/2 of limbus) occurred and limbo-conjuntival autograft from normal contralateral eye was performed; the cornea was clear 6 months after injury. Case 2 showed severe corneal edema, Descemet’s membrane folds and more than 1/2 limbal ischemia immediately after injury, and the cornea became clear from periphery 1 month later. Partial limbal deficiency (1/2 of limbus) occurred and limbo-conjuntival autograft from normal contralateral eye was performed. Then, the cornea became more transparent and visual acuity improved to 20/30. Case 3 also showed severe corneal edema, Descemet’s membrane folds and total limbal ischemia immediately after injury. The cornea became transparent from the periphery 1 month after injury, and total limbal deficiency was showed. Limbo-conjuntival autograft from normal contralateral eye was performed, and central edema and peripheral transparency occurred 6 months after injury. Visual acuity improved from hand movements to 20/40. CCT measurements by ultrasound pachymetry (Fig 1B, Table 2) were large immediately after injury (1056.7 ± 86.2 μm). CCT was significantly reduced at 6 and 9 months after injury compared to immediately after injury (p = 0.014 and p = 0.012, respectively, paired t-test; Table 2). Raw data may be found in S1 Dataset.


Recovery of Corneal Endothelial Cells from Periphery after Injury.

Choi SO, Jeon HS, Hyon JY, Oh YJ, Wee WR, Chung TY, Shin YJ, Kim JW - PLoS ONE (2015)

Photographs of anterior segments (A) and central corneal thickness data (CCT; B).A. Chemical injury of the cornea causes severe corneal edema and endothelial damage immediately after chemical injury. Slit lamp examination shows severe edematous and opaque cornea, and Descemet’s membrane folds. Endothelial cells are absent under specular microscopy. Corneal edema is reduced from the periphery to the center over time. Case 1 shows severe corneal edema and Descemet’s membrane fold immediately after injury, central edema and peripheral transparency 1 month after injury, and a clear cornea 6 months after injury. Case 2 shows severe corneal edema and Descemet’s membrane folds immediately after injury; the cornea becomes more transparent from periphery 1 month after injury. Case 3 shows severe corneal edema and Descemet’s membrane folds immediately after injury and the cornea becoming clear from the periphery 1 month after injury. This case also shows transparency of the central edema and periphery 6 months after injury. B. CCT is greater immediately after injury but decreases significantly 6 and 9 months later (p = 0.014 and 0.012, respectively, paired t-test) * Statistically significant by paired t-test
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4574742&req=5

pone.0138076.g001: Photographs of anterior segments (A) and central corneal thickness data (CCT; B).A. Chemical injury of the cornea causes severe corneal edema and endothelial damage immediately after chemical injury. Slit lamp examination shows severe edematous and opaque cornea, and Descemet’s membrane folds. Endothelial cells are absent under specular microscopy. Corneal edema is reduced from the periphery to the center over time. Case 1 shows severe corneal edema and Descemet’s membrane fold immediately after injury, central edema and peripheral transparency 1 month after injury, and a clear cornea 6 months after injury. Case 2 shows severe corneal edema and Descemet’s membrane folds immediately after injury; the cornea becomes more transparent from periphery 1 month after injury. Case 3 shows severe corneal edema and Descemet’s membrane folds immediately after injury and the cornea becoming clear from the periphery 1 month after injury. This case also shows transparency of the central edema and periphery 6 months after injury. B. CCT is greater immediately after injury but decreases significantly 6 and 9 months later (p = 0.014 and 0.012, respectively, paired t-test) * Statistically significant by paired t-test
Mentions: Chemical injury of the cornea caused severe corneal edema and endothelial damage immediately after chemical injury (Fig 1A). Slit lamp examination showed severe edematous, opaque corneas, Descemet’s membrane folds, and more than 1/2 limbal ischemia while specular microscopy revealed an absence of endothelial cells. Corneal edema reduced from the periphery to the center over time. Case 1 showed severe corneal edema, Descemet’s membrane folds and more than 1/2 limbal ischemia immediately after injury, and central edema and peripheral transparency 1 month later. Partial limbal deficiency (1/2 of limbus) occurred and limbo-conjuntival autograft from normal contralateral eye was performed; the cornea was clear 6 months after injury. Case 2 showed severe corneal edema, Descemet’s membrane folds and more than 1/2 limbal ischemia immediately after injury, and the cornea became clear from periphery 1 month later. Partial limbal deficiency (1/2 of limbus) occurred and limbo-conjuntival autograft from normal contralateral eye was performed. Then, the cornea became more transparent and visual acuity improved to 20/30. Case 3 also showed severe corneal edema, Descemet’s membrane folds and total limbal ischemia immediately after injury. The cornea became transparent from the periphery 1 month after injury, and total limbal deficiency was showed. Limbo-conjuntival autograft from normal contralateral eye was performed, and central edema and peripheral transparency occurred 6 months after injury. Visual acuity improved from hand movements to 20/40. CCT measurements by ultrasound pachymetry (Fig 1B, Table 2) were large immediately after injury (1056.7 ± 86.2 μm). CCT was significantly reduced at 6 and 9 months after injury compared to immediately after injury (p = 0.014 and p = 0.012, respectively, paired t-test; Table 2). Raw data may be found in S1 Dataset.

Bottom Line: Corneal edema subsided from the periphery to the center, CEC density increased, and central corneal thickness decreased over time.In the animal study, corneal edema was greater in the NaOH group compared to the control at both day 1 and day 7.The peripheral corneal endothelium may act as a cell resource for the recovery of corneal endothelium.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Hallym University College of Medicine, Seoul, Republic of Korea.

ABSTRACT

Background: Wound healing of the endothelium occurs through cell enlargement and migration. However, the peripheral corneal endothelium may act as a cell resource for the recovery of corneal endothelium in endothelial injury.

Aim: To investigate the recovery process of corneal endothelial cells (CECs) from corneal endothelial injury.

Methods: Three patients with unilateral chemical eye injuries, and 15 rabbit eyes with corneal endothelial chemical injuries were studied. Slit lamp examination, specular microscopy, and ultrasound pachymetry were performed immediately after chemical injury and 1, 3, 6, and 9 months later. The anterior chambers of eyes from New Zealand white rabbits were injected with 0.1 mL of 0.05 N NaOH for 10 min (NaOH group). Corneal edema was evaluated at day 1, 7, and 14. Vital staining was performed using alizarin red and trypan blue.

Results: Specular microscopy did not reveal any corneal endothelial cells immediately after injury. Corneal edema subsided from the periphery to the center, CEC density increased, and central corneal thickness decreased over time. In the animal study, corneal edema was greater in the NaOH group compared to the control at both day 1 and day 7. At day 1, no CECs were detected at the center and periphery of the corneas in the NaOH group. Two weeks after injury, small, hexagonal CECs were detected in peripheral cornea, while CECs in mid-periphery were large and non-hexagonal.

Conclusions: CECs migrated from the periphery to the center of the cornea after endothelial injury. The peripheral corneal endothelium may act as a cell resource for the recovery of corneal endothelium.

No MeSH data available.


Related in: MedlinePlus