Hua-Qing Gong1, Hua Gao, Li-Xin Xie, Wei-Yun Shi. 1. State Key Lab Cultivation Base, Shandong Provincial Key Lab of Ophthalmology, Shandong Eye Institute, Qingdao, China.
Abstract
OBJECTIVE: To study the ultrastructure changes of failed graft caused by chronic corneal allograft dysfunction (CCAD) after penetrating keratoplasty (PK), and to reveal the possible mechanism of these changes. METHODS: In CCAD group, corneas of 12 patients fulfilling the diagnostic criteria for CCAD who underwent repeated PK operation were studied. The average interval of these 12 patients between two PK operations was 69 months. All but two patients suffered at least once acute rejection episode during follow-up period. The mean time that the first acute immune rejection occurred was 39.4 months. Five healthy donor corneas were also studied as the control group. Both failed corneal grafts and healthy corneas were examined by light and electron microscopy. RESULTS: Compared with normal cornea, the cornea epithelium of CCAD became thinner, the quantity of microvillus apparently reduced, number of dark cells was increased, fibers of cornea stroma arranged disorderly, and there was no obvious invasion of inflammation cell into the stroma. The thickness of Descemet's membrane was uneven, abnormal lacuna and red cell could be seen between the Descemet's membrane and the endothelium. The number of cornea endothelial cells was decreased, cells became thinner, the organelle was reduced obviously, notch appeared in the cell nucleus, chromatin was condensed and inflammatory cells was adherent to the endothelium. CONCLUSIONS: The special ultrastructure changes of CCAD grafts consist of atrophic changes of the endothelium and fibrosis without inflammatory cells. Chronic subclinical alloantigen specific and non-alloantigen specific factors are both contributed to the CCAD process. Acute immune rejection perhaps induces and accelerates the occurrence and development of CCAD.
OBJECTIVE: To study the ultrastructure changes of failed graft caused by chronic corneal allograft dysfunction (CCAD) after penetrating keratoplasty (PK), and to reveal the possible mechanism of these changes. METHODS: In CCAD group, corneas of 12 patients fulfilling the diagnostic criteria for CCAD who underwent repeated PK operation were studied. The average interval of these 12 patients between two PK operations was 69 months. All but two patients suffered at least once acute rejection episode during follow-up period. The mean time that the first acute immune rejection occurred was 39.4 months. Five healthy donor corneas were also studied as the control group. Both failed corneal grafts and healthy corneas were examined by light and electron microscopy. RESULTS: Compared with normal cornea, the cornea epithelium of CCAD became thinner, the quantity of microvillus apparently reduced, number of dark cells was increased, fibers of cornea stroma arranged disorderly, and there was no obvious invasion of inflammation cell into the stroma. The thickness of Descemet's membrane was uneven, abnormal lacuna and red cell could be seen between the Descemet's membrane and the endothelium. The number of cornea endothelial cells was decreased, cells became thinner, the organelle was reduced obviously, notch appeared in the cell nucleus, chromatin was condensed and inflammatory cells was adherent to the endothelium. CONCLUSIONS: The special ultrastructure changes of CCAD grafts consist of atrophic changes of the endothelium and fibrosis without inflammatory cells. Chronic subclinical alloantigen specific and non-alloantigen specific factors are both contributed to the CCAD process. Acute immune rejection perhaps induces and accelerates the occurrence and development of CCAD.