ABSTRACT
In this article we present the histopathological picture of common eyelid and anterior segment diseases, and directly compare histological and correlating clinical features for each disease. In addition to common benign eyelid tumours and cysts, malignant tumours of the lid are shown. For example, in such cases the histopathological characteristics can illustrate why certain tumours require a closer follow-up. Slit-lamp examination results are compared to the histological picture of relevant corneal diseases, followed by affections of the iris and anterior chamber.
Subject(s)
Anterior Eye Segment/pathology , Corneal Diseases/pathology , Diagnostic Techniques, Ophthalmological , Eyelid Diseases/pathology , Iris Diseases/pathology , HumansABSTRACT
PURPOSE: Corneal endothelial cells (EC) are crucial for maintaining corneal clarity before and after keratoplasty. Since it is thought that corneal graft rejection leads to irreversible EC loss and transplant failure, we quantified immune mediated EC loss in the rat keratoplasty model and analyzed whether the EC layer would then regenerate. METHODS: Rats were subjected to orthotopic penetrating keratoplasty. We compared endothelial responses to immunological EC loss following allogeneic transplantations between Fisher and Lewis rats (group R) to those following mechanical EC removal in a syngeneic setting between Lewis rats (group S). Animals were followed clinically for corneal opacity for up to one year. Bulbi were excised and prepared for histological examination at different time points: ECs were defined and characterized using Alicarin red S/ DAPI staining on corneal flatmounts. Ki-67/ DAPI staining on flatmount preparations served to detect cell proliferation. Immunohistochemical staining of corneal cryosections was used to characterize infiltrating immune cells. RESULTS: GROUP R: After about two weeks the allografts were completely opaque, which was accompanied by a massive leukocyte infiltration in conjunction with EC destruction, signifying rejection. EC loss without an immune reaction (group S) resulted only in medium opacity levels. In both groups, all grafts regained clarity in the following weeks to months, and a newly-formed endothelial cell layer with irregular and enlarged ECs became apparent on the formerly EC free grafts. Scattered Ki-67 positive cells within the endothelial cell layer were observed during re-endothelialization. In addition to re-endothelialization, the immunological infiltration seen in the allografts at the time of rejection had subsided after one year. CONCLUSIONS: Re-endothelialization following keratoplasty takes place in the rat in vivo and restores graft clarity, following both immunological or surgical destruction of ECs. Following rejection, EC replacement is accompanied by a reduction of immune infiltrates. Peripheral recipient ECs are a sufficient source for graft re-endothelialization, as seen in rats following EC removal. Our results suggest that ECs both proliferate and enlarge during re-endothelialization in the rat keratoplasty model.
Subject(s)
Corneal Transplantation , Endothelial Cells/pathology , Endothelium, Corneal/pathology , Endothelium, Corneal/physiology , Regeneration/physiology , Animals , Corneal Opacity/pathology , Corneal Opacity/surgery , Endothelium, Corneal/immunology , Endothelium, Corneal/surgery , Graft Rejection/immunology , Rats , Transplantation, HomologousABSTRACT
Patient 1 developed snowflake-like keratitis without inflammatory response in a decompensated corneal allograft. Patient 2, who had a history of repeated corneal grafting, also developed corneal opacification which initially appeared thread-like but quickly expanded. In both patients regrafting was necessary. Histological examination of the excised corneas demonstrated dense populations of Gram-positive bacteria in the interlamellar spaces. A surrounding inflammatory reaction was lacking, which is typical for infectious crystalline keratopathy (ICK).