PURPOSE: The purpose of this study was to image the pathology of vitreoretinal adhesion and cellular proliferation at the macular hole rim for a better understanding of macular hole formation. METHODS: Internal limiting membrane (ILM) peeling, ILM flat-mount preparation, phase contrast and interference microscopy, transmission electron microscopy, and immunocytochemistry of the macular hole rim were performed in 10 eyes with idiopathic macular holes. RESULTS: Phase contrast and interference microscopy showed cellular proliferation on the vitreal side of the ILM in all specimens. There were single cells in three eyes, cell clusters in six eyes, and continuous proliferation in one eye. Surrounding the macular hole, only a few cells were present. Cellular proliferation started at a distance of 80 mum to 940 mum from the macular hole edge. Transmission electron microscopy showed vitreous adhesion at the macular hole rim. In ultrastructural terms, there was a continuous insertion of vitreous collagen fibers into the ILM. Immunocytochemistry was positive for collagen type II, laminin, and fibronectin in the area of vitreous attachment. Cells were stained with markers for glial cells, retinal pigment epithelial cells, and hyalocytes. CONCLUSION: There is ultrastructural evidence that macular hole formation is caused by an insertion of the cortical vitreous into the foveal ILM. Vitreous collagen fibers may exert vitreofoveal traction, resulting in a foveal tear. Cellular proliferation is not continuously distributed surrounding the macular hole but separated from the macular hole edge and seems to originate from cell clusters forming centers of proliferation distant from the macular hole rim.
PURPOSE: The purpose of this study was to image the pathology of vitreoretinal adhesion and cellular proliferation at the macular hole rim for a better understanding of macular hole formation. METHODS: Internal limiting membrane (ILM) peeling, ILM flat-mount preparation, phase contrast and interference microscopy, transmission electron microscopy, and immunocytochemistry of the macular hole rim were performed in 10 eyes with idiopathic macular holes. RESULTS: Phase contrast and interference microscopy showed cellular proliferation on the vitreal side of the ILM in all specimens. There were single cells in three eyes, cell clusters in six eyes, and continuous proliferation in one eye. Surrounding the macular hole, only a few cells were present. Cellular proliferation started at a distance of 80 mum to 940 mum from the macular hole edge. Transmission electron microscopy showed vitreous adhesion at the macular hole rim. In ultrastructural terms, there was a continuous insertion of vitreous collagen fibers into the ILM. Immunocytochemistry was positive for collagen type II, laminin, and fibronectin in the area of vitreous attachment. Cells were stained with markers for glial cells, retinal pigment epithelial cells, and hyalocytes. CONCLUSION: There is ultrastructural evidence that macular hole formation is caused by an insertion of the cortical vitreous into the foveal ILM. Vitreous collagen fibers may exert vitreofoveal traction, resulting in a foveal tear. Cellular proliferation is not continuously distributed surrounding the macular hole but separated from the macular hole edge and seems to originate from cell clusters forming centers of proliferation distant from the macular hole rim.
Authors: David R P Almeida; Eric K Chin; Ryan M Tarantola; James C Folk; H Culver Boldt; Jessica M Skeie; Robert F Mullins; Stephen R Russell; Vinit B Mahajan Journal: Invest Ophthalmol Vis Sci Date: 2015-05 Impact factor: 4.799
Authors: Shao Chong Bu; Roel Kuijer; Roelofje J van der Worp; Xiao Rong Li; Johanna M M Hooymans; Leonoor I Los Journal: PLoS One Date: 2015-07-31 Impact factor: 3.240