L Classen1, T Kivelä, A Tarkkanen. 1. Department of Ophthalmology, Helsinki University Central Hospital, Finland.
Abstract
PURPOSE: To analyze histopathologically and immunohistochemically the filtration bleb after unsuccessful glaucoma seton implantation. METHODS: A von Denffer implant and two Molteno implants that were nonfunctional at three months, at 11 months, and at five years after implantation, respectively, were compared by evaluating the adjacent bleb with light microscopy and a panel of 11 antibodies to epithelial, mesenchymal, and inflammatory cells. RESULTS: The wall of the filtration bleb three months after implantation consisted of loosely arranged collagenous connective tissue with relatively abundant fibroblasts labeled with monoclonal antibodies (MAbs) V9 and Vim 3B4 to vimentin. At 11 months and at five years, the collagenous layers had become increasingly thick and the fibroblasts scarce. All blebs showed metaplastic myofibroblasts surrounded by tenascin, as identified by MAb 1A4 to alpha-smooth muscle actin and TN2 to tenascin, respectively. One bleb was lined by a monolayer of cells that reacted with MAb CAM 5.2 and CY-90 to cytokeratin 8 and 18, respectively, and was apparently derived from the identically reacting proliferating corneal endothelial cells. Another bleb harbored many macrophages and foreign-body giant cells. Little evidence of chronic inflammation around the seton was detected. CONCLUSIONS: A glaucoma seton may induce several processes that potentially decrease filtration. In addition to formation of a collagenous cyst, presence of myofibroblasts suggests long-standing scar modulation that potentially leads to compaction of the filtration membrane. Furthermore, macrophages and corneal endothelial cells may invade the filtration bleb.
PURPOSE: To analyze histopathologically and immunohistochemically the filtration bleb after unsuccessful glaucoma seton implantation. METHODS: A von Denffer implant and two Molteno implants that were nonfunctional at three months, at 11 months, and at five years after implantation, respectively, were compared by evaluating the adjacent bleb with light microscopy and a panel of 11 antibodies to epithelial, mesenchymal, and inflammatory cells. RESULTS: The wall of the filtration bleb three months after implantation consisted of loosely arranged collagenous connective tissue with relatively abundant fibroblasts labeled with monoclonal antibodies (MAbs) V9 and Vim 3B4 to vimentin. At 11 months and at five years, the collagenous layers had become increasingly thick and the fibroblasts scarce. All blebs showed metaplastic myofibroblasts surrounded by tenascin, as identified by MAb 1A4 to alpha-smooth muscle actin and TN2 to tenascin, respectively. One bleb was lined by a monolayer of cells that reacted with MAb CAM 5.2 and CY-90 to cytokeratin 8 and 18, respectively, and was apparently derived from the identically reacting proliferating corneal endothelial cells. Another bleb harbored many macrophages and foreign-body giant cells. Little evidence of chronic inflammation around the seton was detected. CONCLUSIONS: A glaucoma seton may induce several processes that potentially decrease filtration. In addition to formation of a collagenous cyst, presence of myofibroblasts suggests long-standing scar modulation that potentially leads to compaction of the filtration membrane. Furthermore, macrophages and corneal endothelial cells may invade the filtration bleb.
Authors: Alka Mahale; Maha W Othman; Sami Al Shahwan; Ibrahim Al Jadaan; Ohood Owaydha; Zahid Khan; Deepak P Edward Journal: PLoS One Date: 2015-04-16 Impact factor: 3.240
Authors: Alka Mahale; Fatma Fikri; Khitam Al Hati; Sami Al Shahwan; Ibrahim Al Jadaan; Hind Al Katan; Rajiv Khandekar; Azza Maktabi; Deepak P Edward Journal: PLoS One Date: 2017-11-09 Impact factor: 3.240