HISTOPATHOLOGIC AND IMMUNOHISTOCHEMICAL ANALYSIS OF THE FILTRATION BLEB AFTER UNSUCCESSFUL GLAUCOMA SETON IMPLANTATION

Citation
L. Classen et al., HISTOPATHOLOGIC AND IMMUNOHISTOCHEMICAL ANALYSIS OF THE FILTRATION BLEB AFTER UNSUCCESSFUL GLAUCOMA SETON IMPLANTATION, American journal of ophthalmology, 122(2), 1996, pp. 205-212
Citations number
27
Categorie Soggetti
Ophthalmology
ISSN journal
00029394
Volume
122
Issue
2
Year of publication
1996
Pages
205 - 212
Database
ISI
SICI code
0002-9394(1996)122:2<205:HAIAOT>2.0.ZU;2-G
Abstract
PURPOSE: To analyze histopathologically and immunohistochemically the filtration bleb after unsuccessful glaucoma seton implantation. METHOD S: A von Denffer implant and two Molteno implants that were nonfunctio nal at three months, at 11 months, and at five years after implantatio n, respectively, were compared by evaluating the adjacent bleb with li ght microscopy and a panel of 11 antibodies to epithelial, mesenchymal , and inflammatory cells. RESULTS: The wall of the filtration bleb thr ee months after implantation consisted of loosely arranged collagenous connective tissue with relatively abundant fibroblasts labeled with m onoclonal antibodies (MAbs) V9 and Vim 3B4 to vimentin. At 11 months a nd at five years, the collagenous layers had become increasingly thick and the fibroblasts scarce, All blebs showed metaplastic myofibroblas ts surrounded by tenascin, as identified by MAb 1A4 to alpha-smooth mu scle 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 cytokera tin 8 and 18, respectively, and was apparently derived from the identi cally reacting proliferating corneal endothelial cells, Another bleb h arbored 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 potentia lly leads to compaction of the filtration membrane, Further more, macr ophages and corneal endothelial cells may invade the filtration bleb.