Otago glaucoma surgery outcome study: cytology and immunohistochemical staining of bleb capsules around Molteno implants.
OBJECTIVE
To describe the cytology and immunohistochemistry of Molteno implant capsules from cases of primary and secondary glaucoma.


METHODS
Histologic features of capsules including cell cytology, the distribution of activated (proliferating) cells, apoptosing cells, and membrane bound vesicles (presumed death messengers) were assessed by light microscopy and correlated with clinicopathological features in 10 noninflamed eyes with good intraocular pressure control (nine autopsy and one enucleation) obtained from 2 months to 16.8 years after insertion of Molteno implants.


RESULTS
All bleb capsules demonstrated two distinct layers. The thin external layer was cellular with fairly numerous small blood vessels coursing through normally staining, regularly arranged collagen fibers. The thicker, deeper layer was avascular, relatively acellular, and characterized by regularly arranged swollen and fragmented collagen fibers. Most cells in the external layer appeared normal; however, between 5% (in recently formed blebs) and approximately 50% (in well established blebs) showed cytological and/or immunohistochemical changes characteristic of metabolic activation and/or apoptosis. All cells in the deeper layer, regardless of time after surgery, also demonstrated cytological and/or immunohistochemical staining characteristic of metabolic activation and/or apoptosis. In addition, the deeper layer evidenced large numbers of minute membrane-bound vesicles (presumed death messengers).


CONCLUSIONS
The balance between activation and apoptosis regulates the thickness and permeability of bleb capsules, and the normal lifecycle of bleb capsules includes continual inner surface degeneration and external surface renewal.
Molteno
Anthony C B
AC
Ophthalmology Section, Medical and Surgical Sciences, University of Otago Dunedin School of Medicine, Dunedin, New Zealand. acb.molteno@stonebow.otago.ac.nz
Suter
Antony J
AJ
Fenwick
Mark
M
Bevin
Tui H
TH
Dempster
Alex G
AG
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D017209:Apoptosis; D001768:Blister / Q000378:metabolism / Q000473:pathology*; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D002452:Cell Count; D049109:Cell Proliferation; D003228:Conjunctiva / Q000378:metabolism / Q000473:pathology*; D003238:Connective Tissue / Q000378:metabolism / Q000473:pathology*; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D005901:Glaucoma / Q000378:metabolism / Q000601:surgery*; D006801:Humans; D007124:Immunoenzyme Techniques; D020287:In Situ Nick-End Labeling; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008566:Membranes / Q000378:metabolism / Q000473:pathology; D008875:Middle Aged; D018465:Molteno Implants; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D053148:Caspase 3; D020169:Caspases; D018809:Proliferating Cell Nuclear Antigen; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C505407:CASP3 protein, human