OBJECTIVEUse xenologous sclera (pig sclera) as wrapping materials for hydroxyapatite (HA) ocular implants in enucleated New Zealand white rabbits.

METHODSTen rabbits were unilaterally enucleated and the sockets implanted with 10 mm HA spherical implants. All implants were wrapped with pig sclera. The rabbits were killed 4 weeks later and the sockets were examined clinically for inflammation and implant exposure. Exenterated specimens were assessed histopathologically for inflammation and vascularization.

RESULTSNo clinical evidence of implant exposure or extrusion was detected in rabbits receiving pig sclera wrapped implants. Histopathologically the xenologous (pig) sclera displayed moderate inflammation, as well as maintain its lamellar arrangement without disruption. Fibrovascular ingrowth was complete in all implants.

CONCLUSIONXenologous (pig) sclera behaves similar clinically to homologous sclera as a wrapping material for spherical HA ocular implants in a rabbit model, and may represent a reasonable alternative to sclera in such procedures in humans.

Animals ; Durapatite ; Neovascularization, Pathologic ; Orbital Implants ; Prosthesis Implantation ; methods ; Rabbits ; Sclera ; blood supply ; pathology ; transplantation ; Swine ; Transplantation, Heterologous

Glaucoma is characterized by loss of retinal ganglion cells (RGCs) and their axons. Retrograde axoplasmic transport blockade and excitotoxicity were proposed to be a major cause of RGC apoptosis. We conducted this study to characterize the episcleral vessel cauterization glaucoma model in the rat with respect to decreased retrograde axoplasmic flow and subsequent apoptotic RGC death. After episcleral vessels were cauterized in Sprague-Dawley rats, Fluorogold was injected into their superior colliculi by stereotactic method. Retrograde axoplasmic flow and TUNEL-stained apoptotic dead cells were observed microscopically. Elevated intraocular pressure was maintained for up to 6 weeks during follow-up. Retrograde axoplasmic flow to the rat retina was significantly decreased. Apoptotic RGC was selectively TUNELstained in the retina, especially at the ganglion cell layers. We concluded that elevated intraocular pressure caused apoptotic RGC death through retrograde axoplasmic flow blockage. Further studies will elucidate the neuroprotection strategies in glaucoma patients.
Animals ; *Apoptosis ; Axonal Transport ; Disease Models, Animal ; In Situ Nick-End Labeling ; *Intraocular Pressure ; Male ; Ocular Hypertension/*complications ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/*pathology ; Retrograde Degeneration/etiology ; Sclera/blood supply