The Effect of Amniotic Membrane on the Fibrosis between Orbital Connective Tissue and Porous Polyethylene Sheet Iimplant

PURPOSE: Soft tissue or muscle adhesion to the Porous Polyethylene Sheet Implant (PPSI) can cause postoperative extraocular motility disturbance after orbital fracture repairs using PPSI. This study was designed to examine the efficacy of amniotic membrane transplantation in the suppression of fibrosis between orbital connective tissue and PPSI. METHODS: Twelve New Zealand white rabbits were grouped as A, B, and C and conventional PPSI were implanted between orbital connective tissue and orbital floor in group A; PPSI with a barrier surface (PPSI-B) in group B; PPSI with amniotic membrane transplantation in group C. The implants were harvested at 8 weeks postoperatively, and stained with Masson trichrome and hemaoxylin and eosin staining techniques. RESULTS: In group A, the PPSI demonstrated dense adhesion on both the soft tissue implant and the bone implant interfaces. A lot of fibroblasts were observed on the surface of PPSI. In group B, the PPSI-B demonstrated less fibrosis over the barrier surface, and less fibroblasts than in group A. In group C, the PPSI with amniotic membrane transplantation manifested least fibrous adhesion among three groups. CONCLUSIONS: In orbital fracture repair, amniotic membrane transplantation could reduce the fibrosis between orbital connective tissue and PPSI, and might prevent the postoperative extraocualr motility disturbance.

Pilocarpine Induced Expression of Nitric Oxide Synthase in R18A5 Retinal Ganglion Cell Line

Pilocarpine is a direct cholinergic agonist and reduces intraocular pressure by enhancing aqueous outflow. A recent study reveals that pilocarpine induces apoptotic cell death in retinal ganglion cells; activation of bax and caspase-3 is a possible mechanism of the cell death. The objective of this study is to determine whether nitric oxide is involved in apoptotic retinal ganglion cell death which is induced by pilocarpine. R18A5 retinal ganglion cells were treated with 1 mM pilocarpine. After 20 hours of incubation, NADPH-d staining assay and immunocytochemistry of nNOS, iNOS, and NF-KB were performed. In retinal ganglion cells treated with pilocarpine, intense NADPH-d histochemical reactivity was present, whereas NADPH-d reactivity was weak in control. The immunoreactivity of iNOS was increased significantly and the immunoreactivity of nNOS was increased slightly in retinal ganglion cells treated with pilocarpine. The activation of NF-KB was demonstrated by staining of nuclei in retinal ganglion cells exposed to pilocarpine, whereas such features were not seen in untreated control cells. This study provides the first evidence that nitric oxide synthase is increased in retinal ganglion cells treated with pilocarpine, and nitric oxide may be a mediator of the cell death mechanism.

The Effect of Minoxidil on Cultured Mouse Fibroblast

Proliferative vitreoretinopathy is characterized by proliferation of retinal pigment epithelial cells, fibroblasts, glial cells and excessive fibrous tissue production. Recently minoxidil has been found to inhibit the proliferation of cultured fibroblast and retinal pigment epithelium. Minoxidil also inhibits the mRNA expression and protein production of lysyl hydroxylase, a key-enzyme involved in cross-linking of collagen. Therefore, the author investigated the effects of minoxidil on cultured mouse fibroblast and the result was compared with those of 5-fluorouracil and dexamethasone. Dexamethasone demonstrated bimodal effect of stimulation of proliferation at low concentrations and inhibition at higher concentrations. Fifty percent inhibition of growth (ID50) was seen at a concentration of 316mg/L. 5-fluorouracil had the most potent antiproliferative activity with ID50 of 0.8mg/L. Minoxidil had more potent antiproliferative properties on cultured mouse fibroblasts than dexamethasone. Fifty percent inhibition of growth (ID50) was 200mg/L. Reduction in cell number was seen after a 30 minute treatment and was half-maximal after 48 hours of treatment with 1000mg/L minoxidil.