[Variation of inflammatory reaction of ciliary body--harmony between clinic and basic science].

Histopathological findings of ciliary epithelium and muscle were discussed in the inflammatory conditions that are induced in endophthalmitis, blood-aqueous barrier destruction, cyclocryotherapy and cyclophotocoagulation. The clinical results were also discussed regarding the reduction of aqueous production and uveoscleroplasty which are introduced by the experimental cyclophotocoagulation at the pars plicata/pars plana. Tissue destruction by inflammatory reaction occurred in not only the ciliary body but also in the retina if the endophthalmitis had progressed to the point of severity. The post-inflammatory reactive hypertrophy of nonpigmented and pigmented ciliary epithelium was mild at pars plicata and the anterior portion of the pars plana. On the other hand, it was severe at the posterior portion of the pars plana and the ora serrata, and it was clear that the cyclitic membrane developed into proliferative vitreoretinopathy. Adult pig cultured nonpigmented ciliary epithelium showed proliferated tissue resembling the cyclitic membrane. These results show that nonpigmented ciliary epithelium has a strong proliferative activity as much the same as fibroblasts. The destruction of the blood-aqueous barrier was produced by corneal perforation, paracentesis, prostaglandin E1 (PGE1) subconjunctival injection, and hyperosmotic agent intraophthalmic artery injection. The localization of the tissue destruction was made clear at the beginning portion of the ciliary process and the posterior part of the pars plana. The repetitive instillation of latanoprost and cyclosporin A eye drops showed the same localization of the tissue damage. These results suggest that the beginning portion of the ciliary process is vulnerable to inflammatory agents. Cyclosporin A might produce a toxic reaction on nonpigmented ciliary epithelium, and latanoprost destroys the blood-aqueous barrier. Cyclocryotherapy produces severe necrosis of the pigmented ciliary epithelium and melanocytes, and atrophy of pigmented ciliary epithelium and ciliary muscle, and the proliferation of nonpigmented ciliary epithelium follows. Because cyclocryotherapy is a blind therapy, hypotony and phthisis bulbi will occur if the pars plicata is damaged severely, and the intraocular pressure (IOP) decrease will not be achieved if pars plana is damaged locally. Finally, we demonstrated that it is difficult to predict the therapeutic outcome of cyclocryotherapy. Cyclophotocoagulation of the pars plicata and the pars plana produced severe necrosis of pigmented ciliary epithelium and melanocytes, and atrophy of pigmented ciliary epithelium and ciliary muscle, and the proliferation of nonpigmented ciliary epithelium followed. Cyclitic membrane was developed from the proliferation of nonpigmented ciliary epithelium depending on the severity of photocoagulation. From these experiments the complete destruction of the pars plicata might result in for hypotony and phthisis bulbi. The reduction of aqueous production for angle-closure glaucoma was achieved by moderate cyclophotocoagulation of the pars plicata. On the other hand, moderate cyclophotocoagulation of the pars plicata for open-angle glaucoma produced the obstruction of uveoscleral aqueous outflow which compensated for the reduction of aqueous production. From these results we suggested that moderate cyclophotocoagulation of the pars plana for open-angle glaucoma might be necessary to effect the increase of uveoscleral aqueous outflow. Moderate and severe cyclophotocoagulation of the transit area between the pars plicata and the pars plana might bring about reduction of aqueous production and the increase of uveoscleral aqueous outflow.