Glaucoma is a common cause of blindness in industrialized countries and is the most frequent cause of irreversible
blindness worldwide. Since raised intraocular pressure (IOP) has been implicated as the major risk factor, the
main goal of all glaucoma treatment is to reduce IOP sufficiently to prevent continuous irreversible retinal ganglion cell
damage and progression of visual field loss. Pharmacological reduction of IOP is first-line therapy, followed by laser
treatment of the trabecular meshwork and filtering glaucoma surgery, and cyclophotocoagulation of the ciliary body or allogenic
implants. The most important glaucoma implants are presented (MOLTENO, AHMED, BAERVELDT, KRUPIN) together
with more recent developments (Ex-Press, Eyepass, iStent, Gold micro shunt). Drainage into the suprachoroidal
space is a promising option, but is also limited by scarring of the new created outflow route due to proliferation and adhesion
of fibroblasts. A deeper understanding of fibroblasts in the related eye compartments is required. Characterization of
scleral, choroidal, and, as a reference, Tenon fibroblast subtypes, is possible based on gene expression patterns. Alongside
mitomycin C and 5-fluorouracil, newer drugs to prevent fibrosis have been proposed, offering effects that are more specific
and more physiological. Effectors involved in wound healing phases and signaling pathways are potential targets for
pharmaceutical intervention. Downregulation of growth factors like TGF-ß and their downstream effectors may suppress
proliferation and differentiation of fibroblasts, extracellular matrix deposition, wound contraction, and neovascularization.
Furthermore, current approaches to local drug delivery in glaucoma implant technology are briefly summarized.