Primary open angle glaucoma (POAG) is defined as an optic neuropathy which is characterised by the loss of optic nerve axons and the related retinal ganglion cells. The reason for these changes is still unknown. In the pathogenesis of POAG several factors like increased intraocular pressure and a reduction of ocular blood supply are discussed. Morphological and biochemical analyses of the trabecular meshwork (TM) of POAG patients revealed loss of cells, increased accumulation of extracellular matrix (ECM), changes in the cytoskeleton, cellular senescence and the process of subclinical inflammation. One factor becoming more likely to be involved in the pathogenesis of POAG is oxidative stress. Treatment of TM cells with oxidative stress induced POAG-typical changes like ECM accumulation, cell death, disarrangement of the cytoskeleton, advanced senescence and the release of inflammatory markers. By pretreatment with antioxidants, prostaglandin analogues, beta-blockers or local carbonic anhydrase inhibitors, these effects were markedly reduced. In conclusion, oxidative stress is able to induce characteristic glaucomatous TM changes in vitro and these oxidative stress-induced TM changes can be minimised by the use of antioxidants and IOP-lowering substances. It is tempting to speculate that prevention of oxidative stress exposure to the TM may help to reduce the progression of POAG.