Photodynamic therapy (PDT) of tumours is based on a dual selectivity, i.e. preferential uptake and retention of a photosensitiser by tumours and irradiation of the tumour area with light wavelengths specifically absorbed by the photosensitiser. The photoexcited sensitiser generates highly reactive oxygen species that induce irreversible damage to neoplastic cells and vessels. Following sensitiser accumulation and irradiation, damage to sensitive sites within the microvasculature, namely to endothelial cells and the vascular basement membrane, is induced and leads to the establishment of thrombogenic sites within the vessel lumen. This initiates a physiological cascade of responses including platelet aggregation, the release of vasoactive molecules, leukocyte adhesion, increases in vascular permeability and vessel constriction. These result in tumour destruction by vascular collapse, blood flow stasis and tissue hemorrhages. Several photosensitisers are able to induce severe vasculature damage, although by variously different mechanisms. Due to its efficient vascular interactions, photodynamic treatment is also increasingly used for non-cancerous lesions. Successful application of PDT mainly for vessel occlusion and thrombosis in intimal hyperplasia, restenosis, atherosclerotic plaques, corneal and choroidal neovascularisation and port-wine stains is reported.