Background Elongated and tortuous capillary loops are distinctive features of psoriasis. The significance of these microvascular changes in the pathogenesis of plaques, however, remains unclear.Objectives To determine what part the expanded superficial capillary bed plays in the pathogenesis of clinical lesions by selectively thermolysing psoriatic capillaries with a pulsed dye laser (PDL).Methods Cutaneous lesions were biopsied before and after treatment and sections assessed by standard immunohistochemical techniques for changes in known indicators of angiogenesis, including endothelial surface area, endothelial cell proliferation and endothelial cell expression of adhesion molecules. We also measured lymphocytic infiltration and epidermal thickness, and quantified the presence of a marker of keratinocyte proliferation before and after treatment.Results The effect of the PDL was limited to the superficial capillary bed, with no changes in the microvessels (including venules and arterioles) of the upper reticular dermis. Although there was significant clinical improvement in plaques after treatment (P = 0·02), complete clearance of lesions was not achieved. Thermolysis of psoriatic capillaries caused a reduction in both endothelial surface area (P < 0·01) and endothelial cell proliferation in the superficial dermis (P = 0·04). Endothelial expression of surface adhesion molecules (integrins and E-selectin) important in angiogenesis was not, however, altered by treatment. The CD4+ and CD8+ T-cell infiltrate was significantly reduced in the superficial papillary dermis (P = 0·02 and P = 0·04, respectively), but not in the epidermis or upper reticular dermis. Laser treatment significantly reduced epidermal thickness (P = 0·001), but did not alter epidermal keratinocyte proliferation (P = 0·2).Conclusions The results demonstrate that dermal capillary changes alone are unlikely to be causal in psoriasis. They indicate that the expanded psoriatic capillaries may be important in facilitating the access of activated T cells to the skin and in maintaining the psoriatic plaque. These results do not refute the consensus view that plaque formation may be mediated by the release of growth factors/cytokines from activated epidermal T cells/keratinocytes.