Abstract
Background and Objectives
Pulsed dye laser (PDL) therapy is effective in clearing psoriasis plaques, but the mechanism of action is only partially understood. Local narrow‐band ultraviolet B (NB‐UVB), which has a better‐defined mode of action, is an effective standard treatment for psoriasis. Our aim was to evaluate the cellular and molecular effects of PDL and to compare them with those of local NB‐UVB in order to gain further insight into their mechanisms of action in psoriasis.
Study Design/Patients and Methods
Nineteen patients with stable plaque‐type psoriasis were treated either with PDL or NB‐UVB. Lesional punch biopsies were obtained from all patients before treatment. Additional biopsies were obtained at 3 and 24 hours after PDL treatment in five of these patients. In 14 patients additional biopsies were taken after 7 and 13 weeks of treatment. Samples were histopathologically examined for the level of dermal T cell infiltrate, and the expression of epidermal β‐defensin 2, immune cell‐derived tumor necrosis factor (TNF)‐α, endothelial E‐selectin, vascular endothelial growth factor receptor (VEGFR) 2 and 3, and the expression of interleukin (IL)‐23 before and after treatment.
Results
The expression of VEGFR2, VEGFR3, and E‐selectin was decreased in clinically high responders within 24 hours after PDL treatment. The expression of IL‐23, TNF‐α mRNA, and E‐selectin protein were significantly reduced after two PDL treatments, whereas the expression of all epidermal markers and dermal T cell infiltrates had normalized after four treatments. The expression of epidermal activation markers and E‐selectin were significantly reduced after 13 weeks of NB‐UVB treatment.
Conclusions
The expression of epidermal activation markers and the dermal T cell infiltrates were decreased after both treatments. The decreased expression of VEGFR2 and VEGFR3 followed by the down‐regulation of TNF‐α and IL‐23p19 may be contributory factors in the efficacy of PDL in stable plaque‐type psoriasis. Lasers Surg. Med. 42:201–210, 2010. © 2010 Wiley‐Liss, Inc.