Flashlamp pulsed dye laser (PDL) suppression of keloid proliferation through down-regulation of TGF-beta1 expression and extracellular matrix expression.

Abstract:

BACKGROUND AND OBJECTIVES:Keloids have been treated with flashlamp pulsed dye lasers (PDLs) with good results. We investigated whether PDL treatments induced keloid regression by decreasing growth factor-beta(1) (TGF-beta(1)) induction, thereby reducing fibroblast proliferation and collagen deposition. STUDY DESIGN/MATERIALS AND METHODS:Clinical evaluation and photography documented keloid height/texture, erythema, and pliability before and after PDL treatments scheduled at 2-month intervals in 30 patients. Fluence per pulse was 10-18 J/cm(2) (mean 14.0 J/cm(2)). Immunohistochemical (IHC) staining of TGF-beta(1), proliferating cell nuclear antigen (PCNA), and collagen (types I and III) in extra-cellular matrix was performed on 10 intra-lesional or punch biopsies obtained before and 7 days after PDL treatments. RESULTS:Twelve months after final PDL treatments, keloid regression ( >/= 50%) had occurred in 26/30 patients in whom erythema and surface irregularities had been reduced and pliability had been increased. In 4/30 patients, no changes in keloids had occurred after 12 months. Multiple treatments ( > 6) yielded better results than fewer treatments: 79% versus 50%, respectively. Marked keloid regression ( >/= 90%) occurred in two patients who had received more than 10 treatments. IHC staining indicated that expression of TGF-beta(1), PCNA and collagen type III, but not type I, was significantly reduced in keloid fibroblasts after PDL irradiation. CONCLUSIONS:Keloids regressed following PDL-induced reduction in TGF-beta(1) expression, fibroblast proliferation, and collagen type III deposition. More than six PDL treatments at 2-month intervals provided the best results.

journal_name

Lasers Surg Med

authors

Kuo YR,Jeng SF,Wang FS,Chen TH,Huang HC,Chang PR,Yang KD

doi

10.1002/lsm.10206

subject

Has Abstract

pub_date

2004-01-01 00:00:00

pages

104-8

issue

2

eissn

0196-8092

issn

1096-9101

journal_volume

34

pub_type

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