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Control of hypertrophic scar growth using selective photothermolysis
Author(s) -
Reiken Steven R.,
Wolfort Sean F.,
Berthiaume Francois,
Compton Carolyn,
Tompkins Ronald G.,
Yarmush Martin L.
Publication year - 1997
Publication title -
lasers in surgery and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.888
H-Index - 112
eISSN - 1096-9101
pISSN - 0196-8092
DOI - 10.1002/(sici)1096-9101(1997)21:1<7::aid-lsm2>3.0.co;2-u
Subject(s) - laser , implant , scars , histology , energy density , extracellular matrix , pulse (music) , pulse duration , hypertrophic scar , wavelength , biomedical engineering , chemistry , nuclear medicine , materials science , medicine , pathology , surgery , optics , optoelectronics , biochemistry , physics , detector , theoretical physics
Background and Objective Previous studies have shown a clinical improvement of hypertrophic scars (HS) after treatment with a pulsed dye laser. The objective of this study was to investigate the effects of variations in pulse wavelength and energy density on HS tissue using human HS implanted in athymic mice. Study Design/Materials and Methods Small pieces (∼1 mm 3 ) of HS tissue were implanted into athymic mice and allowed to grow for 5 days. The implant site was then exposed to a single 450 μs pulse, and implant growth and histology were monitored for an additional 12 days. Laser wavelength and energy density ranges tested were 585–600 nm and 2–10 J/cm 2 , respectively. Results Using a wavelength of 585 nm, laser treatment inhibited implant growth by 70% at 6 J/cm 2 and 92% at 10 J/cm 2 , respectively. The inhibitory effect decreased as the laser wavelength was increased from 585 to 600 nm. A widespread destruction of the implant microvasculature with a minor effect on surrounding extracellular matrix at the highest light dose were observed. Conclusion Pulsed laser treatment inhibits HS implant growth in nude mice. This effect is likely mediated by selective photothermolysis of the implant microvasculature. Lasers Surg. Med. 21:7–12, 1997. © 1997 Wiley‐Liss, Inc.