TY - GEN
T1 - Wound healing stimulation in mice by low-level light
AU - Demidova, Tatiana N.
AU - Herman, Ira M.
AU - Salomatina, Elena V.
AU - Yaroslavsky, Anna N.
AU - Hamblin, Michael R.
PY - 2006
Y1 - 2006
N2 - It has been known for many years that low levels of laser or non-coherent light (LLLT) accelerate some phases of wound healing. LLLT can stimulate fibroblast and keratinocyte proliferation and migration. It is thought to work via light absorption by mitochondrial chromophores leading to an increase in ATP, reactive oxygen species and consequent gene transcription. However, despite many reports about the positive effects of LLLT on wound healing, its use remains controversial. Our laboratory has developed a model of a full thickness excisional wound in mice that allows quantitative and reproducible light dose healing response curves to be generated. We have found a biphasic dose response curve with a maximum positive effect at 2 J/cm 2 of 635-nm light and successively lower beneficial effects from 3-25 J/cm 2, the effect is diminished at doses below 2J/cm 2 and gradually reaches control healing levels. At light doses above 25 J/cm 2 healing is actually worse than controls. The two most effective wavelengths of light were found to be 635 and 820-nm. We found no difference between filtered 635±15-nm light from a lamp and 633-nm light from a HeNe laser. The strain and age of the mouse affected the magnitude of the effect. Light treated wounds start to contract after illumination while control wounds initially expand for the first 24 hours. Our hypothesis is that a single brief light exposure soon after wounding affects fibroblast cells in the margins of the wound. Cells may be induced to proliferate, migrate and assume a myofibroblast phenorype. Our future work will be focused on understanding the mechanisms underlying effects of light on wound healing processes.
AB - It has been known for many years that low levels of laser or non-coherent light (LLLT) accelerate some phases of wound healing. LLLT can stimulate fibroblast and keratinocyte proliferation and migration. It is thought to work via light absorption by mitochondrial chromophores leading to an increase in ATP, reactive oxygen species and consequent gene transcription. However, despite many reports about the positive effects of LLLT on wound healing, its use remains controversial. Our laboratory has developed a model of a full thickness excisional wound in mice that allows quantitative and reproducible light dose healing response curves to be generated. We have found a biphasic dose response curve with a maximum positive effect at 2 J/cm 2 of 635-nm light and successively lower beneficial effects from 3-25 J/cm 2, the effect is diminished at doses below 2J/cm 2 and gradually reaches control healing levels. At light doses above 25 J/cm 2 healing is actually worse than controls. The two most effective wavelengths of light were found to be 635 and 820-nm. We found no difference between filtered 635±15-nm light from a lamp and 633-nm light from a HeNe laser. The strain and age of the mouse affected the magnitude of the effect. Light treated wounds start to contract after illumination while control wounds initially expand for the first 24 hours. Our hypothesis is that a single brief light exposure soon after wounding affects fibroblast cells in the margins of the wound. Cells may be induced to proliferate, migrate and assume a myofibroblast phenorype. Our future work will be focused on understanding the mechanisms underlying effects of light on wound healing processes.
KW - Biomodulation
KW - Biostimulation
KW - Cold laser
KW - Excisional wound healing
KW - Low level light therapy
UR - http://www.scopus.com/inward/record.url?scp=33745353774&partnerID=8YFLogxK
U2 - 10.1117/12.646310
DO - 10.1117/12.646310
M3 - Conference contribution
AN - SCOPUS:33745353774
SN - 0819461830
SN - 9780819461834
T3 - Progress in Biomedical Optics and Imaging - Proceedings of SPIE
BT - Mechanisms for Low-Light Therapy
T2 - Mechanisms for Low-Light Therapy
Y2 - 22 January 2006 through 24 January 2006
ER -