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Wound Healing Stimulation by Low-Level Light

It has been known for many years that low levels of laser or noncoherent 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 cytochromes, increase in 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/cm2 of 635-nm light and successively lower beneficial effects from 3–25 J/cm2, the effect is diminished at doses below 2 J/cm2 and gradually reaches control healing levels. At light doses above 25 J/cm2 healing is actually worse than controls. Although analysis of action spectra revealed the most effective light to be 635 nm, dose response curves are likely to be of similar shape for different wavelengths of light but at different absolute fluences. We found no difference between filtered 635 ± 15-nm light from a lamp and 633-nm HeNe laser. Light alone (or a combination with other agents such as photosensitive dyes or matrix degrading enzymes) could be used for stimulation of wound healing. Our future work will be focused on understanding the mechanisms underlying effects of light on wound healing processes. We propose to examine various knockout and overexpressing mice to determine the precise mechanisms operating and to study mouse models of impaired wound healing to more closely define which patients might most benefit from LLLT.