Can we treat ‘light as a drug’ for Photobiomodulation therapy? To satisfy the definition of an active pharmaceutical agent, the substance should be absorbed and capable of changing bodily function that light satisfies. Our understanding of our visual cycle and Vitamin D metabolism are clear evidences for this phenomenon. Advances in optophotonic technologies along with a better understanding of light-tissue interactions, especially in in vivo optical imaging and optogenetics, are spearheading the popularity of biophotonics in biology and medicine. This therapy is defined as the non-thermal use of non-ionizing forms of photonic devices including lasers, LEDs and broad-band light to alleviate pain, inflammation, modulate immune responses and promote wound healing and tissue regeneration. This presentation will provide a brief overview of the two most well understood phenomenon namely, an intracellular mechanism involving cytochrome c oxidase in the mitochondria and an extracellular mechanism involving activation of a latent growth factor, TGF-β1. Surprisingly, despite vast volumes of scientific literature from both clinical and laboratory studies noting the phenomenological evidences for this innovative therapy, there has been inconsistent, non-reproducible clinical outcomes. It is hoped that outlining the molecular mechanism will enable development of more robust, safe and efficacious PBM clinical regimens.
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