LLLT Mechanism of Action

Stress or damage to cells causes an increased production of nitric oxide (NO) in the mitochondria.

The increased NO binds to cytochrome c oxidase (Cox) displacing oxygen, thereby inhibiting cellular respiration in the mitochondria.

Low level laser therapy (LLLT) dissociates NO from Cox, allowing immediate influx of oxygen and resumption of respiration.

Increased cellular respiration generates reactive oxygen species (ROS). ROS are small molecules that include oxygen ions like superoxide, free radicals such as hydroxyl radicals, and hydrogen peroxide as well as organic peroxides.

NO may also be released from hemoglobin and myoglobin.

This released NO has an effect on cyclic guanine monophosphate (cGMP) causing vasodilation.

ROS (and RNS) are involved with signaling pathways between mitochondria and nuclei which regulates nucleic acid synthesis, protein synthesis, and activation of enzymes.

Therefore LLLT shifts cell redox potential toward increased oxidation, increased ROS and cell redox activity.

This leads to transcription of protective and stimulatory gene products.

Cellular Effects: Prevention of cell apoptosis
Enhance cell proliferation: Fibroblasts
Keratinocytes
Endothelial cells
Lymphocytes
Tissue Effects: Neovascularization
Angiogenesis
Collagen synthesis

Therefore LLLT promotes healing of : Nerves
Tendons and ligaments
Cartilage and bones
Muscle (both cardiac and skeletal)
Internal organs

And, LLLT Reduces pain and inflammation
Repairs ischemia of skeletal and cardiac muscle
Reduces damage from strokes, brain and spinal cord injuries

Note: Too much NO and ROS can actually cause damage, hence the Biphasic Dose Response of LLLT. Other direct cytotoxic pathways have been proposed as well.