Alopecia - Hair Loss

Photobiomodulation (PBM) for Alopecia

Androgenetic alopecia (AGA)

The results of PBM for AGA suggest that the fraction of all the hair follicle (HF) in the anagen phase is
increased. This may be due to the ability of PBM to stimulate the mitochondria in the bulge stem cells. Stem cells are quiescent cells that have adapted to survive in their hypoxic niche. One of the most
damaging agents to the longevity of cells is oxidative damage to DNA and other biomolecules, caused by the ROS that are an inevitable by-product of aerobic respiration. Therefore stem cells tend to have
an overall anaerobic metabolism characterized by low mitochondrial activity and high expression of glycolytic enzymes.

Alopecia areata (AA)

The mechanism of action of PBM has some differences with that outlined above for AGA. Because AA is an autoimmune disease, the principle molecular signatures are characteristic of a pro-inflammatory nvironment in the HF. PBM has long been known to have a pronounced anti-inflammatory effect, but it is only recently that the possible mechanism for this has become apparent. Cells in the macrophage lineage can assume a diversity of phenotypes, and retain the capability to shift their function to maintain tissue homeostasis.

Chemotherapy-induced alopecia (CIA)

The mechanism of PBM is likely to operate via a different set of signaling pathways. It has long been known that PBM is able to protect cells at risk of dying. Many in vitro models have been utilized to show that PBM can inhibit apoptosis in different cells triggered by a number of different toxic substances. This
effect occurs due to the up-regulation of anti-apoptotic proteins, possible in the mitochondria. Another group of chromophores was identified in the HF, namely opsins. Opsins are blue-light responsive
signaling molecules, that were responsible for reducing apoptosis and prolonging the anagen phase in ex vivo HF that were treated with 3.2 J/cm2 of 453 nm LED light.

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