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The anagen stage represents the growth stage of the hair cycle and may last 2 to 6 years. The cagaten stage, which generally lasts 1 to 2 weeks, is when transitioning of club hair is observed as it progresses towards the skin pore and the dermal papilla begins to separate from the hair follicle. The telogen stage which lasts from 5 to 6 weeks, exhibits complete dermal papillary separation from the hair follicle. Lastly, the cycle progresses again towards the anagen stage as the dermal papilla joins up with the hair follicle and the hair matrix starts synthesizing new hair. Androgenetic alopecia (AGA) is the most common form of hair loss in men affecting almost 50% of the male population [18]. As the name suggests, AGA refers to hair loss induced in genetically susceptible individuals due to the effects of androgens such as testosterone – a lipophilic hormone that diffuses across the cell membrane to carry out its function, and its derivative dihydrotestosterone (DHT), which is a more active form of testosterone. The enzyme responsible for the conversion of testosterone to DHT is 5-α reductase. Two types of 5-α reductase enzymes exist; Type 1 which is prevalent in keratinocytes, fibroblasts, sweat glands, and sebocytes, and Type 2 found in skin and the inner root sheath of hair follicles [19]. DHT acts by binding to its nuclear androgen receptor (AR) which is responsible for regulation of gene expression [19]. Abnormal androgen signaling is responsible for disruption of epithelial progenitor cell activation and transient amplifying cell proliferation which forms the essential pathophysiological basis for AGA[20]. The exact genes associated with the process of hair loss are not entirely known however, a few of the genes proposed for hair growth include desmoglein, activin, epidermal growth factor (EGF), fibroblast growth factor (FGF), lymphoid-enhancer factor-1 (LEF-1), and sonic hedgehog [19]. Presently, amongst the treatment options available, the most common include use of minoxidil, finasteride or surgical hair transplantation [18]. Recently, the United States Food and Drug Administration (FDA) has approved the use of LLLT as a novel treatment modality for hair loss (Figure 3) [21]. Figure 3: Examples of LLLT devices for treatment of hair loss. 2.2 LLLT for Treatment of Hair Loss: In 2007, the FDA approved LLLT as a possible treatment modality for hair loss (Figure 4) [21]. It is believed that LLLT can stimulate reentry of anagen hair follicles into telgoen stage, bring about greater rates of proliferation in active anagen follicles, prevent development of premature catagen stage and extend the duration of the anagen phase [21, 22]. Although the exact underlying mechanism as to how LLLT brings about hair growth is not known, there have been several proposals. There is evidence suggestive of the action of LLLT on mitochondria leading to increased adenosine triphosphate (ATP) production, modulation of reactive oxygen species (ROS) and stimulation Proc. of SPIE Vol. 8932 89320X-4PDF Image | Low-level light therapy (LLLT) for cosmetics and dermatology
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