The hair follicle cells can undergo either a programmed cell death (apoptosis) whereby they retain the ability to regenerate at the initiation of next growth cycle, or they can undergo a necrotic cell death where they lose their ability to regenerate. One of the markers of cell viability in hair follicle is Bcl-2, which is known to suppress apoptosis in a variety of cell systems [74, 75]. Throughout the hair cycle, Bcl-2 protein is prominently expressed in the follicular dermal papilla [34]. Several studies suggest a positive relationship of hair follicle activity and Bcl-2 levels in the dermal papilla cells. For example, Bcl-2 expression increases in the dermal papilla in response to treatment with the hair growth stimulatory agent minoxidil [83]. Elevated levels of follicle Bcl-2 have also been associated with a decreased sensitivity to chemotherapy-induced alopecia [69]. On the other hand, inhibitory effects of testosterone and 5-alpha-dihydrotestosterone on hair follicle activity are accompanied by a decreased expression of Bcl-2 protein in dermal papilla cells [84]. The dermal papilla Bcl-2 level seems to be an excellent marker for hair follicle viability, and might be useful in studying laser-induced changes in the follicle.
While high laser fluences and energy levels can cause permanent reduction in hair desired by many consumers, it has the potential for collateral skin damage. The level of efficacy versus dermal side effects is generally dependent on the difference in eumelanin levels between epidermis and the target hair follicle. To understand the mechanism of laser-induced changes in hair growth reduction, whether temporary or permanent, or changes in hair character after treatment, or to determine the treatment regimen for maximal hair reduction benefit, it is important to understand the impact that laser has on key biochemical and molecular targets that regulate hair growth, character, and cycling.