As mentioned earlier, P. acnes, which colonize the lower infundibulum, can digest triglycerides in the sebum and then release free fatty acids to produce inflammation or release cytokines to stimulate abnormal keratinization and inflammation. P acnes also produces high amount of porphyrin, particularly corpoporphyrin, which is called an endogenous photosensitizer. 5-Aminolevolunic acid (ALA) is another chemical substance which can induce exogenous porphyrin synthesis, particularly uroporphyrin, coproporphylin, and protoporphyrin IX. When these porphyrins are exposed to the light, especially to 381-560 nm wavelength, they can produce singlet oxygen which is a cytotoxic agent (Fig. 17.2) [29].
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Figure 17.2 Mechanism of action of light therapy. |
This agent can destroy P acnes, or in high amounts especially obtained from exogenous ALA application, it can cause damage to sebaceous glands [30].
Porphyrins have a wide range of absorption spectrum from UV to visible light. They have the greatest absorption to wavelengths near 400-420 nm, with their highest absorption peak (called the Soret band) occurring at 415 nm. Further, additional small peaks (Q bands) occur at longer wavelengths between 450 and 700 nm (509, 544, 584 and 634 nm) (Fig. 17.3) [31,32].
Violet/blue light source, with peak wavelengths between 400-420 nm (Soret band), is a popular treatment for acne. It has been very effective, with no reports of mutagenicity, and low side effects when the target is endogenous porphyrin, which is produced by P. acnes. Blue light also has antiinflammatory effects for inflamed acne by down-regulating interleukin (IL)-1, a proinflammatory cytokine, which is a chemo-attractant of inflammatory cells, and a stimulant of other inflammatory mediators [33].