Objective: The purpose of this study was to evaluate the relationship of 625, 525, and 425 nm wavelengths, providing average power output and effects on three common pathogenic bacteria. Background data: Ultraviolet (UV) light kills bacteria, but the bactericidal effects of UV may not be unique, as 425 nm produces a similar effect. The bactericidal effects of light-emitting diode (LED) wavelengths such as 625 and 525 nm have not been described. Before conducting clinical trials, the appropriate wavelength with reasonable dose and exposure time should be established. Materials and methods: The bactericidal effects of 625, 525, and 425 nm wavelength LED irradiation were investigated in vitro for the anaerobic bacterium Porphyromonas gingivalis and two aerobes (S taphylococcus aureus and Escherichia coli DH5α). Average power output was 6 mW/cm ² for 1 h. The bacteria were exposed to LED irradiation for 1, 2, 4, and 8 h (21.6, 43.2, 86.4, and 172.8 J/cm ² , respectively). LED irradiation was performed during growth on agar and in broth. Control bacteria were incubated without LED irradiation. Bacterial growth was expressed in colony-forming units (CFU) and at an optical density at 600 nm in agar and broth. Results: The bactericidal effect of LED phototherapy depended upon wavelength, power density, bacterial viable number, and bacteria species. The bactericidal effect of 425 and 525 nm irradiation varied depending upon the bacterial inoculation, compared with unirradiated samples and samples irradiated with red light. Especially, P. gingivalis and E. coli DH5α were killed by 425 nm, and S. aureus growth was inhibited by 525 nm. However, the wavelength of 625 nm was not bactericidal for P. gingivalis , E. coli DH5α, or S. aureus . Conclusions: Irradiation at 625 nm light was not bactericidal to S. aureus , E. coli, and P. gingivalis , whereas wavelengths of 425 and 525 nm had bactericidal effects. S. aureus was also killed at 525 nm.

Oxidative stress, in which the amount of oxidants exceeds the capacity of antioxidant defense system, is a well-accepted pathogenesis of several human diseases. Light-emitting diode irradiation (LEDI) is an efficient strategy to counteract this condition. The biological effect of phototherapy, using visible light, has attracted recent attention especially in dermatological practice. However, little is known about the molecular mechanism of the anti-oxidant and anti-inflammatory effects of red light irradiation. We evaluated these effects of LEDI in HaCaT human keratinocyte cells under phorbol-12-myristate-13-acetate (PMA) induced reactive oxygen species (ROS). Microarray analysis revealed changes in 309 genes after LEDI. LEDI at 625 nm produced ROS scavenging and anti-inflammatory effects. One of the most important genes identified by microarray analysis was sphingosine kinase-1 (SPHK1), which is a key molecule in sphingolipid metabolism. SPHK1 knock-down drastically reduced ROS scavenging efficiency as well as expression levels of inflammation-related proteins in PMA-treated HaCaT cells. These results not only indicate the potential for the clinical application of 625-nm LEDI in treating skin disorders via ROS and/or inflammation, but also suggest SPHK1 as a potential therapeutic target in phototherapy.