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Biphasic dose response in low level light therapy FIGURE 5. Reactive oxygen species (ROS) formed as a result of LLLT effects in mitochondria may activate the redox-sensitive transcription factor NF-κB (relA-p50) via protein kinase D (PKD). activated after LLLT and is instrumental in causing transcription of pro- tective and stimulatory gene products. 2.7. Downstream cellular response Although the underlying mechanism of LLLT are still not completely understood, in vitro studies, animal experiments and clinical studies have all tended to indicate that LLLT delivered at low doses may produce a bet- ter result when compared to the same light delivered at high doses. LLLT can prevent cell apoptosis and improve cell proliferation, migration and adhesion at low levels of red/NIR light illumination (see Figure 6). LLLT at low doses has been shown to enhance cell proliferation in vitro in several types of cells: fibroblasts (Lubart et al. 1992; Yu et al. 1994), keratinocytes (Grossman et al. 1998), endothelial cells (Moore et al. 2005), and lymphocytes (Agaiby et al. 2000; Stadler et al. 2000). The mechanism of proliferation was proposed to involve photostimulatory effects in mitochondria processes, which enhanced growth factor release, and ultimately led to cell proliferation (Bjordal et al. 2007). Kreisler et al showed (Kreisler et al. 2003) that the attachment and proliferation of human gingival fibroblasts were enhanced by LLLT in a dose-dependent manner. LLLT modulated matrix metalloproteinase activity and gene expression in porcine aortic smooth muscle cells (Gavish et al. 2006). Shefer at el. showed (Shefer et al. 2002) that LLLT could activate skeletalPDF Image | BIPHASIC DOSE RESPONSE IN LOW LEVEL LIGHT THERAPY
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