Clinical protocols are recommended in device guidelines outlined for treating many diseases on empirical basis.
However, effects of low-intensity infrared lasers at fluences used in clinical protocols on DNA are controversial.
Excitation of endogenous chromophores in tissues and free radicals generation could be described as a consequence of
laser used. DNA lesions induced by free radicals cause changes in DNA structure, chromatin organization, ploidy
degrees and cell death. In this work, we investigated whether low-intensity infrared laser therapy could alter the
fibroblasts nuclei characteristics and induce DNA fragmentation. Tendons of <i>Wistar</i> rats were exposed to low-intensity
infrared laser (830 nm), at different fluences (1, 5 and 10 J/cm<sup>2</sup>), in continuous wave (power output of 10mW, power
density of 79.6 mW/cm<sup>2</sup>). Different frequencies were analyzed for the higher fluence (10 J/cm<sup>2</sup>), at pulsed emission
mode (2.5, 250 and 2500 Hz), with the laser source at surface of skin. Geometric, densitometric and textural parameters
obtained for Feulgen-stained nuclei by image analysis were used to define nuclear phenotypes. Significant differences
were observed on the nuclear phenotype of tendons after exposure to laser, as well as, high cell death percentages was
observed for all fluences and frequencies analyzed here, exception 1 J/cm<sup>2</sup> fluence. Our results indicate that low-intensity
infrared laser can alter geometric, densitometric and textural parameters in tendon fibroblasts nuclei. Laser can also
induce DNA fragmentation, chromatin lost and consequently cell death, using fluences, frequencies and emission modes
took out from clinical protocols.
Low-level therapy laser is a phototherapy treatment that involves the application of low power light in the red or infrared wavelengths in various diseases such as arthritis. In this work, we investigated whether low-intensity infrared laser therapy could cause death by caspase-6 apoptosis or DNA damage pathways in cartilage cells after zymosaninduced articular inflammatory process. Inflammatory process was induced in C57BL/6 mouse by intra-articular injection of zymosan into rear tibio-tarsal joints. Thirty animals were divided in five groups: (I) control, (II) laser, (III) zymosan-induced, (IV) zymosan-induced + laser and (V). Laser exposure was performed after zymosan administration with low-intensity infrared laser (830 nm), power 10 mW, fluence 3.0 J/cm<sup>2</sup> at continuous mode emission, in five doses. Twenty-four hours after last irradiation, the animals were sacrificed and the right joints fixed and demineralized. Morphological analysis was observed by hematoxylin and eosin stain, pro-apoptotic (caspase-6) was analyzed by immunocytochemistry and DNA fragmentation was performed by TUNEL assay in articular cartilage cells. Inflammatory process was observed in connective tissue near to articular cartilage, in IV and V groups, indicating zymosan effect. This process was decreased in both groups after laser treatment and dexamethasone. Although groups III and IV presented higher caspase-6 and DNA fragmentation percentages, statistical differences were not observed when compared to groups I and II. Our results suggest that therapies based on low-intensity infrared lasers could reduce inflammatory process and could not cause death by caspase-6 apoptosis or DNA damage pathways in cartilage cells after zymosan-induced articular inflammatory process.