Although orthodontic treatment is common, orthodontic force often induced pain. Low-level laser therapy (LLLT) has been investigated to improve therapeutic comfort. In dentistry, LLLT is mainly applied using two types of lasers, CO 2 and diode lasers, whose biological actions are thought to be associated with wavelength (CO 2 : 10,600 nm; diode: 808 nm). The analgesic effect of LLLT on orthodontic treatment-related pain is widely reported but inconsistent. This study aimed to (1) determine whether irradiation with a CO 2 or diode laser attenuates orthodontic treatment-related pain using the jaw-opening reflex model, (2) elucidate the optimal irradiation protocol for both lasers to obtain the maximal analgesic effect, (3) evaluate the effects of laser irradiation on other biological features [e.g., tooth movement, glial fibrillary acidic protein (GFAP) expression, and temperature alterations] and (4) investigate the mechanism underlying the analgesic effect of laser irradiation. In this animal model, orthodontic treatment-induced pain manifested as a significantly reduced the threshold for inducing the jaw-opening reflex on the orthodontically treated side compared with the contralateral side. GFAP expression in the bilateral trigeminal ganglia (TGs) was significantly increased by the application of orthodontic force. CO 2 laser irradiation of the orthodontically treated region significantly increased the threshold for inducing the jaw-opening reflex and the peripheral temperature. Similar reductions in jaw-opening reflex excitability were induced by surface anesthesia and thermal stimulation but not, the diode laser. Neither CO 2 nor diode laser irradiation altered GFAP expression in the TGs. Infiltration anesthesia also significantly increased the threshold for inducing the jaw-opening reflex on each anesthetized side. Irradiation (30 s) by either laser immediately after orthodontic force application (preirradiation) significantly decreased jaw-opening reflex excitability and GFAP expression in the bilateral TGs the next day. However, thermal stimulation immediately after orthodontic force application failed to alter jaw-opening reflex excitability the next day. Laser irradiation did not alter tooth movement; however, Tsuchiya et al.Beneficial Effects of CO 2 Laser an optimized irradiation protocol for aiding tooth movement is suggested. In conclusion, both CO 2 and diode lasers are able to prevent orthodontic treatment-related pain. Furthermore, the involvement of temperature alterations and surface anesthesia in the analgesic effect induced by CO 2 laser irradiation is suggested.

The electrical stimulation to gingiva induced the jaw-opening reflex (JOR). We have previously reported that the threshold for inducing jaw-opening reflex (JOR-TH) is significantly reduced by application of orthodontic force to teeth, and the intraperitoneal administration of TRPV1 antagonist recovers the JOR-TH. However, serious adverse side effects (e.g., hyperthermia) are reported by general administration of TRPV1 antagonists, and effective and safety application has to be established. In this study, TRPV1 and or TRPA1 antagonists were topically applied to gingiva, and the orthodontic force-induced JOR excitation was investigated with other features (e.g., trigeminal excitation, inflammatory cytokine alteration, rectal and gingival temperatures, and temperature sensitivity of the plantar and gingiva). Topical application of TRP antagonists immediately (D0)or one-day (D1)after orthodontic force application significantly increased JOR-TH the next day in dose-dependent and synergistic manner. On the other hand, there were no alterations in rectal and gingival temperature. In D0, the analgesic effect was associated with a significant reduction of CINC2 (cytokine-induced neutrophil chemoattractant-2) in the periodontium. In addition, chemical application-induced increase in temperature sensitivity was only observed in plantar. Taken together, topical application of TRP antagonists cocktail may reduce clinical orthodontic pain via CINC-2 reduction without adverse side effects.

Electrical stimulation to periodontal ligament induces the jaw-opening reflex. Due to pain, the threshold for inducing jaw-opening reflex was significantly reduced when orthodontic force was applied to the tooth. The application of orthodontic force excites the trigeminal ganglia, as well as other peripheral pain, which is associated with expression of GFAP (Glial fibrillary acidic protein) in the satellite glial cells in V 1 and V 2 regions. In addition, the intraperitoneal administration of TRPV1 antagonist or the thermal stimulation (e.g., laser irradiation) to periodontium significantly inhibited orthodontic force-induced excitation of jaw-opening reflex and trigeminal ganglia. Recently, the conjugational function of TRPV1 and TRPA1 to inflammation has been reported, and both receptors are widely present in peripheral nervous systems. Thus, the effects of topical administration of TRPV1 and or TRPA1 antagonists to cervical gingiva on alteration of the tooth movement-related pain and the trigeminal excitability were examined. Each TRP antagonist expressed an analgesic effect on tooth movement-related pain; however, trigeminal excitation was not inhibited. Moreover, the co-administration of both TRP antagonists significantly increased the analgesic effect without inducing general/local temperature alteration. Taken together, the cooperative effect of TRP antagonists may play a critical role in controlling tooth movement-related pain.

The many patients complain about orthodontic force-induced pain. It has reported that jaw-opening reflex (JOR) excitability is increased in 1 (D1) day and is decreased in 7 days (D7) after orthodontic force application in rats. In this model, potential analgesic role of Receptor Potential Vanilloid 1 (TRPV1) antagonism in orthodontic forceinduced pain and related features were investigated. Rats were applied continuous orthodontic force to right maxillary first molar. TRPV1 antagonists (A-889425: 5-10 mmol/kg, AMG9810: 10-15 mmol/kg) or aspirin (560 mmol/kg) was applied to D1-D7. Inflammatory cytokines were measured by antibody arrays. Excitation of trigeminal ganglia (TG) was evaluated by expression of Glial fibrillary acidic protein (GFAP) in satellite glial cells. And, expression of mature osteoclasts was measured by TRAP staining. All chemicals significantly reduced JOR excitability at D1. Temporal alteration of JOR excitability was associated with GFAP expression and that was significantly reduced by TRPV1 antagonists and aspirin. Although these chemicals reduced expression of mature osteoclasts at D7 significantly, distance of tooth movement was not altered. Significant increase of CINC2 and IL-6 was induced by orthodontic force application. Both TRPV1 antagonists significantly reduced CINC2 and IL-6, however, aspirin failed to reduce CINC2. Taken together, TRPV1 antagonism, in both peripheral and central, induced broad effects on orthodontic forceinduced physiological and morphological alterations. Poster Sessions

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