OBJECTIVE: This study examined the effects of low-level laser therapy (LLLT) on osteoblasts via insulin-like growth factor I (IGF-I) signal transduction. BACKGROUND: Because orthodontic treatment is usually accompanied by bone formation, if bone formation can be promoted, the treatment and retention periods will be shorter. Recently, we reported the stimulatory effects of LLLT on bone formation. It was dependent on increased IGF-I, which plays an essential role in the anabolic regulation of bone metabolism. However, the signal transduction of IGF-I stimulated by LLLT was not elucidated. MATERIALS AND METHODS: Mouse osteoblastic MC3T3-E1 cells were cultured with or without LLLT (0.96-3.82 J/cm(2)), and the expression of IGF-I and Runt-related transcription factor 2 (Runx2) and the phosphorylation of extracellular-signal-regulated kinase (ERK) were determined by using real-time PCR and Western blot analysis. RESULTS: LLLT at 1.91 J/cm(2) significantly increased the expression of IGF-I and Runx2 and of ERK phosphorylation. Cyclolignan picropodophyllin (PPP; an IGF-I receptor inhibitor) partly inhibited the LLLT-induced expression of these factors. Moreover, when conditioned medium from the LLLT (1.91 J/cm(2)) cells was added to the MC3T3-E1 culture, the calcium content in the mineralized nodules increased significantly. PPP or noggin [a bone morphogenetic protein (BMP) antagonist] partly inhibited the LLLT-induced change in calcium content, and the addition of both PPP and noggin inhibited most of the LLLT-induced change in calcium content. CONCLUSION: These results suggest that LLLT stimulates in vitro mineralization through increased IGF-I and BMP production, through Runx2 expression and ERK phosphorylation in osteoblasts.
OBJECTIVE: This study examined the effects of low-level laser therapy (LLLT) on osteoblasts via insulin-like growth factor I (IGF-I) signal transduction. BACKGROUND: Because orthodontic treatment is usually accompanied by bone formation, if bone formation can be promoted, the treatment and retention periods will be shorter. Recently, we reported the stimulatory effects of LLLT on bone formation. It was dependent on increased IGF-I, which plays an essential role in the anabolic regulation of bone metabolism. However, the signal transduction of IGF-I stimulated by LLLT was not elucidated. MATERIALS AND METHODS:Mouse osteoblastic MC3T3-E1 cells were cultured with or without LLLT (0.96-3.82 J/cm(2)), and the expression of IGF-I and Runt-related transcription factor 2 (Runx2) and the phosphorylation of extracellular-signal-regulated kinase (ERK) were determined by using real-time PCR and Western blot analysis. RESULTS: LLLT at 1.91 J/cm(2) significantly increased the expression of IGF-I and Runx2 and of ERK phosphorylation. Cyclolignan picropodophyllin (PPP; an IGF-I receptor inhibitor) partly inhibited the LLLT-induced expression of these factors. Moreover, when conditioned medium from the LLLT (1.91 J/cm(2)) cells was added to the MC3T3-E1 culture, the calcium content in the mineralized nodules increased significantly. PPP or noggin [a bone morphogenetic protein (BMP) antagonist] partly inhibited the LLLT-induced change in calcium content, and the addition of both PPP and noggin inhibited most of the LLLT-induced change in calcium content. CONCLUSION: These results suggest that LLLT stimulates in vitro mineralization through increased IGF-I and BMP production, through Runx2 expression and ERK phosphorylation in osteoblasts.
Authors: Farzane Hendudari; Abbas Piryaei; Seyedeh-Nafiseh Hassani; Hasan Darbandi; Mohammad Bayat Journal: Lasers Med Sci Date: 2016-03-16 Impact factor: 3.161
Authors: Carla Roberta Tim; Karina Nogueira Zambone Pinto; Bruno Rafael Orsini Rossi; Kelly Fernandes; Mariza Akemi Matsumoto; Nivaldo Antonio Parizotto; Ana Claudia Muniz Rennó Journal: Lasers Med Sci Date: 2013-03-21 Impact factor: 3.161