Molecular effects of low-energy laser irradiation during orthodontic tooth movement

Abstract

Since orthodontic treatments usually take around 2–3 years, it can be a great burden for both patients and providers. Therefore, shortening the duration of treatment is both desirable and beneficial to the orthodontists as long treatment duration is associated with increased risks of gingival inflammation, decalcification, dental caries, and root resorption. Several novel modalities have been reported to accelerate orthodontic tooth movement including low-level laser therapy, pulsed electromagnetic fields, electrical currents, corticotomy, distraction osteogenesis, and mechanical vibration. Low-level laser therapy (LLLT) is an effective method to prompt wound healing, bone repair, and modeling after surgery. These biostimulatory effects of LLLT have been related to increased fibroblast and osteoblast activities. Similarly, LLLT has been suggested to play a role in accelerated tooth movement. In vivo rat studies have demonstrated that low-level laser irradiation (LLLI) increases osteoclastogenesis on the compression side via stimulation of the receptor activator of nuclear factor-κB (RANK)/RANK ligand (RANKL) and the c-fms/macrophage colony-stimulating factor (M-CSF) during experimental tooth movement. On the tension side, LLLI stimulates bone formation and has been associated with increased expression of type I collagen (COL1), fibronectin (FN), and osteopontin (OPN). Furthermore, In vivo studies have shown that LLLI induces differentiation and activation of osteoblasts and osteoclasts. Therefore, LLLI facilitates the turnover of connective tissues and accelerates the bone remodeling process by stimulating osteoblast and osteoclast proliferation and function during orthodontic tooth movement. This article reviews the current knowledge of the biological effects of laser irradiation and its molecular effect on orthodontic tooth movement. Since orthodontic treatments usually take around 2–3 years, it can be a great burden for both patients and providers. Therefore, shortening the duration of treatment is both desirable and beneficial to the orthodontists as long treatment duration is associated with increased risks of gingival inflammation, decalcification, dental caries, and root resorption. Several novel modalities have been reported to accelerate orthodontic tooth movement including low-level laser therapy, pulsed electromagnetic fields, electrical currents, corticotomy, distraction osteogenesis, and mechanical vibration. Low-level laser therapy (LLLT) is an effective method to prompt wound healing, bone repair, and modeling after surgery. These biostimulatory effects of LLLT have been related to increased fibroblast and osteoblast activities. Similarly, LLLT has been suggested to play a role in accelerated tooth movement. In vivo rat studies have demonstrated that low-level laser irradiation (LLLI) increases osteoclastogenesis on the compression side via stimulation of the receptor activator of nuclear factor-κB (RANK)/RANK ligand (RANKL) and the c-fms/macrophage colony-stimulating factor (M-CSF) during experimental tooth movement. On the tension side, LLLI stimulates bone formation and has been associated with increased expression of type I collagen (COL1), fibronectin (FN), and osteopontin (OPN). Furthermore, In vivo studies have shown that LLLI induces differentiation and activation of osteoblasts and osteoclasts. Therefore, LLLI facilitates the turnover of connective tissues and accelerates the bone remodeling process by stimulating osteoblast and osteoclast proliferation and function during orthodontic tooth movement. This article reviews the current knowledge of the biological effects of laser irradiation and its molecular effect on orthodontic tooth movement.