Abstract

PurposeIn orthodontic tooth movement, osteoclasts play a crucial role in bone resorption on the compression side of the alveolar bone. It has been reported that nitric oxide is involved in bone remodeling caused by mechanical loading, and we previously reported that NOC-18, a long-acting nitric oxide donor, augmented RANKL-induced osteoclast differentiation in mouse monocytic RAW264 cells as well as mouse bone marrow macrophages. In this study, we investigated whether NOC-18 facilitated experimental tooth movement in mice. Materials and methodsEight-week-old male ddY mice were used. Experimental tooth movement was induced by the insertion of an orthodontic elastic between the left maxillary first molar and second molar. Just after the insertion of the elastic, NOC-18 was intraperitoneally administered once, and mice were killed after 3 days. For the detection of osteoclasts, HE staining, TRAP staining, and immunostaining for cathepsin K were performed. ResultsAn intraperitoneal injection of NOC-18 significantly increased the distance of experimental tooth movement. Furthermore, the number and area of osteoclasts on the compression side of the alveolar bone surface was significantly higher in the NOC-18 group. ConclusionThese results suggested that systemic administration of NOC-18 might have some effect to facilitate experimental tooth movement in mice via the augmentation of osteoclast differentiation on the compression side of the alveolar bone.

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