Role of CCR2 in orthodontic tooth movement
Introduction Cytokines and chemokines regulate bone remodeling during orthodontic tooth movement. CC chemokine ligand 2 (CCL2) is involved in osteoclast recruitment and activity, and its expression is increased in periodontal tissues under mechanical loading. In this study, we investigated whether t...
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Veröffentlicht in: | American journal of orthodontics and dentofacial orthopedics 2012-02, Vol.141 (2), p.153-160.e1 |
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Sprache: | eng |
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Zusammenfassung: | Introduction Cytokines and chemokines regulate bone remodeling during orthodontic tooth movement. CC chemokine ligand 2 (CCL2) is involved in osteoclast recruitment and activity, and its expression is increased in periodontal tissues under mechanical loading. In this study, we investigated whether the CC chemokine receptor 2 (CCR2)-CCL2 axis influences orthodontic tooth movement. Methods A coil spring was placed in CCR2-deficient (CCR2−/− ), wild-type, vehicle-treated, and P8A-treated (CCL2 analog) mice. In a histopathologic analysis, the amounts of orthodontic tooth movement and numbers of osteoclasts were determined. The expression of mediators involved in bone remodeling was evaluated by real-time polymerase chain reaction. Results Orthodontic tooth movement and the number of TRAP-positive cells were significantly decreased in CCR2−/− and P8A-treated mice in relation to wild-type and vehicle-treated mice, respectively. The expressions of RANKL, RANK, and osteoblasts markers (COL-1 and OCN) were lower in CCR2−/− than in wild-type mice. No significant difference was found in osteoprotegerin levels between the groups. Conclusions These data suggested a reduction of osteoclast and osteoblast activities in the absence of CCR2. The CCR2-CCL2 axis is positively associated with osteoclast recruitment, bone resorption, and orthodontic tooth movement. Therefore, blockage of the CCR2-CCL2 axis might be used in the future for modulating the extent of orthodontic tooth movement. |
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ISSN: | 0889-5406 1097-6752 |
DOI: | 10.1016/j.ajodo.2011.07.019 |