The Role of RANKL on Bone Remodeling at the Compression Sites during Tooth Movement in Rat.
Qiu Song-b
Abstract
Qiu Song-b
Abstract
Objective: To investigate the role of RANKL on the induction of osteoclasts and bone remodeling at the compression site during tooth movement. Methods: The orthodontic tooth movement of upper molars was performed in Wistar rats. The expression of RANKL protein at the compression sites was detected by immunohistochemical staining technique. Furthermore, we observed the effect of RANKL on the osteoclast formation in bone marrow culture of adult rats. Results: Immunohistochemical staining revealed that expression of RANKL protein was detected in periodontal ligament cells and osteoclasts which mostly located in resorption lacunae. RANKL protein was expressed strongly at the compressive site at 3, 5, and 7 days after experimental tooth movement, RANKL expression increased in parallel with the changes in the numbers of osteoclasts. When bone marrow cells were cultured with increasing concentrations of RANKL in the presence of M-CSF (50 ng/ml), TRAP-positive cells increased in a dose-dependent manner. Conclusion: We found that RANKL up-regulation at the compressive site of experimental tooth movement induced osteoclastogenesis, and brought about alveolar bone resorption.
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Objective: To investigate the role of RANKL on the induction of osteoclasts and bone remodeling at the compression site during tooth movement. Methods: The orthodontic tooth movement of upper molars was performed in Wistar rats. The expression of RANKL protein at the compression sites was detected by immunohistochemical staining technique. Furthermore, we observed the effect of RANKL on the osteoclast formation in bone marrow culture of adult rats. Results: Immunohistochemical staining revealed that expression of RANKL protein was detected in periodontal ligament cells and osteoclasts which mostly located in resorption lacunae. RANKL protein was expressed strongly at the compressive site at 3, 5, and 7 days after experimental tooth movement, RANKL expression increased in parallel with the changes in the numbers of osteoclasts. When bone marrow cells were cultured with increasing concentrations of RANKL in the presence of M-CSF (50 ng/ml), TRAP-positive cells increased in a dose-dependent manner. Conclusion: We found that RANKL up-regulation at the compressive site of experimental tooth movement induced osteoclastogenesis, and brought about alveolar bone resorption.
Key concepts: RANKL, Osteoclast, Periodontal fiber, Bone remodeling, Dental alveolus, Bone resorption, Resorption, Immunohistochemistry