Department of Orthodontics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Institute of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Clin Oral Investig. 2018 Jul;22(6):2345-2351. doi: 10.1007/s00784-018-2335-z. Epub 2018 Jan 18.
Craniofacial sutures are important growth sites for skull development and are sensitive to mechanical stress. In order to determine the role of bone resorption in stress-mediated sutural bone growth, midpalatal suture expansion was performed in mice receiving alendronate, an anti-resorptive bisphosphonate.
The midpalatal sutures of 8-week-old C57BL/6 mice were expanded by orthodontic wires over the period of 2 weeks. Mice with maxillary expansion without drug treatment as well as untreated animals served as controls. Skulls were analyzed with micro-computed tomography (micro-CT), immunohistochemistry and histology.
Maxillary expansion in mice without drug treatment resulted in an increase of TRAP-positive osteoclasts. In contrast, no increase in osteoclasts was observed in expanded sutures of mice with bisphosphonate treatment. Double calcein labeling demonstrated rapid bone formation on the oral edges of the expanded sutures in mice without bisphosphonate treatment. Less bone formation was observed in bisphosphonate-treated mice after expansion. Histology revealed that the sutural architecture was reestablished in expanded sutures of mice without bisphosphonate treatment. In contrast, the sutural architecture was disorganized and the cartilage had an irregular form, following expansion in bisphosphonate-treated mice. Finally, micro-CT imaging demonstrated that the total amount of maxillary expansion was significantly lower in mice with bisphosphonate treatment as compared to those of mice without drug treatment.
In conclusion, our results indicate that osteoclast-mediated bone resorption is needed for maxillary suture expansion and reorganization of sutural architecture.
Orthodontic palatal expansion can be complicated in patients with inherited or drug-induced diseases of osteoclast dysfunction.
颅面骨缝是颅骨发育的重要生长部位，对机械应力敏感。为了确定骨吸收在应激介导的骨缝骨生长中的作用，在接受阿伦膦酸盐（一种抗吸收双膦酸盐）治疗的小鼠中进行了正中缝扩张。
在 8 周龄 C57BL/6 小鼠的正中缝上用正畸丝扩张 2 周。作为对照，对接受上颌扩张但未接受药物治疗的小鼠以及未接受治疗的动物进行了研究。使用微计算机断层扫描（micro-CT）、免疫组织化学和组织学对颅骨进行了分析。
未经药物治疗的小鼠上颌扩张导致 TRAP 阳性破骨细胞增加。相比之下，在接受双膦酸盐治疗的小鼠中，扩张的缝中没有观察到破骨细胞增加。双钙黄素标记显示，在未接受双膦酸盐治疗的小鼠中，扩张缝的口腔边缘有快速的骨形成。在接受双膦酸盐治疗的小鼠中，扩张后观察到的骨形成较少。组织学显示，在未接受双膦酸盐治疗的小鼠中，扩张缝的缝结构得到了重建。相比之下，在接受双膦酸盐治疗的小鼠中，扩张后缝结构紊乱，软骨形态不规则。最后，micro-CT 成像显示，与未接受药物治疗的小鼠相比，接受双膦酸盐治疗的小鼠的上颌扩张总量明显降低。
总之，我们的结果表明，破骨细胞介导的骨吸收是上颌缝扩张和缝结构重建所必需的。
遗传性或药物诱导的破骨细胞功能障碍性骨病患者的正畸腭扩张可能会变得复杂。
