ABSTRACT
Nowadays, orthodontic treatment has become increasingly popular. However, the biological mechanisms of orthodontic tooth movement (OTM) have not been fully elucidated. We were aiming to summarize the evidences regarding the mechanisms of OTM. Firstly, we introduced the research models as a basis for further discussion of mechanisms. Secondly, we proposed a new hypothesis regarding the primary roles of periodontal ligament cells (PDLCs) and osteocytes involved in OTM mechanisms and summarized the biomechanical and biological responses of the periodontium in OTM through four steps, basically in OTM temporal sequences, as follows: (1) Extracellular mechanobiology of periodontium: biological, mechanical, and material changes of acellular components in periodontium under orthodontic forces were introduced. (2) Cell strain: the sensing, transduction, and regulation of mechanical stimuli in PDLCs and osteocytes. (3) Cell activation and differentiation: the activation and differentiation mechanisms of osteoblast and osteoclast, the force-induced sterile inflammation, and the communication networks consisting of sensors and effectors. (4) Tissue remodeling: the remodeling of bone and periodontal ligament (PDL) in the compression side and tension side responding to mechanical stimuli and root resorption. Lastly, we talked about the clinical implications of the updated OTM mechanisms, regarding optimal orthodontic force (OOF), acceleration of OTM, and prevention of root resorption.
Subject(s)
Humans , Osteoblasts , Osteoclasts , Periodontal Ligament , Periodontium , Root Resorption , Tooth Movement TechniquesABSTRACT
ABSTRACT Objective This study aimed to investigate the potential role of CAMK II pathway in the compression-regulated OPG expression in periodontal ligament cells (PDLCs). Material and Methods The PDL tissue model was developed by 3-D culturing human PDLCs in a thin sheet of poly lactic-co-glycolic acid (PLGA) scaffolds, which was subjected to static compression of 25 g/cm2 for 3, 6 and 12 h, with or without treatment of KN-93. After that, the expression of OPG, RANKL and NFATC2 was investigated through real-time PCR and western blot analysis. Results After static compression, the NFATC2 and RANKL expression was significantly up-regulated, while partially suppressed by KN-93 for 6 and 12 h respectively. The OPG expression was significantly down-regulated by compression in 3 h, started to elevate in 6 h, and significantly up-regulated in 12 h. The up-regulation after 12 h was significantly suppressed by KN-93. Conclusions Long-term static compression increases OPG expression in PDLCs, at least partially, via the CAMK II pathway.
Subject(s)
Humans , /metabolism , Osteogenesis/physiology , Osteoprotegerin/metabolism , Periodontal Ligament/cytology , Benzylamines/pharmacokinetics , Blotting, Western , Bone Resorption/metabolism , Cells, Cultured , Down-Regulation , NFATC Transcription Factors/metabolism , Pressure , Protein Kinase Inhibitors/pharmacokinetics , RANK Ligand/analysis , RANK Ligand/metabolism , Random Allocation , Real-Time Polymerase Chain Reaction , Sulfonamides/pharmacokinetics , Time Factors , Up-RegulationABSTRACT
Objective To evaluate the effectiveness of Typodont-based table clinic competition (TCC) on undergraduate orthodontic education. Methods Students who have finished basic orthodon-tic courses made diagnosis,treatment strategy and performed orthodontic treatment for malocclusion cases on Typodonts. A self-design questionnaire was employed to investigate their perception to this pedagogy. Results The majority of participants(82.2%-92.9%) highly evaluated Typodont-based TCC. Conclu-sions Typodont-based TCC course is conducive to arousing students' study internets and to promoting association between theory and practice.