title: Local RANKL gene transfer to the periodontal tissue accelerates orthodontic tooth movement.
abstract: It has been reported that not only selective alveolar-bone resorption, but also receptor activator of nuclear factor kappa B ligand (RANKL) expression is induced on the compressed side of an orthodontically moving tooth. Numerous reports have described the pharmacological acceleration of tooth movement (TM) through the activation of osteoclasts. However, because of rapid flush out by blood circulation, daily systemic administration or daily local injection is needed. Previously, we discovered that every-3-days OPG gene transfer to the periodontal-tissue inhibited RANKL-mediated osteoclastogenesis and diminished experimental TM. Therefore, we hypothesized that local RANKL gene transfer into the periodontal tissue would accelerate TM. The upper first molars of 6-week-old male Wistar rats were moved palatally using fixed orthodontic wires. The inactivated hemagglutinating-virus of Japan (HVJ) envelope vector containing the mouse RANKL expression plasmid was injected periodically into the palatal periodontal tissue of the upper first molars during TM. Local RANKL gene transfer significantly enhanced RANKL expression and osteoclastogenesis in periodontal tissue without any systemic effects. The TM rate was significantly increased in the RANKL gene transfer side. In conclusion, we demonstrated that transfer of the RANKL gene to the periodontal-tissue activated osteoclastogenesis and accelerated the amount of experimental TM. Local RANKL gene transfer might be a useful tool not only for shortening orthodontic treatment, but also for moving ankylosed teeth where teeth, fuse to the surrounding bone.
authors.affiliation: Department of Oral Health and Development Sciences, Division of Orthodontics and Dentofacial Orthopedics, Graduate School of Dentistry, Tohoku University, Sendai 980-8575, Japan. kanzaki@mail.tains.tohoku.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Kanzaki
authors.forename: M
authors.initials: M
authors.lastname: Chiba
authors.forename: K
authors.initials: K
authors.lastname: Arai
authors.forename: I
authors.initials: I
authors.lastname: Takahashi
authors.forename: N
authors.initials: N
authors.lastname: Haruyama
authors.forename: M
authors.initials: M
authors.lastname: Nishimura
authors.forename: H
authors.initials: H
authors.lastname: Mitani
mesh_terms: D000818:Animals; D002352:Carrier Proteins / Q000032:analysis / Q000235:genetics* / Q000378:metabolism; D015316:Genetic Therapy / Q000379:methods*; D005822:Genetic Vectors / Q000008:administration & dosage / Q000235:genetics; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis / Q000235:genetics* / Q000378:metabolism; D010010:Osteoclasts / Q000166:cytology; D010012:Osteogenesis; D010519:Periodontium / Q000737:chemistry / Q000378:metabolism*; D053245:RANK Ligand; D051381:Rats; D017208:Rats, Wistar; D053246:Receptor Activator of Nuclear Factor-kappa B; D029082:Sendai virus / Q000235:genetics; D013314:Stress, Mechanical; D014087:Tooth Movement Techniques / Q000379:methods*; D014161:Transduction, Genetic / Q000379:methods*
chemical_list: D002352:Carrier Proteins; D008562:Membrane Glycoproteins; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; C505687:Tnfrsf11a protein, mouse; C505689:Tnfsf11 protein, mouse