title: Osteoclast induction in periodontal tissue during experimental movement of incisors in osteoprotegerin-deficient mice.
abstract: Osteoprotegerin (OPG) is a novel secreted member of the tumor necrosis factor (TNF) receptor superfamily that negatively regulates osteoclastogenesis. The receptor activator of the NFKB ligand (RANKL) is one of the key regulatory molecules in osteoclast formation and binds to OPG. In this study, it was suggested that OPG and RANKL are involved in alveolar bone remodeling during orthodontic tooth movement. We examined RANKL localization and osteoclast induction in periodontal tissues during experimental movement of incisors in OPG-deficient mice. To produce orthodontic force, an elastic band was inserted between the upper right and left incisors for 2 or 5 days, and the dissected maxillae were examined for cytochemical and immunocytochemical localization of tartrate-resistant acid phosphatase (TRAP), vacuolar-type H(+)-ATPase, and RANKL. Compared to wild-type OPG (+/+) littermates, TRAP-positive multinucleated cells were markedly induced in the periodontal ligament (PDL) on the compressed side and in the adjacent alveolar bone of OPG-deficient mice. These multinucleated cells exhibited intense vacuolar-type H(+)-ATPase along the ruffled border membranes. Because of accelerated osteoclastic resorption in OPG-deficient mice, alveolar bone was severely destroyed and partially perforated at 2 and 5 days after force application. In both wild-type and OPG-deficient mice, RANKL expression became stronger at 2 and 5 days after force application than before force application. There was no apparent difference in intensity of RANKL expression between OPG (+/+) littermates and OPG-deficient mice. In both wild-type and OPG-deficient mice, expression of RANKL protein was detected in osteoblasts, fibroblasts, and osteoclasts mostly located in resorption lacunae. These results suggest that during orthodontic tooth movement, RANKL and OPG in the periodontal tissues are important determinants regulating balanced alveolar bone resorption.
authors.affiliation: Department of Orthodontics, School of Dentistry, Showa University, Tokyo, Japan.
authors.forename: Takahiro
authors.initials: T
authors.lastname: Oshiro
authors.forename: Aya
authors.initials: A
authors.lastname: Shiotani
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Shibasaki
authors.forename: Takahisa
authors.initials: T
authors.lastname: Sasaki
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D016723:Bone Remodeling / Q000502:physiology; D002352:Carrier Proteins / Q000032:analysis; D006023:Glycoproteins / Q000172:deficiency* / Q000235:genetics; D007124:Immunoenzyme Techniques; D007180:Incisor / Q000502:physiology; D007527:Isoenzymes / Q000032:analysis; D008562:Membrane Glycoproteins / Q000032:analysis; D051379:Mice; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D010010:Osteoclasts / Q000737:chemistry / Q000166:cytology / Q000502:physiology*; D053244:Osteoprotegerin; D010519:Periodontium / Q000737:chemistry / Q000166:cytology / Q000502:physiology*; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D018160:Receptors, Cytoplasmic and Nuclear / Q000172:deficiency* / Q000235:genetics; D018124:Receptors, Tumor Necrosis Factor / Q000172:deficiency* / Q000235:genetics; D000071681:Tartrate-Resistant Acid Phosphatase; D014087:Tooth Movement Techniques
chemical_list: D002352:Carrier Proteins; D006023:Glycoproteins; D007527:Isoenzymes; D008562:Membrane Glycoproteins; D053244:Osteoprotegerin; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C505687:Tnfrsf11a protein, mouse; C506031:Tnfrsf11b protein, mouse; C505689:Tnfsf11 protein, mouse; D000255:Adenosine Triphosphate; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase