title: Soluble cytokine receptor treatment in experimental orthodontic tooth movement in the rat.
abstract: Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-alpha), are believed to play a role in the biological processes involved in the course of orthodontic tooth movement and especially in root resorption. The inhibition of cytokine activity, e.g. by soluble receptors, could be beneficial in reducing this unwanted side-effect. The aim of this study was to investigate the role of cytokines IL-1 and TNF-alpha in the course of experimentally induced tooth movement. The upper left first molar was moved orthodontically in 80 male Wistar rats using a coil spring with a force of 0.5 N. Starting at day -1, three groups of 20 animals each received daily intraperitoneal injections (ip) of 2 ml of 1 mug/ml soluble receptors (a) to IL-1(sIL-RII), (b) to TNF-alpha (sTNF-alpha-RI) and (c) a combination of (a) and (b). Twenty animals served as the control. After 3, 6, 9 and 12 days, the animals were killed in groups of five. The amount of tooth movement was registered and the maxillae were prepared for histological and histomorphometric analysis. Osteoclasts and odontoclasts were identified using tartrate-resistant acid phosphatase (TRAP) histochemistry. The amount of tooth movement was reduced in all receptor-treated groups by approximately 50 per cent. At the same time, the number of TRAP-positive cells on the desmodontal bone surface and on the surface of the roots was reduced. Thus, systemic application of soluble receptors to IL-1 and TNF-alpha following experimental induction of tooth movement in the rat reduced the number of osteoclasts as well as odontoclasts.
authors.affiliation: Department of Orthodontics, University of Bonn, Germany.
authors.forename: Andreas
authors.initials: A
authors.lastname: Jäger
authors.forename: Dongliang
authors.initials: D
authors.lastname: Zhang
authors.forename: Afshar
authors.initials: A
authors.lastname: Kawarizadeh
authors.forename: Rene
authors.initials: R
authors.lastname: Tolba
authors.forename: Bert
authors.initials: B
authors.lastname: Braumann
authors.forename: Stefan
authors.initials: S
authors.lastname: Lossdörfer
authors.forename: Werner
authors.initials: W
authors.lastname: Götz
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D007274:Injections, Intraperitoneal; D007375:Interleukin-1 / Q000502:physiology; D007527:Isoenzymes / Q000032:analysis; D008297:Male; D008437:Maxilla / Q000473:pathology; D008963:Molar / Q000473:pathology; D009804:Odontoblasts / Q000473:pathology; D009969:Orthodontic Wires; D010010:Osteoclasts / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D017472:Receptors, Interleukin-1 / Q000008:administration & dosage / Q000627:therapeutic use*; D053574:Receptors, Interleukin-1 Type II; D018124:Receptors, Tumor Necrosis Factor / Q000008:administration & dosage / Q000627:therapeutic use*; D012391:Root Resorption / Q000473:pathology / Q000517:prevention & control; D000071681:Tartrate-Resistant Acid Phosphatase; D013997:Time Factors; D014087:Tooth Movement Techniques / Q000295:instrumentation; D014092:Tooth Root / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D015415:Biomarkers; D007375:Interleukin-1; D007527:Isoenzymes; D017472:Receptors, Interleukin-1; D053574:Receptors, Interleukin-1 Type II; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase