title: Orally administered liposomal lactoferrin inhibits inflammation-related bone breakdown without interrupting orthodontic tooth movement.
abstract: BACKGROUND
  Bovine lactoferrin (bLF) modulates the production of tumor necrosis factor-alpha (TNF-α) and inhibits alveolar bone breakdown associated with periodontitis. This study is designed to examine the effects of orally administered liposomal bLF (LbLF) on orthodontic force (OF)-induced alveolar bone remodeling during experimental tooth movement.
  
  
  METHODS
  Two groups of male Wistar rats were treated with either LbLF or control solution in drinking water 7 days before OF application. Lipopolysaccharide (LPS) was injected into the gingival sulcus in half the rats in each group. Thus, four groups: OF, OF+LbLF, OF+LPS, and OF+LPS+LbLF were established.
  
  
  RESULTS
  Orally administered LbLF significantly reduced apical migration of junctional epithelium in the OF and OF+LPS groups. In OF+LPS, osteoclast number in the alveolar crestal area was increased by LPS treatment, whereas osteoclast number was significantly reduced in OF+LPS+LbLF through suppression of TNF-α production. Osteoclastic induction in the middle part, mainly from OF application, was not affected by LbLF administration. Inhibition of tooth movement was not induced by LbLF.
  
  
  CONCLUSIONS
  Orally administered LbLF significantly inhibits LPS-induced alveolar bone resorption but not OF-induced bone remodeling. LbLF could be a potent therapeutic and preventive agent to control periodontal inflammation in patients undergoing orthodontic treatment.
authors.affiliation: Department of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Kawazoe
authors.forename: T
authors.initials: T
authors.lastname: Inubushi
authors.forename: M
authors.initials: M
authors.lastname: Miyauchi
authors.forename: A
authors.initials: A
authors.lastname: Ishikado
authors.forename: E
authors.initials: E
authors.lastname: Tanaka
authors.forename: K
authors.initials: K
authors.lastname: Tanne
authors.forename: T
authors.initials: T
authors.lastname: Takata
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000284:Administration, Oral; D016301:Alveolar Bone Loss / Q000473:pathology / Q000517:prevention & control; D000539:Alveolar Process / Q000187:drug effects* / Q000473:pathology; D000818:Animals; D000890:Anti-Infective Agents / Q000008:administration & dosage*; D016723:Bone Remodeling / Q000187:drug effects*; D002417:Cattle; D002452:Cell Count; D004846:Epithelial Attachment / Q000187:drug effects / Q000473:pathology; D004926:Escherichia coli; D007527:Isoenzymes / Q000032:analysis; D007781:Lactoferrin / Q000008:administration & dosage*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008081:Liposomes; D008297:Male; D010010:Osteoclasts / Q000187:drug effects; D010518:Periodontitis / Q000473:pathology / Q000517:prevention & control; D010865:Pilot Projects; D053245:RANK Ligand / Q000032:analysis; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013314:Stress, Mechanical; D000071681:Tartrate-Resistant Acid Phosphatase; D019237:Tooth Cervix / Q000473:pathology; D014087:Tooth Movement Techniques / Q000379:methods*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000890:Anti-Infective Agents; D007527:Isoenzymes; D008070:Lipopolysaccharides; D008081:Liposomes; D053245:RANK Ligand; D014409:Tumor Necrosis Factor-alpha; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; D007781:Lactoferrin