title: Increased bone loss and amount of osteoclasts in kinin B1 receptor knockout mice.
abstract: OBJECTIVE
  The pathophysiology of periodontal diseases involves aspects of immunity and bone remodelling. Considering the role of the kinin B1 receptor (Bdkrb1) in inflammation and healing, the purpose of this study was to evaluate the contribution of Bdkrb1 to the pathogenesis of periodontitis.
  
  
  METHODS
  We used a model of ligature-induced experimental periodontitis (LIEP) in mice lacking Bdkrb1 (Bdkrb1(-/-) ) to test the role of this receptor in bone loss and cytokine secretion by lymph nodes cells. Angiotensin-converting enzyme inhibitor (ACEi) was used as a pharmacological strategy to support the genetic model. Also, autonomous effect of Bdkrb1 deletion was evaluated in osteoclasts precursors from bone marrow.
  
  
  RESULTS
  Bdkrb1(-/-) mice exhibit increased bone loss and IL-17 secretion in response to LIEP when compared to wild type. LIEP does not modify TNF-α, IFN-γ and IL-10 levels in Bdkrb1(-/-) mice after 21 days. Bone marrow cells from Bdkrb1(-/-) displayed increased differentiation into functional osteoclasts with consistent artificial calcium phosphate degradation. Furthermore, treatment of mice with ACEi prevented bone destruction.
  
  
  CONCLUSIONS
  Bdkrb1 participates in the pathogenesis of LIEP bone loss possibly through mechanisms that involve modulation of the TH 17 response, thereby demonstrating its role in the development of periodontitis.
authors.affiliation: Departamento de Biofísica, Universidade Federal de São Paulo, São Paulo, Brazil.
authors.forename: Thais Oliveira
authors.initials: TO
authors.lastname: Gonçalves-Zillo
authors.forename: Lívia Souza
authors.initials: LS
authors.lastname: Pugliese
authors.forename: Vicência Micheline Toledo
authors.initials: VM
authors.lastname: Sales
authors.forename: Marcelo Alves da Silva
authors.initials: MA
authors.lastname: Mori
authors.forename: Carla Cristina
authors.initials: CC
authors.lastname: Squaiella-Baptistão
authors.forename: Ieda Maria
authors.initials: IM
authors.lastname: Longo-Maugéri
authors.forename: José Daniel
authors.initials: JD
authors.lastname: Lopes
authors.forename: Suzana Macedo
authors.initials: SM
authors.lastname: de Oliveira
authors.forename: Ana Carolina
authors.initials: AC
authors.lastname: Monteiro
authors.forename: João Bosco
authors.initials: JB
authors.lastname: Pesquero
mesh_terms: D016301:Alveolar Bone Loss / Q000209:etiology / Q000473:pathology* / Q000517:prevention & control; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D001854:Bone Marrow Cells / Q000473:pathology; D002130:Calcium Phosphates / Q000378:metabolism; D002452:Cell Count; D002454:Cell Differentiation / Q000502:physiology; D048430:Cell Shape; D002478:Cells, Cultured; D004656:Enalapril / Q000627:therapeutic use; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010010:Osteoclasts / Q000473:pathology*; D010518:Periodontitis / Q000209:etiology* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D043783:Receptor, Bradykinin B1 / Q000235:genetics / Q000502:physiology*; D013601:T-Lymphocytes / Q000502:physiology; D058504:Th17 Cells / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D002130:Calcium Phosphates; C556062:IL10 protein, mouse; D020381:Interleukin-17; D043783:Receptor, Bradykinin B1; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D004656:Enalapril; D007371:Interferon-gamma; C020243:calcium phosphate