Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/36524
Title: Increased bone loss and amount of osteoclasts in kinin B1 receptor knockout mice
Authors: Gonçalves-Zillo, Thais Oliveira [UNIFESP]
Pugliese, Livia Souza [UNIFESP]
Toledo Sales, Vicencia Micheline [UNIFESP]
Silva Mori, Marcelo Alves da [UNIFESP]
Squaiella-Baptistao, Carla Cristina
Longo-Maugeri, Ieda Maria [UNIFESP]
Lopes, Jose Daniel [UNIFESP]
Oliveira, Suzana Macedo de [UNIFESP]
Monteiro, Ana Carolina
Pesquero, Joao Bosco [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Inst Butantan
MEDEX
Keywords: Bdkrb1
bone loss
kinin
osteoclast
periodontitis
Issue Date: 1-Jul-2013
Publisher: Wiley-Blackwell
Citation: Journal of Clinical Periodontology. Hoboken: Wiley-Blackwell, v. 40, n. 7, p. 653-660, 2013.
Abstract: Aim 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. Material and 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-, IFN- and IL-10 levels in Bdkrb1-/- mice after 21days. 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. Conclusion Bdkrb1 participates in the pathogenesis of LIEP bone loss possibly through mechanisms that involve modulation of the TH17 response, thereby demonstrating its role in the development of periodontitis.
URI: http://repositorio.unifesp.br/handle/11600/36524
ISSN: 0303-6979
Other Identifiers: http://dx.doi.org/10.1111/jcpe.12097
Appears in Collections:Em verificação - Geral

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