Increased bone loss and amount of osteoclasts in kinin B1 receptor knockout mice

Author(s)

Goncalves-Zillo, Thais Oliveira ^[1] ; Pugliese, Livia Souza ^[2] ; Toledo Sales, Vicencia Micheline ^[1] ; da Silva Mori, Marcelo Alves ^[1] ; Squaiella-Baptistao, Carla Cristina ^[3] ; Longo-Maugeri, Ieda Maria ^[2] ; Lopes, Jose Daniel ^[2] ; de Oliveira, Suzana Macedo ^[1] ; Monteiro, Ana Carolina ^[4] ; Pesquero, Joao Bosco ^[1]

Affiliation

^[1] Univ Fed Sao Paulo, Dept Biofis, BR-04039032 Sao Paulo - Brazil

^[2] Univ Fed Sao Paulo, Dept Microbiol Imunol & Parasitol, Disciplina Imunol, BR-04039032 Sao Paulo - Brazil

^[3] Inst Butantan, Lab Imunoquim, Sao Paulo - Brazil

^[4] MEDEX, Inst Nacl Canc CPQ, Rio De Janeiro - Brazil

• Document type: Journal article
• Source: JOURNAL OF CLINICAL PERIODONTOLOGY; v. 40, n. 7, p. 653-660, JUL 2013.
• Web of Science Citations: 15

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. (AU)

• FAPESP's process: 08/06676-8 - Cellular and molecular biology of the kallikrein-kinin and renin-angiotensin systems
• Grantee: João Bosco Pesquero
• Support Opportunities: Research Projects - Thematic Grants