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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

iNOS-Derived Nitric Oxide Stimulates Osteoclast Activity and Alveolar Bone Loss in Ligature-Induced Periodontitis in Rats

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Author(s):
Herrera, Bruno S. [1] ; Martins-Porto, Rodrigo [1] ; Maia-Dantas, Aline [1] ; Campi, Paula [1] ; Spolidorio, Luis C. [1] ; Costa, Soraia K. P. [1] ; Van Dyke, Thomas E. [2] ; Gyurko, Robert [2] ; Muscara, Marcelo N. [1]
Total Authors: 9
Affiliation:
[1] State Univ Sao Paulo, Dept Physiol & Pathol, Araraquara Dent Sch, BR-14801590 Araraquara, SP - Brazil
[2] Boston Univ, Dept Periodontol & Oral Biol, Goldman Sch Dent Med, Boston, MA 02215 - USA
Total Affiliations: 2
Document type: Journal article
Source: Journal of Periodontology; v. 82, n. 11, p. 1608-1615, NOV 2011.
Web of Science Citations: 33
Abstract

Background: Inflammatory stimuli activate inducible nitric oxide synthase (iNOS) in a variety of cell types, including osteoclasts (OC) and osteoblasts, resulting in sustained NO production. In this study, we evaluate the alveolar bone loss in rats with periodontitis under long-term iNOS inhibition, and the differentiation and activity of OC from iNOS-knockout (KO) mice in vitro. Methods: Oral aminoguanidine (an iNOS inhibitor) or water treatment was started 2 weeks before induction of periodontitis. Rats were sacrificed 3, 7, or 14 days after ligature placement, and alveolar bone loss was evaluated. In vitro OC culture experiments were also performed to study the differentiation of freshly isolated bone marrow cells from both iNOS KO and wild-type C57BL/6 mice. OC were counted 6 days later after tartrate-resistant acid phosphatase staining (a marker of osteoclast identity), and bone resorption activity was assessed by counting the number of resorption pits on dentin disks. Results: Rats with ligature showed progressive and significant alveolar bone loss compared to sham animals, and aminoguanidine treatment significantly inhibited ligature-induced bone loss at 7 and 14 days after the induction. In comparison to bone marrow cells from wild-type mice, cells from iNOS KO mice showed decreased OC growth and the resulting OC covered a smaller culture dish area and generated fewer resorption pit counts. Conclusion: Our results demonstrate that iNOS inhibition prevents alveolar bone loss in a rat model of ligature-induced periodontitis, thus confirming that iNOS-derived NO plays a crucial role in the pathogenesis of periodontitis, probably by stimulating OC differentiation and activity. J Periodontol 2011;82:1608-1615. (AU)

FAPESP's process: 08/02893-4 - Set-up and standardization of human osteoblast and osteoclast cell cultures as tools for the study of the mechanisms involved in the alveolar bone loss secondary to periodontitis
Grantee:Bruno Schneider Herrera
Support Opportunities: Scholarships in Brazil - Post-Doctoral