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iNOS -derived Nitric Oxide Modulates Infection-stimulated Bone Loss

¹ Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Av. Bandeirantes 3900, Monte Alegre, 14049-900, Ribeirão Preto SP, São Paulo, Brazil;
² Department of Oral Surgery and Pathology, School of Dentistry, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil;
³ Department of Biological Sciences, School of Dentistry of Bauru, University of São Paulo, Bauru, São Paulo, Brazil;
⁴ Department of Microbiology, Institute of Biomedical Sciences, University of Sao Paulo, São Paulo, Brazil; and
⁵ Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil

Correspondence: ^* corresponding author, fdqcunha{at}fmrp.usp.br

Nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) plays an important role in host defense, as well as in inflammation-induced tissue lesions. Here we evaluated the role of NO in bone loss in bacterial infection-induced apical periodontitis by using iNOS-deficient mice (iNOS^–/–). The iNOS^–/– mice developed greater inflammatory cell recruitment and osteolytic lesions than WT mice. Moreover, tartrate-resistant acid-phosphatase-positive (TRAP⁺) osteoclasts were significantly more numerous in iNOS^–/– mice. Furthermore, the increased bone resorption in iNOS^–/– mice also correlated with the increased expression of receptor activator NF-kappaB (RANK), stromal-cell-derived factor-1 (SDF-1/CXCL12), and reduced expression of osteoprotegerin (OPG). These results show that NO deficiency was associated with an imbalance of bone-resorption-modulating factors, leading to severe infection-stimulated bone loss.

Key Words: Nitric oxide • osteoclastogenesis • RANK • RANKL • OPG • SDF-1/CXCL12

Journal of Dental Research, Vol. 87, No. 12, 1155-1159 (2008)
DOI: 10.1177/154405910808701207


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