iNOS -derived Nitric Oxide Modulates Infection-stimulated Bone Loss

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Abstract
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-1α (SDF-1α/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.