title: The role of iNOS and PHOX in periapical bone resorption.
abstract: Nitric oxide (NO) and reactive oxygen species (ROS) are key molecules in resistance to pathogens. Little is known about their role in pathogenesis of periapical lesions. To address this issue, we induced periapical lesions in mice lacking nitric oxide synthase (iNOS(-/-)) or phagocyte oxidase (PHOX(-/-)). iNOS(-/-) mice expressed higher levels of IL-1β, TNF-α, RANK, RANKL, and MCP-1 than C57BL/6 and PHOX(-/-). Apical thickening of the periodontal ligament was also greater in iNOS(-/-) compared with other groups. Interestingly, ROS production did not interfere in periapical lesion progression, but seemed to be essential for the appearance of multinucleated TRAP-positive cells. Thus, periapical lesion progression in iNOS(-/-) was associated with an imbalance of pro-inflammatory cytokines (IL-1β and TNF-α), bone-resorptive modulators (RANK and RANKL), and MCP-1. We conclude that NO, but not ROS, controls progression of bone resorption in a murine experimental model of apical periodontitis.
authors: Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, CP 486, 30161-970 Belo Horizonte, MG, Brazil.
authors: M J B
authors: MJ
authors: Silva
authors: L M A
authors: LM
authors: Sousa
authors: V P L
authors: VP
authors: Lara
authors: F P
authors: FP
authors: Cardoso
authors: G M
authors: GM
authors: Júnior
authors: A H
authors: AH
authors: Totola
authors: M V
authors: MV
authors: Caliari
authors: O B
authors: OB
authors: Romero
authors: G A B
authors: GA
authors: Silva
authors: A P
authors: AP
authors: Ribeiro-Sobrinho
authors: L Q
authors: LQ
authors: Vieira
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D016301:Alveolar Bone Loss / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D018932:Chemokine CCL2 / Q000032:analysis; D016207:Cytokines / Q000032:analysis; D004195:Disease Models, Animal; D018450:Disease Progression; D018836:Inflammation Mediators / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D007527:Isoenzymes / Q000032:analysis; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D019255:NADPH Oxidases / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology; D052247:Nitric Oxide Synthase Type II / Q000502:physiology*; D010485:Periapical Periodontitis / Q000201:enzymology* / Q000473:pathology; D010513:Periodontal Ligament / Q000201:enzymology / Q000473:pathology; D010586:Phagocytes / Q000201:enzymology*; D053245:RANK Ligand / Q000032:analysis; D017382:Reactive Oxygen Species / Q000494:pharmacology; D053246:Receptor Activator of Nuclear Factor-kappa B / Q000032:analysis; D000071681:Tartrate-Resistant Acid Phosphatase; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D015415:Biomarkers; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D016207:Cytokines; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D007527:Isoenzymes; D053245:RANK Ligand; D017382:Reactive Oxygen Species; D053246:Receptor Activator of Nuclear Factor-kappa B; C505687:Tnfrsf11a protein, mouse; C505689:Tnfsf11 protein, mouse; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D019255:NADPH Oxidases; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase