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.
The objective of this study was to determine the ecological relationships between bacterial species that colonize infected root canals. Root canal bacteria recovered from one patient with pulp canal necrosis were evaluated in vitro for synergistic and antagonistic activities determined by mono and co-culture growth kinetics and the production of bacteriocin-like substances using the double layer diffusion method.Peptostreptococcus prevotii triggered a significant increase of Fusobacterium nucleatum growth, while the former bacteria did not affect the growth of P. prevotii. The bacterial species did not produce antagonism activity against itself or against any of the other two species. Despite many studies have demonstrated the capability of root canal microorganisms to produce antagonistic substances, these in vitro experimental tests show the synergistic effect of P. prevotii on the growth of F. nucleatum.
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