Purpose To evaluate the kinetics of
apical periodontitis development in vivo , induced either by contamination of the root canals by microorganisms from the oral cavity or by inoculation of bacterial
lipopolysaccharide (LPS) and the regulation of major
enzymes and receptors involved in the
arachidonic acid metabolism. Methodology
Apical periodontitis was induced in C57BL6 mice (n=96), by root canal exposure to oral cavity (n=48 teeth) or inoculation of LPS (10 µL of a
suspension of 0.1 µg/µL) from E. coli into the root canals (n= 48 teeth). Healthy teeth were used as control (n=48 teeth). After 7, 14, 21 and 28 days the animals were euthanized and tissues removed for histopathological and qRT-PCR analyses. Histological analysis data were analyzed using two-way ANOVA followed by Sidak's test, and qRT-PCR data using two-way ANOVA followed by Tukey's test (α=0.05). Results Contamination by microorganisms led to the development of
apical periodontitis, characterized by the recruitment of inflammatory cells and bone tissue resorption, whereas inoculation of LPS induced inflammatory cells recruitment without
bone resorption. Both stimuli induced
mRNA expression for
cyclooxygenase-2 and
5-lipoxygenase enzymes. Expression of
prostaglandin E 2 and
leukotriene B 4 cell surface receptors were more stimulated by LPS. Regarding nuclear
peroxisome proliferator-activated receptors (
PPAR), oral contamination induced the synthesis of
mRNA for PPARδ, differently from inoculation of LPS, that induced PPARα and PPARγ expression. Conclusions Contamination of the root canals by microorganisms from oral cavity induced the development of
apical periodontitis differently than by inoculation with LPS, characterized by less bone loss than the first model. Regardless of the model used, it was found a local increase in the synthesis of
mRNA for the
enzymes 5-lipoxygenase and
cyclooxygenase-2 of the
arachidonic acid metabolism, as well as in the surface and
nuclear receptors for the
lipid mediators
prostaglandin E2 and
leukotriene B4.