Abstract
PurposeTo 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.MethodologyApical 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).ResultsContamination 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.ConclusionsContamination 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.
Highlights
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
Contamination of root canals after coronary opening to the oral environment led to the development of apical periodontitis, initially characterized by the thickening of the apical periodontal ligament in the period of 7 days, the recruitment of neutrophils and macrophages at 14 days, the presence of bone resorption at 21 days, culminating in intense infiltration of inflammatory cells, edema and extensive periapical bone resorption at 28 days (Figure 1)
Summary
The importance of microorganisms for the genesis of apical periodontitis was demonstrated in a classic study in which the dental pulp, when exposed to the oral environment in a germ-free mice, did not lead to bone loss; whereas in conventional laboratory animals lesions were detected after 15 days of exposure. Until the 1970s, the isolation of microorganisms from root canals demonstrated a predominantly aerobic and anaerobic facultative composition. Subsequently, it was observed that most of the microorganisms present in the infections of the root canal system of teeth with chronic periapical lesions were anaerobes, Gram-negative. Gram-negative bacteria present bacterial lipopolysaccharide (LPS) or endotoxin as a component of the cellular wall, and contain both lipid components and polysaccharide moieties, with lipid A being considered the toxic portion of the molecule. LPS is released during the occurrence of cellular stress, multiplication or bacterial death, stimulating a tissue immune-inflammatory reaction and bone resorption.6,8-10Studies that perform the apical periodontitis induction procedure in their methodology show variations, either by the inoculation of a mixture of pathogens, a single species such as Fusobacterium nucleatum, LPS6 or by the contamination of oral root canals by microorganisms from the oral cavity. De Rossi, et al. (2008) inducted the apical periodontitis by coronary opening, and inoculated a mixture of 4 pathogens (Porphyromonas gingivalis, Prevotella nigrescens, Actinomyces viscosus and Fusobacterium nucleatum subsp.polymorphum) into the root canals; later, the cavity was kept open to the oral environment. De Rossi, et al. (2008) inducted the apical periodontitis by coronary opening, and inoculated a mixture of 4 pathogens (Porphyromonas gingivalis, Prevotella nigrescens, Actinomyces viscosus and Fusobacterium nucleatum subsp.polymorphum) into the root canals; later, the cavity was kept open to the oral environment. In another study, carried out to analyze the effect of calcium hydroxide on bacterial endotoxins, the process of inoculating LPS into the root canal promoted extensive bone resorption.. In another study, carried out to analyze the effect of calcium hydroxide on bacterial endotoxins, the process of inoculating LPS into the root canal promoted extensive bone resorption.6 Notwithstanding, another way of inducing periapical lesion is to perform a coronary opening, remove the pulp tissue and leave the cavity open for contamination by microorganisms from the oral cavity. In another study, carried out to analyze the effect of calcium hydroxide on bacterial endotoxins, the process of inoculating LPS into the root canal promoted extensive bone resorption. Notwithstanding, another way of inducing periapical lesion is to perform a coronary opening, remove the pulp tissue and leave the cavity open for contamination by microorganisms from the oral cavity.
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