ABSTRACT
Background: This study aimed to assess the prevalence of apical periodontitis (AP) and its association with the presence/quality of root canal filling (RCF) and coronal restoration (CR) in Iraqi population. Material and Methods: A total of 385 CBCT scans of patients (18-45) yrs. old with 9250 teeth were examined. The teeth were grouped according to the presence/absence of apical radiolucency, presence/radiographic quality of RCF, and CR. Chi-square and Kappa were used to assess associations and intra-consensus reliability. Logistic regression was used to predict risk factors associated with AP. The significant level was set at p<0.05. Results: AP was prevalent in 17.7 and 80.2% of teeth without RCT and with RCT (p<0.05), respectively. AP in root canal-treated teeth with missed canals (93.2%) was higher than that in root canal-treated teeth with no missing canal (78.3%) (p<0.05). AP in teeth with inadequate RCF (87%) was higher than that in teeth with adequate RCF (63%) (P<0.05). No difference in the prevalence of AP in teeth with adequate vs inadequate CR ((79.7%) vs (81%), respectively) (p>0.05). The presence of AP was significantly associated with inadequate RCF (vs adequate RCF) (OR=4.16, CI 95% 2.29-7.56, P<0.05), and was not associated with inadequate CR (vs adequate CR) (OR=-0.71, CI 95% 0.35-1.42, P>0.05). Intra-consensus reliability was (0.9) for AP and (0.82) for RCF and CR quality. Conclusions: AP was highly prevalent in teeth with previous root canal filling compared to non-treated teeth. AP was significantly associated with inadequacy of root canal filling but not with the inadequacy of coronal restoration. Key words:Apical periodontitis, cone beam computed tomography, root canal treatment, endodontics.
ABSTRACT
Metabolism of cancer cells is characterized by aerobic glycolysis, or the Warburg effect. Aerobic glycolysis reduces pyruvate flux into mitochondria, preventing a complete oxidation of glucose and shunting glucose to anabolic pathways essential for cell proliferation. Here we tested a new strategy, mitochondrial uncoupling, for its potential of antagonizing the anabolic effect of aerobic glycolysis and for its potential anticancer activities. Mitochondrial uncoupling is a process that facilitates proton influx across the mitochondrial inner membrane without generating ATP, stimulating a futile cycle of acetyl- CoA oxidation. We tested two safe mitochondrial uncouplers, NEN (niclosamide ethanolamine) and oxyclozanide, on their metabolic effects and anti-cancer activities. We used metabolomic NMR to examine the effect of mitochondrial uncoupling on glucose metabolism in colon cancer MC38 cells. We further tested the anti-cancer effect of NEN and oxyclozanide in cultured cell models, APCmin/+ mouse model, and a metastatic colon cancer mouse model. Using a metabolomic NMR approach, we demonstrated that mitochondrial uncoupling promotes pyruvate influx to mitochondria and reduces various anabolic pathway activities. Moreover, mitochondrial uncoupling inhibits cell proliferation and reduces clonogenicity of cultured colon cancer cells. Furthermore, oral treatment with mitochondrial uncouplers reduces intestinal polyp formation in APCmin/+ mice, and diminishes hepatic metastasis of colon cancer cells transplanted intrasplenically. Our data highlight a unique approach for targeting cancer cell metabolism for cancer prevention and treatment, identified two prototype compounds, and shed light on the anti-cancer mechanism of niclosamide.
