Association between hypertension, oral microbiome and salivary nitric oxide: A case-control study

Nitric Oxide ◽  
2021 ◽  
Vol 106 ◽  
pp. 66-71
Author(s):  
Pamela Barbadoro ◽  
Elisa Ponzio ◽  
Erminia Coccia ◽  
Emilia Prospero ◽  
Andrea Santarelli ◽  
...  
Gut ◽  
2016 ◽  
Vol 67 (1) ◽  
pp. 120-127 ◽  
Author(s):  
Xiaozhou Fan ◽  
Alexander V Alekseyenko ◽  
Jing Wu ◽  
Brandilyn A Peters ◽  
Eric J Jacobs ◽  
...  

ObjectiveA history of periodontal disease and the presence of circulating antibodies to selected oral pathogens have been associated with increased risk of pancreatic cancer; however, direct relationships of oral microbes with pancreatic cancer have not been evaluated in prospective studies. We examine the relationship of oral microbiota with subsequent risk of pancreatic cancer in a large nested case–control study.DesignWe selected 361 incident adenocarcinoma of pancreas and 371 matched controls from two prospective cohort studies, the American Cancer Society Cancer Prevention Study II and the National Cancer Institute Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. From pre-diagnostic oral wash samples, we characterised the composition of the oral microbiota using bacterial 16S ribosomal RNA (16S rRNA) gene sequencing. The associations between oral microbiota and risk of pancreatic cancer, controlling for the random effect of cohorts and other covariates, were examined using traditional and L1-penalised least absolute shrinkage and selection operator logistic regression.ResultsCarriage of oral pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, were associated with higher risk of pancreatic cancer (adjusted OR for presence vs absence=1.60 and 95% CI 1.15 to 2.22; OR=2.20 and 95% CI 1.16 to 4.18, respectively). Phylum Fusobacteria and its genus Leptotrichia were associated with decreased pancreatic cancer risk (OR per per cent increase of relative abundance=0.94 and 95% CI 0.89 to 0.99; OR=0.87 and 95% CI 0.79 to 0.95, respectively). Risks related to these phylotypes remained after exclusion of cases that developed within 2 years of sample collection, reducing the likelihood of reverse causation in this prospective study.ConclusionsThis study provides supportive evidence that oral microbiota may play a role in the aetiology of pancreatic cancer.


2008 ◽  
Vol 158 (5) ◽  
pp. 615-622 ◽  
Author(s):  
Fatma Sen ◽  
Mustafa Demirturk ◽  
Neslihan Abaci ◽  
Ebru Golcuk ◽  
Huseyin Oflaz ◽  
...  

ObjectiveEndothelial nitric oxide synthase (eNOS) intron 4a/b polymorphism is associated with plasma NO concentrations and coronary artery disease/hypertension in various populations. GH deficiency in adulthood predisposes to reduced NO concentrations and premature atherosclerosis. Our aim was to determine whether intron 4a/b polymorphism of eNOS gene influences endothelial function and early atherosclerotic changes in GH-deficient hypopituitary patients.DesignThirty-three hypopituitary GH-deficient patients on conventional replacement therapy other than GH and 43 age-, sex-, and body mass index (BMI)-matched controls were studied in this cross-sectional case–control study.MethodsEarly atherosclerotic changes were determined by flow-mediated dilation (FMD) of brachial artery and carotid artery intima-media thickness (IMT). eNOS4a/b polymorphism was detected by PCR.ResultsHypopituitary patients had significantly higher total/low-density lipoprotein cholesterol and fat mass and lower IGF-I concentrations compared with controls. IMT was significantly higher in patients (0.777±0.23 vs 0.639±0.17 mm, P<0.01). No significant difference was observed with respect to FMD measurements. eNOS4a/b genotype frequencies were similar between patients and controls. Patients carrying ‘a’ allele (a/a and a/b) had significantly higher IMT compared with controls carrying ‘a’ allele and bb genotype (P<0.05). However, logistic regression analysis revealed that presence of hypopituitarism, age≥45 years, and BMI≥27.9 kg/m2 were significant independent predictors of IMT≥0.65 mm.ConclusionNo compelling data are evident to suggest that eNOS4a/b polymorphism modifies the atherosclerotic process in GH-deficient situations. A large case–control study is needed to confirm our findings.


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