Browsing by Author "Petrovic, Sanja Matic (56539393600)"

Objectives: Aiming to show that periodontitis (PD) and type 2 diabetes (T2D) are bidirectionally related and potentially linked by inflammatory cytokines, we searched for association between −308 G/A Tumor necrosis factor-alpha (TNFα), +252A/G Lymphotoxin-alpha (LTα), +36A/G Tumor necrosis factor receptor 1 (TNFR1) and +676 T/G tumor necrosis factor receptor 2 (TNFR2) single nucleotide polymorphisms (SNPs) and: risk of PD or PD + T2D; periodontitis parameters in PD and PD + T2D; serum levels of cytokines/their receptors. Relationship between periodontal inflammation and serum cytokine/receptor levels was also assessed. Design: Subjects were stratified as: 57 healthy controls (HC); 58 PD; 65 PD + T2D. Sociodemographic, environmental, behavioral and periodontal clinical data were recorded. SNPs were genotyped using polymerase chain reaction-restriction fragment length polymorphism, while cytokines/receptors levels were quantified by enzyme-linked immunosorbent assay. Impact of periodontal inflammation was measured using periodontal inflamed surface area (PISA). Results: TNFα AA genotype showed protective effect in T2D + PD compared to PD, even adjusted for behavioral/environmental factors (OR 0.18; 95 %CI 0.037−0.886; p = 0.035). LTα AG heterozygotes had increased risk of PD (OR 3.27; 95 %CI 1.35−7.96; p = 0.016), while TNFR2 TG genotype had protective effect (OR = 0.44; 95 %CI 0.954−0.9794; p = 0.043). TNFR1 AA was predictor of periodontal pocket depth and clinical attachment loss in PD. Correlation between TNFR2 concentration and PISA was negative in PD, positive in PD + T2D. Conclusions: None of the SNPs showed cross-susceptibility between PD and T2D. + 252A/G LTα and +676 T/G TNFR2 SNPs are associated with PD risk. Periodontal destruction in healthy individuals is influenced by TNFR1 genotype. Impact of periodontal on systemic inflammation is masked by T2D. © 2020 Elsevier Ltd

Objectives: Aiming to show that periodontitis (PD) and type 2 diabetes (T2D) are bidirectionally related and potentially linked by inflammatory cytokines, we searched for association between −308 G/A Tumor necrosis factor-alpha (TNFα), +252A/G Lymphotoxin-alpha (LTα), +36A/G Tumor necrosis factor receptor 1 (TNFR1) and +676 T/G tumor necrosis factor receptor 2 (TNFR2) single nucleotide polymorphisms (SNPs) and: risk of PD or PD + T2D; periodontitis parameters in PD and PD + T2D; serum levels of cytokines/their receptors. Relationship between periodontal inflammation and serum cytokine/receptor levels was also assessed. Design: Subjects were stratified as: 57 healthy controls (HC); 58 PD; 65 PD + T2D. Sociodemographic, environmental, behavioral and periodontal clinical data were recorded. SNPs were genotyped using polymerase chain reaction-restriction fragment length polymorphism, while cytokines/receptors levels were quantified by enzyme-linked immunosorbent assay. Impact of periodontal inflammation was measured using periodontal inflamed surface area (PISA). Results: TNFα AA genotype showed protective effect in T2D + PD compared to PD, even adjusted for behavioral/environmental factors (OR 0.18; 95 %CI 0.037−0.886; p = 0.035). LTα AG heterozygotes had increased risk of PD (OR 3.27; 95 %CI 1.35−7.96; p = 0.016), while TNFR2 TG genotype had protective effect (OR = 0.44; 95 %CI 0.954−0.9794; p = 0.043). TNFR1 AA was predictor of periodontal pocket depth and clinical attachment loss in PD. Correlation between TNFR2 concentration and PISA was negative in PD, positive in PD + T2D. Conclusions: None of the SNPs showed cross-susceptibility between PD and T2D. + 252A/G LTα and +676 T/G TNFR2 SNPs are associated with PD risk. Periodontal destruction in healthy individuals is influenced by TNFR1 genotype. Impact of periodontal on systemic inflammation is masked by T2D. © 2020 Elsevier Ltd

Introduction: There is a known connection between periodontitis and atherosclerosis and the presence of periopathogens in blood vessels. However, changes of the oral microflora related to the aging process and its possible effects on atherosclerosis, have yet to be analyzed. The aim of this study was to assess temporal changes in the frequency of periodontal bacteria in the subgingival plaque and in atherosclerotic blood vessels of patients with atherosclerosis. Methodology:The study included 100 patients with atherosclerosis and periodontitis, divided into two groups, below and over 60 years of age. Clinical examinations were performedand subgingival plaque specimens were collected as well as biopsy specimens from the following arteries: coronary (34), carotid (29), abdominal (10), femoral (10), mammary (13) and iliac (4). Subgingival and artery specimens were subjected to PCR detection of 5 major periodontal pathogens: Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Aggregatibacter actinomycetemcomitans (Aa), Tannerella forsythensis (Tf) and Treponema denticola (Td). Results:Tf was the most and Td the least frequent bacteria in both age groups and in both types of samples. The frequencies of bacteria in subgingival versus atherosclerotic samples were: Tf (76%:53%), Pi (71%:31%), Pg (60%:38%), Aa (39%:14%) and Td (21%:6%). Only Aa and Pi showed a significant difference of prevalence between younger and older patients. The most colonized artery was a. coronaria, followed by a. carotis, a. abdominalis, a. mammaria, and a. femoralis. Conclusions: Patient’s age and the distance of a given blood vessel from the oral cavity influenced microbiological findings in the atherotic plaque. © 2018 Kannosh et al.

Introduction: There is a known connection between periodontitis and atherosclerosis and the presence of periopathogens in blood vessels. However, changes of the oral microflora related to the aging process and its possible effects on atherosclerosis, have yet to be analyzed. The aim of this study was to assess temporal changes in the frequency of periodontal bacteria in the subgingival plaque and in atherosclerotic blood vessels of patients with atherosclerosis. Methodology:The study included 100 patients with atherosclerosis and periodontitis, divided into two groups, below and over 60 years of age. Clinical examinations were performedand subgingival plaque specimens were collected as well as biopsy specimens from the following arteries: coronary (34), carotid (29), abdominal (10), femoral (10), mammary (13) and iliac (4). Subgingival and artery specimens were subjected to PCR detection of 5 major periodontal pathogens: Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Aggregatibacter actinomycetemcomitans (Aa), Tannerella forsythensis (Tf) and Treponema denticola (Td). Results:Tf was the most and Td the least frequent bacteria in both age groups and in both types of samples. The frequencies of bacteria in subgingival versus atherosclerotic samples were: Tf (76%:53%), Pi (71%:31%), Pg (60%:38%), Aa (39%:14%) and Td (21%:6%). Only Aa and Pi showed a significant difference of prevalence between younger and older patients. The most colonized artery was a. coronaria, followed by a. carotis, a. abdominalis, a. mammaria, and a. femoralis. Conclusions: Patient’s age and the distance of a given blood vessel from the oral cavity influenced microbiological findings in the atherotic plaque. © 2018 Kannosh et al.