| 1. |
- Tonetti, Maurizio S, et al.
(författare)
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Periodontitis and atherosclerotic cardiovascular disease : consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases
- 2013
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Ingår i: Journal of periodontology. - 1943-3670. ; 84:4 Suppl, s. S24-S29
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: This consensus report is concerned with the association between periodontitis and atherosclerotic cardiovascular disease (ACVD). Periodontitis is a chronic multifactorial inflammatory disease caused by microorganisms and characterized by progressive destruction of the tooth supporting apparatus leading to tooth loss; as such, it is a major public health issue.AIMS: This report examined biological plausibility, epidemiology and early results from intervention trials. PLAUSIBILITY: Periodontitis leads to entry of bacteria in the blood stream. The bacteria activate the host inflammatory response by multiple mechanisms. The host immune response favors atheroma formation, maturation and exacerbation. Epidemiology: In longitudinal studies assessing incident cardiovascular events, statistically significant excess risk for ACVD was reported in individuals with periodontitis. This was independent of established cardiovascular risk factors. The amount of the adjusted excess risk varies by type of cardiovascular outcome and across populations by age and gender. Given the high prevalence of periodontitis, even low to moderate excess risk is important from a public health perspective. Intervention: There is moderate evidence that periodontal treatment: (i) reduces systemic inflammation as evidenced by reduction in C-reactive protein (CRP) and improvement of both clinical and surrogate measures of endothelial function; but (ii) there is no effect on lipid profiles--supporting specificity. Limited evidence shows improvements in coagulation, biomarkers of endothelial cell activation, arterial blood pressure and subclinical atherosclerosis after periodontal therapy. The available evidence is consistent and speaks for a contributory role of periodontitis to ACVD. There are no periodontal intervention studies on primary ACVD prevention and there is only one feasibility study on secondary ACVD prevention.CONCLUSIONS: It was concluded that: (i) there is consistent and strong epidemiologic evidence that periodontitis imparts increased risk for future cardiovascular disease; and (ii) while in vitro, animal and clinical studies do support the interaction and biological mechanism, intervention trials to date are not adequate to draw further conclusions. Well-designed intervention trials on the impact of periodontal treatment on prevention of ACVD hard clinical outcomes are needed.
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| 2. |
- Tonetti, Maurizio S, et al.
(författare)
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Periodontitis and atherosclerotic cardiovascular disease : consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases
- 2013
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Ingår i: Journal of Periodontology. - : John Wiley & Sons Inc.. - 1943-3670 .- 0022-3492. ; 84:4 Suppl, s. S24-S29
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: This consensus report is concerned with the association between periodontitis and atherosclerotic cardiovascular disease (ACVD). Periodontitis is a chronic multifactorial inflammatory disease caused by microorganisms and characterized by progressive destruction of the tooth supporting apparatus leading to tooth loss; as such, it is a major public health issue. AIMS: This report examined biological plausibility, epidemiology and early results from intervention trials. PLAUSIBILITY: Periodontitis leads to entry of bacteria in the blood stream. The bacteria activate the host inflammatory response by multiple mechanisms. The host immune response favors atheroma formation, maturation and exacerbation. Epidemiology: In longitudinal studies assessing incident cardiovascular events, statistically significant excess risk for ACVD was reported in individuals with periodontitis. This was independent of established cardiovascular risk factors. The amount of the adjusted excess risk varies by type of cardiovascular outcome and across populations by age and gender. Given the high prevalence of periodontitis, even low to moderate excess risk is important from a public health perspective. Intervention: There is moderate evidence that periodontal treatment: (i) reduces systemic inflammation as evidenced by reduction in C-reactive protein (CRP) and improvement of both clinical and surrogate measures of endothelial function; but (ii) there is no effect on lipid profiles--supporting specificity. Limited evidence shows improvements in coagulation, biomarkers of endothelial cell activation, arterial blood pressure and subclinical atherosclerosis after periodontal therapy. The available evidence is consistent and speaks for a contributory role of periodontitis to ACVD. There are no periodontal intervention studies on primary ACVD prevention and there is only one feasibility study on secondary ACVD prevention. CONCLUSIONS: It was concluded that: (i) there is consistent and strong epidemiologic evidence that periodontitis imparts increased risk for future cardiovascular disease; and (ii) while in vitro, animal and clinical studies do support the interaction and biological mechanism, intervention trials to date are not adequate to draw further conclusions. Well-designed intervention trials on the impact of periodontal treatment on prevention of ACVD hard clinical outcomes are needed.
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| 3. |
- Hudson, Thomas J., et al.
(författare)
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International network of cancer genome projects
- 2010
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 464:7291, s. 993-998
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Tidskriftsartikel (refereegranskat)abstract
- The International Cancer Genome Consortium (ICGC) was launched to coordinate large-scale cancer genome studies in tumours from 50 different cancer types and/or subtypes that are of clinical and societal importance across the globe. Systematic studies of more than 25,000 cancer genomes at the genomic, epigenomic and transcriptomic levels will reveal the repertoire of oncogenic mutations, uncover traces of the mutagenic influences, define clinically relevant subtypes for prognosis and therapeutic management, and enable the development of new cancer therapies.
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| 4. |
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| 5. |
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| 6. |
- Panezai, Jeneen, et al.
(författare)
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Periodontal Disease Augments Cardiovascular Disease Risk Biomarkers in Rheumatoid Arthritis
- 2022
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Ingår i: Biomedicines. - : MDPI. - 2227-9059. ; 10:3
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: Periodontal disease (PD) and rheumatoid arthritis (RA) are known chronic conditions with sustained inflammation leading to osteolysis. Cardiovascular diseases (CVD) are frequent comorbidities that may arise from sustained inflammation associated with both PD and RA. In order to determine CVD risk, alterations at the molecular level need to be identified. The objective of this study, therefore, was to assess the relationship of CVD associated biomarkers in RA patients and how it is influenced by PD.METHODS: The study consisted of patient (26 RA with PD, 21 RA without PD, 51 patients with PD only) and systemically and periodontally healthy control (n = 20) groups. Periodontal parameters bleeding on probing, probing pocket depth, and marginal bone loss were determined to characterize the patient groups. Proteomic analysis of 92 CVD-related protein biomarkers was performed using a multiplex proximity extension assay. Biomarkers were clustered using the search tool for retrieval of interacting genes (STRING) to determine protein-protein interaction (PPI) networks.RESULTS: RA patients with PD had higher detection levels for 47% of the measured markers (ANGPT1, BOC, CCL17, CCL3, CD4, CD84, CTRC, FGF-21, FGF-23, GLO1, HAOX1, HB-EGF, hOSCAR, HSP 27, IL16, IL-17D, IL18, IL-27, IL6, LEP, LPL, MERTK, MMP12, MMP7, NEMO, PAPPA, PAR-1, PARP-1, PD-L2, PGF, PIgR, PRELP, RAGE, SCF, SLAMF7, SRC, THBS2, THPO, TNFRSF13B, TRAIL-R2, VEGFD, VSIG2, and XCL1) as compared to RA without PD. Furthermore, a strong biological network was identified amongst these proteins (clustering coefficient = 0.52, PPI enrichment p-value < 0.0001). Coefficients for protein clusters involved in CVD (0.59), metabolic (0.53), and skeletal (0.51) diseases were strongest in the PD group.CONCLUSION: Periodontal disease augments CVD-related biomarkers in RA through shared pathological clusters, concurrently enhancing metabolic and skeletal disease protein interactions, independent of autoimmune status.
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| 7. |
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| 8. |
- Socransky, Sigmund S, et al.
(författare)
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Effect of periodontal therapy on the subgingival microbiota over a 2-year monitoring period. I. Overall effect and kinetics of change.
- 2013
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Ingår i: Journal of clinical periodontology. - : Wiley. - 1600-051X .- 0303-6979. ; 40:8, s. 771-780
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Tidskriftsartikel (refereegranskat)abstract
- AIM: To examine the 2-year post-therapy kinetics of change in the composition of subgingival biofilms. MATERIAL AND METHODS: In this study, 178 chronic periodontitis subjects were recruited and clinically monitored at baseline, 3, 6, 12, 18 and 24months after therapy. All subjects received scaling and root planing and 156 one or more of periodontal surgery, systemically administered amoxicillin+metronidazole or local tetracycline at pockets ≥5mm. Subgingival biofilm samples taken from each subject at each time point were analysed for their content of 40 bacterial species using checkerboard DNA-DNA hybridization. The significance of changes in median species counts over time was sought using the Wilcoxon or Friedman tests and adjusted for multiple comparisons. RESULTS: Mean counts were significantly reduced from baseline to 2years for 30 of the 40 taxa. Marked reductions were observed for periodontal pathogens including Tannerella forsythia, Treponema denticola and Eubacterium nodatum. The kinetics of change differed from species to species. When data were subset according to baseline PD, patterns of change in the microbial profiles were generally similar. CONCLUSION: Periodontal therapy leads to a rapid reduction in periodontal pathogens, followed by a slower reduction in other taxa that can be sustained for at least 2years.
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| 9. |
- Tanner, Anne C R, et al.
(författare)
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Clinical characteristics and microbiota of progressing slight chronic periodontitis in adults.
- 2007
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Ingår i: Journal of Clinical Periodontology. - 0303-6979 .- 1600-051X. ; 34:11, s. 917-930
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Tidskriftsartikel (refereegranskat)abstract
- AIM: This study sought clinical and microbial risk indicators for progressing slight periodontitis. MATERIAL AND METHODS: One hundred and seventeen periodontally healthy or slight periodontitis adults (20-40 years) were monitored clinically at 6-month intervals followed by supragingival cleaning. Inter-proximal sites with >1.5 mm increase in clinical attachment over 18 months were considered disease active. Subgingival plaque was analysed by 78 16S rDNA and 38 whole-genomic DNA probes and by PCR to Porphyromonas gingivalis and Tannerella forsythia. Characteristics were compared between active and inactive subjects. RESULTS: Twenty-two subjects showed disease activity principally at molars. Mean baseline gingival and plaque indices, bleeding on probing, probing depth and clinical attachment level (CAL) were higher in active subjects. DNA probes detected species and not-yet-cultivated phylotypes from chronic periodontitis, although few species were associated with active subjects. By PCR P. gingivalis (p=0.007) and T. forsythia (p=0.075) were detected more frequently during monitoring in active subjects. Stepwise logistic analysis associated baseline levels of gingival index, clinical attachment and bleeding with subsequent clinical attachment loss. CONCLUSIONS: Gingivitis and CAL were significantly associated with progressing slight periodontitis in 20--40-year-old adults. Species associated with moderate and advanced chronic periodontitis were detected in slight periodontitis.
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| 10. |
- Tanner, Anne C R, et al.
(författare)
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Subgingival and tongue microbiota during early periodontitis.
- 2006
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Ingår i: Journal of Dental Research. - : SAGE Publications. - 0022-0345 .- 1544-0591. ; 85:4, s. 318-323
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Tidskriftsartikel (refereegranskat)abstract
- Periodontal infections have a microbial etiology. Association of species with early disease would be useful in determining which microbes initiate periodontitis. We hypothesized that the microbiota of subgingival and tongue samples would differ between early periodontitis and health. A cross-sectional evaluation of 141 healthy and early periodontitis adults was performed with the use of oligonucleotide probes and PCR. Most species differed in associations with sample sites; most subgingival species were associated with subgingival samples. Few species were detected more frequently in early periodontitis by DNA probes. Porphyromonas gingivalis and Tannerella forsythia (Tannerella forsythensis) were associated with early periodontitis by direct PCR. In conclusion, the microbiota of tongue samples was less sensitive than that of subgingival samples in detecting periodontal species, and there was overlap in species detected in health and early periodontitis. Detection of periodontal pathogens in early periodontitis suggests an etiology similar to that of more advanced disease.
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