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Article: Periodontitis and atherogenesis: Causal association or simple coincidence? A pilot intervention study

TitlePeriodontitis and atherogenesis: Causal association or simple coincidence? A pilot intervention study
Authors
KeywordsInflammation
Periodontitis
Periodontal medicine
IL-6
CRP
Clinical trial
Issue Date2004
Citation
Journal of Clinical Periodontology, 2004, v. 31, n. 5, p. 402-411 How to Cite?
AbstractObjectives: The aim of this study was to assess the systemic effects of treating severe widespread periodontitis in a population of otherwise healthy individuals by examining treatment associated changes in markers of inflammation that are also implicated in cardiovascular atherosclerotic diseases. The potential impact of specific polymorphisms in cytokine genes known to influence both periodontitis and cardiovascular diseases was also examined. Materials and Methods: A convenience sample of patients affected with severe generalised periodontitis was enrolled into a prospective single blind longitudinal intervention trial with a 6 months follow-up. Serum C-reactive protein (CRP) and interleukin-6 (IL-6) levels were assessed by high-sensitivity assays. Serological and clinical periodontal parameters were evaluated at baseline, 2 and 6 months after completion of non-surgical periodontal therapy. Results: In the 94 subjects that completed this pilot trial improvements in all clinical periodontal parameters were achieved. These were accompanied with significant reductions in serum IL-6 and CRP concentrations. In a multivariate model, serum CRP levels were significantly associated with the outcome of periodontal treatment after correcting for potential covariates (age, body mass index, gender, smoking) and polymorphisms in the IL-6 (-174 C/G) and IL-1A (-889) genes. A median decrease in serum CRP of 0.5 mg/1 (95% CI 0.4-0.7 mg/l) was observed 6 months after completion of periodontal therapy in this population. Subjects with above average response to periodontal therapy (<30 residual pockets and <30% of sites bleeding on probing) accounted for the observed improvement in serum CRP. Conclusions: Control of periodontitis, achieved with non-surgical periodontal therapy, significantly decreased serum mediators and markers of acute phase response. The significance of the serum response was associated with the half of the population that responded better to non-surgical periodontal therapy. The results of this pilot study indicate that severe generalised periodontitis causes systemic inflammation. This is consistent with a causative role of periodontitis in atherogenesis. © Blackwell Munksgaard, 2004.
Persistent Identifierhttp://hdl.handle.net/10722/230744
ISSN
2023 Impact Factor: 5.8
2023 SCImago Journal Rankings: 2.249
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorD'Aiuto, Francesco-
dc.contributor.authorParkar, Mohammed-
dc.contributor.authorAndreou, Georgios-
dc.contributor.authorBrett, Peter M.-
dc.contributor.authorReady, Derren-
dc.contributor.authorTonetti, Maurizio S.-
dc.date.accessioned2016-09-01T06:06:42Z-
dc.date.available2016-09-01T06:06:42Z-
dc.date.issued2004-
dc.identifier.citationJournal of Clinical Periodontology, 2004, v. 31, n. 5, p. 402-411-
dc.identifier.issn0303-6979-
dc.identifier.urihttp://hdl.handle.net/10722/230744-
dc.description.abstractObjectives: The aim of this study was to assess the systemic effects of treating severe widespread periodontitis in a population of otherwise healthy individuals by examining treatment associated changes in markers of inflammation that are also implicated in cardiovascular atherosclerotic diseases. The potential impact of specific polymorphisms in cytokine genes known to influence both periodontitis and cardiovascular diseases was also examined. Materials and Methods: A convenience sample of patients affected with severe generalised periodontitis was enrolled into a prospective single blind longitudinal intervention trial with a 6 months follow-up. Serum C-reactive protein (CRP) and interleukin-6 (IL-6) levels were assessed by high-sensitivity assays. Serological and clinical periodontal parameters were evaluated at baseline, 2 and 6 months after completion of non-surgical periodontal therapy. Results: In the 94 subjects that completed this pilot trial improvements in all clinical periodontal parameters were achieved. These were accompanied with significant reductions in serum IL-6 and CRP concentrations. In a multivariate model, serum CRP levels were significantly associated with the outcome of periodontal treatment after correcting for potential covariates (age, body mass index, gender, smoking) and polymorphisms in the IL-6 (-174 C/G) and IL-1A (-889) genes. A median decrease in serum CRP of 0.5 mg/1 (95% CI 0.4-0.7 mg/l) was observed 6 months after completion of periodontal therapy in this population. Subjects with above average response to periodontal therapy (<30 residual pockets and <30% of sites bleeding on probing) accounted for the observed improvement in serum CRP. Conclusions: Control of periodontitis, achieved with non-surgical periodontal therapy, significantly decreased serum mediators and markers of acute phase response. The significance of the serum response was associated with the half of the population that responded better to non-surgical periodontal therapy. The results of this pilot study indicate that severe generalised periodontitis causes systemic inflammation. This is consistent with a causative role of periodontitis in atherogenesis. © Blackwell Munksgaard, 2004.-
dc.languageeng-
dc.relation.ispartofJournal of Clinical Periodontology-
dc.subjectInflammation-
dc.subjectPeriodontitis-
dc.subjectPeriodontal medicine-
dc.subjectIL-6-
dc.subjectCRP-
dc.subjectClinical trial-
dc.titlePeriodontitis and atherogenesis: Causal association or simple coincidence? A pilot intervention study-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1600-051X.2004.00580.x-
dc.identifier.pmid15086624-
dc.identifier.scopuseid_2-s2.0-2442605651-
dc.identifier.volume31-
dc.identifier.issue5-
dc.identifier.spage402-
dc.identifier.epage411-
dc.identifier.isiWOS:000220839500012-
dc.identifier.issnl0303-6979-

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