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Periodontitis and atherogenesis: causal association or simple coincidence?
Author(s) -
D'Aiuto Francesco,
Parkar Mohammed,
Andreou Georgios,
Brett Peter M.,
Ready Derren,
Tonetti Maurizio S.
Publication year - 2004
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.2004.00580.x
Subject(s) - medicine , periodontitis , c reactive protein , gastroenterology , body mass index , population , bleeding on probing , periodontal examination , chronic periodontitis , clinical attachment loss , prospective cohort study , inflammation , environmental health
Objectives: 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/l (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.