Periodontitis-associated up-regulation of systemic inflammatory mediator level may increase the risk of coronary heart disease.
OBJECTIVE
Although an elevation in the concentration of high-sensitivity C-reactive protein (hs-CRP) as a result of periodontal infection may account for an increased risk of developing coronary heart disease (CHD), the effect of periodontal infection on the level of hs-CRP in an otherwise healthy Japanese population has not yet been reported. The aim of the present study was to confirm, on a larger scale, our previous pilot study findings that both chronic periodontitis and subsequent periodontal treatment alter the serum levels of C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).


METHODS
The concentrations of serum hs-CRP, IL-6 and TNF-alpha were measured in 78 periodontitis patients at baseline and at re-assessment, and in 40 periodontally healthy subjects at the time of examination.


RESULTS
The concentrations of hs-CRP and IL-6 in the sera of periodontitis patients were significantly higher than those in control subjects. By contrast, the concentration of TNF-alpha was significantly lower in periodontitis patients than in control subjects. Whereas periodontal treatment decreased the levels of serum hs-CRP and IL-6, no such effect was observed for TNF-alpha. When the patients were subdivided into four groups according to their initial concentration of hs-CRP, only the CRP and IL-6 concentrations of the highest quartile group showed a significant reduction following periodontal treatment. No significant difference in the initial clinical parameters was observed in any quartile.


CONCLUSIONS
Although periodontal infection does affect the concentration of hs-CRP and IL-6 in serum, a subgroup of patients exist who are highly susceptible to an increased risk of CHD associated with periodontitis, suggesting that there may be subjects who have an elevated risk of CHD independent of susceptibility to periodontal tissue destruction per se.
Nakajima
T
T
Laboratory of Periodontology and Immunology, Department of Oral Health and Welfare, Niigata University Faculty of Dentistry, Niigata, Japan.
Honda
T
T
Domon
H
H
Okui
T
T
Kajita
K
K
Ito
H
H
Takahashi
N
N
Maekawa
T
T
Tabeta
K
K
Yamazaki
K
K
D016301:Alveolar Bone Loss / Q000097:blood / Q000145:classification; D002097:C-Reactive Protein / Q000032:analysis; D055113:Chronic Periodontitis / Q000097:blood* / Q000145:classification / Q000628:therapy; D003327:Coronary Disease / Q000209:etiology*; D012534:Dental Scaling; D004198:Disease Susceptibility; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D017622:Periodontal Attachment Loss / Q000097:blood / Q000145:classification; D010514:Periodontal Pocket / Q000097:blood / Q000145:classification; D012307:Risk Factors; D016745:Root Planing; D012907:Smoking; D013524:Surgical Flaps; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D015854:Up-Regulation / Q000502:physiology*
D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein