Abstract
Background: Periodontitis
is a local inflammatory process mediating destruction of periodontal
tissues triggered by bacterial insult. However, this disease is also
characterized by systemic inflammatory host responses that may
contribute, in part, to the recently reported higher risk for
cardiovascular disease (CVD) among patients with periodontitis. Moderate
elevation of C-reactive protein (CRP) has been found to be a predictor of
increased risk for CVD. Elevated CRP levels in periodontal patients have
been reported by several groups. In this study, we examined whether CRP
plasma levels are increased in periodontitis and if there is a relation
to severity of periodontal disease and to the periodontal microflora.
Methods: CRP serum levels
were assessed using radial immunodiffusion assay in 174 subjects, 59 with
moderate mean clinical attachment loss (AL) (2.39 ± 0.29 mm) and 50 with high AL (3.79 ± 0.86 mm) as compared to 65
periodontally healthy controls (AL, 1.74 ± 0.18 mm). Clinical attachment loss,
probing depths, and percentage of periodontal pocket sites ³5 mm were measured. The presence of periodontal
pathogens Porphyromonas gingivalis (P.g.), Prevotella intermedia
(P.i.), Campylobacter recta (C.r.), and Bacteroides forsythus
(B.f.) in subgingival plaque samples was measured by
immunofluorescence microscopy.
Results: Statistically
significant increases in CRP levels were observed in subjects with
periodontal disease when compared to healthy controls (P = 0.036).
Subjects with high levels of mean clinical attachment loss had
significantly higher mean CRP levels (4.06 ± 5.55 mg/l) than controls
(1.70 ± 1.91 mg/l), P = 0.011. The CRP levels were adjusted for
factors known to be associated with elevated CRP, including age, smoking,
body mass index (BMI), triglycerides, and cholesterol. Age and BMI were
found to be significant covariates. The reported range for CRP as a risk
factor for CVD, peripheral vascular diseases, or stroke is 1.34 mg/l to
6.45 mg/l and the mean of this range is 3 mg/l. The percentage of
subjects with elevated levels of CRP ³ 3 mm was
significantly higher in the high clinical AL group (38%; 95% CI: 26.7%, 49.3%) when compared
to the control group (16.9%; 95% CI: 9.25%, 24.5%), P = 0.011. The
presence of periodontal pathogens P.g., P.i., C.r., and B.f.
in subgingival samples was positively associated with elevated CRP levels
(P = 0.029).
Conclusions: The extent
of increase in CRP levels in periodontitis patients depends on the
severity of the disease after adjusting for age, smoking, body mass
index, triglycerides, and cholesterol. Also, there are elevated levels of
CRP associated with infection with subgingival organisms often associated
with periodontal disease, including P.g., P.i., C.r., and B.f.
Recent investigations emphasized the role of moderate elevated CRP plasma
levels as a risk factor for CVD. The positive correlation between CRP and
periodontal disease might be a possible underlying pathway in the
association between periodontal disease and the observed higher risk for
CVD in these patients. J Periodontol 2001;72:1221-1227.
KEY WORDS
Periodontal diseases/microbiology;
periodontitis/pathogenesis; C-reactive protein; cardiovascular
diseases/etiology; risk factors.
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