Relationship of destructive periodontal disease to the acute-phase response.
Mots clés
Abstrait
BACKGROUND
Destructive periodontal diseases have been associated with an increased risk of atherosclerotic complications; however, the potential mechanisms are yet to be defined. Inflammation plays a central role in atherosclerosis since C-reactive protein (CRP), an acute-phase protein monitored as a marker of inflammatory status, has been identified as a major risk factor for atherosclerotic complications. Recent reports that destructive periodontal diseases can increase CRP values present the possibility that the acute-phase response may link these 2 disease processes. The objective of the present investigation was to determine the effect of destructive periodontal disease status, severity, and progression on components of the acute-phase response in an urban minority population.
METHODS
Clinical measurements recorded included probing depth, attachment level, gingival erythema, bleeding upon probing, suppuration, and plaque. Disease progression was defined as a >2 mm loss of attachment 2 months post-baseline. Serum antibody was measured by enzyme-linked immunosorbent assay. CRP was measured using a high-sensitivity CRP (hsCRP) assay. A commercial laboratory measured serum glucose (non-fasting), albumin, cholesterol, high-density lipoprotein (HDL), triglycerides, low-density lipoprotein (LDL), and iron.
RESULTS
Increased serum IgG antibody to Porphyromonas gingivalis, but not to 5 other species, was associated with periodontal disease status, increased severity, and progression as were age, male gender, and smoking. Cholesterol and LDL were increased in disease, and HDL and iron were increased in health. hsCRP, glucose, and cholesterol increased with disease progression. By regression analysis, IgG antibody to P. gingivalis correlated with age, probing depth, and hsCRP, and negatively correlated with albumin and iron. By logistic regression, subjects who experienced multiple sites of disease progression and elevated antibody to P. gingivalis increased the odds ratio of hsCRP>2.08 mg/l by 14.1 and 5.6, respectively.
CONCLUSIONS
These results suggest that destructive periodontal disease and disease progression are associated with changes in serum components consistent with an acute-phase response.
