Recent evidences indicate that C-reactive protein (CRP) and CRP inducing cytokines may be involved indirectly as well as directly in the development of atherosclerosis and hence can be validated as CVD predictor. It has been proposed that patients with periodontitis may have elevated circulating levels of these inflammatory markers like c-reactive protein and hence increase the risk for atherosclerosis. The aim of this present study was to determine whether the presence of chronic periodontitis and subsequent non surgical periodontal treatment could influence the serum levels of C-reactive protein (CRP). In this study, a total of 60 patients were assessed for the estimation of serum C-reactive protein. The test group included 30 patients with chronic periodontitis and the control group included 30 periodontally healthy individuals. Serum blood samples were collected at baseline for both the groups and three months after therapy for the study group for the estimation of C-reactive protein levels by immunoturbidometric method. It was found that the mean CRP level of the patients with chronic generalized periodontitis was significantly higher than that of the healthy controls and significant reduction in these levels was observed after non surgical therapy. It was also found that there was no statistically significant difference between the post treatment (90th day) CRP levels of chronic generalized periodontitis group and the healthy controls which indicate that the non surgical therapy brought down the CRP levels of chronic periodontitis patients to levels comparable with that of healthy controls.
Periodontal diseases are chronic gram negative oral infections initiated in the gingiva and leading to alveolar bone destruction and gradual loss of tooth supporting connective tissues. Cumulatively these infections affect more than 70% of the general population.1 Recent evidence associates periodontal disease with a higher risk for atherosclerotic plaque formation that could lead to myocardial infarction, ischemic stroke and peripheral arterial disease. Several pathological mechanisms have been proposed to explain this strong association, including the involvement of systemically elevated inflammatory mediators.
C-reactive protein is a well known acute phase reactant produced by the liver in response to diverse inflammatory stimuli including heat, trauma, infection and hypoxia. Their levels provide useful information for the diagnosis, monitoring and therapy of inflammatory process and associated disease.
C-reactive protein has been shown to play a role in the pathogenesis of atherosclerosis through different mechanisms including binding the phosphocholine of oxidized low density lipoproteins, upregulating the expression of adhesion molecules in endothelial cells, increasing low density lipoprotein uptake into macrophages, inhibiting endothelial nitric oxide synthase expression in aortic endothelial cells, and increasing plasminogen activator inhibitor-1 expression and activity.2
Recent studies have demonstrated a correlation between periodontitis and elevated CRP levels. It was found that after controlling for established risk factors, increased levels of CRP persisted among individuals with extensive periodontal disease. In fact, among dentate individuals with extensive periodontal disease, an increase of approximately one third in mean CRP and a doubled prevalence of elevated CRP were found compared to periodontally healthy subjects. It was also observed that subjects with periodontal disease and cardiovascular disease demonstrated higher levels of CRP than subjects with cardiovascular disease and no periodontitis.3 There was also a significant increase in adjusted mean levels of CRP in subjects with high attachment loss when compared to subjects with healthy periodontium.3
Given the results of various studies, if we can say that periodontal infection does contribute significantly to the systemic levels of CRP, then it would follow that periodontal treatment could result in its reduction also and hence decrease the risk for atherosclerosis. Previous studies have shown that periodontal treatment lead to the reduction of serum CRP levels.4
The present study was undertaken to examine the serum levels of CRP in periodontitis and the effect of periodontal treatment on the serum level of this inflammatory marker.
Materials and methods
A total number of 60 subjects with age range of 30-60 years were selected for this study. They were divided into two groups in which Group I: (Control group) consisted of thirty individuals who were free of periodontal disease and GROUP II (test group) consists of thirty individuals who were diagnosed with generalized mild to moderate chronic periodontitis, with 4-6 mm probing pocket depth along with radiographic evidence of bone loss. Patients under medications like antibiotics, corticosteroids, anti-inflammatory drugs and oral contraceptive pills for the past 3 months, systemic diseases, who have undergone periodontal treatment in the last 6 months, smokers and pregnant woman and patients with less than 24 teeth were excluded from the study. The clinical parameters that were assessed at baseline (0 day) and on 90th day were probing pocket depth and clinical attachment level.
0 day (baseline)
The subjects selected for the study (30 patients with chronic periodontitis and 30 healthy controls) were referred to the biochemistry laboratory of for collection of non fasting venous blood for the estimation of C-reactive protein.
On the same day, the test group patients underwent supragingival scaling with ultrasonic (piezoelectric) scalers. The patients were then recalled after one week for subgingival scaling and root planing which was done with the aid of gracey curettes (area specific). Oral hygiene instructions were given to the patients.
The patients were recalled on the 90th day after non surgical therapy (scaling and root planing). The clinical parameters that were assessed at baseline (probing pocket depth and clnical attachment level) were reassessed. The patients were then referred to the biochemistry laboratory for the collection of serum and estimation of CRP.
Estimation of C-reactive protein
5μl of the serum sample was taken and 450μl of reagent 1 and 50μl of reagent 2 were added to it and the absorbance was read from semi automated analyzer. Serum levels of CRP of each patient were quantified using Particle Enhanced Turbidometric Immunoassay (PETIA) technique. The lower and upper detection limits of the kit being 0.1 – 20mg/ml. All the samples were automatically quantified by the computer assisted semi automated biochemical analyzer.
The mean CRP levels of test group were estimated as 3.317mg/l and 2.260mg/l at baseline and 90th day. The mean CRP level of control group at baseline was found to be 1.93mg/l. The comparative analysis of clinical parameters as well the CRP levels were done using various statistical tools and their outcome is shown in the following tables and graphical representations.
Table 1: CRP levels on day 0 and day 90 in group 1 patients
|TIME POINT||N||Mean CRP Level in mg/l||STD DEVIATION||STD ERROR MEAN|
* ‘p’ value< 0.001 (Statistically significant)