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ORIGINAL RESEARCH Table of Contents   
Year : 2010  |  Volume : 21  |  Issue : 3  |  Page : 326-329
Evaluation of the C-reactive protein serum levels in periodontitis patients with or without atherosclerosis


Department of Periodontics and Implantology, Sharad Pawar Dental College, Deemed University, Sawangi (Meghe), Wardha - 442 001, Maharashtra, India

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Date of Submission19-Jun-2009
Date of Decision05-Sep-2009
Date of Acceptance01-Oct-2009
Date of Web Publication29-Sep-2010
 

   Abstract 

Background : Several studies suggested an association between periodontal disease and cardiovascular disease (CVD). C- reactive protein is elevated in periodontitis patients and has been found to be a predictor of increased risk for cardiovascular disease. Since, CRP is known to play a role in pathogenesis of atherosclerosis, the present study was undertaken to evaluate the serum levels of CRP in periodontitis patients with or without atherosclerosis.
Materials and Methods : A total of 45 patients, 15 chronic periodontitis patients with atherosclerosis (Group A), 15 chronic periodontitis patients with no history of any systemic disease (Group B), and 15 clinically healthy individuals with no history of periodontal or systemic disease (Group C) within age range of 30 to 55 years were selected for the study. PI, PBI, PPD, CAL and radiographic marginal alveolar bone level were assessed in all the three groups. CRP levels were assessed with 'Turbi-latex' kit using turbidimetric analysis.
Results : The mean CAL recorded was 4.9mm in group A, 4.6mm in group B and 1.9 mm in group C. The mean radiographic marginal bone level was 45 to 50% in group A, 45 to 50% in group B and 90 to 95% in group C. Mean serum C-reactive protein level was significantly higher in group A (8.9 mg/l), as compared to group B (4.9 mg/l) as well as group C (0.9 mg/l).
Conclusion : Within the limits of this study it was concluded that periodontitis may add to the inflammatory burden of the individual and may result in increased risk of atherosclerosis based on serum C-reactive protein concentrations.

Keywords: Atherosclerosis, C-reactive protein, periodontitis

How to cite this article:
Thakare KS, Deo V, Bhongade ML. Evaluation of the C-reactive protein serum levels in periodontitis patients with or without atherosclerosis. Indian J Dent Res 2010;21:326-9

How to cite this URL:
Thakare KS, Deo V, Bhongade ML. Evaluation of the C-reactive protein serum levels in periodontitis patients with or without atherosclerosis. Indian J Dent Res [serial online] 2010 [cited 2019 Dec 6];21:326-9. Available from: http://www.ijdr.in/text.asp?2010/21/3/326/70787
Periodontal disease is an infectious disease characterized by an inflammation and destruction of supporting tissues of the teeth in response to subgingival gram negative anaerobes. Gram negative anaerobes are present in large numbers in subgingival dental plaque in periodontal pockets. Endotoxins derived from gram negative microorganisms interact with toll like receptors (TLR) expressed on the surface of neutrophils and monocytes, which are abundant in periodontal inflammation. TLR-ligand complexes activate signal transduction pathways in both the innate and adaptive immune systems leading to the production of cytokines, which co-ordinate the local and systemic inflammatory response. [1] Pro-inflammatory cytokines originating at the site of local pathology activate hepatocytes to produce acute phase proteins including C-reactive protein (CRP) [2] and this forms part of the non specific response. Atherosclerosis is a progressive vascular disease characterized by patchy sub intimal thickening (atheroma formation) of large to medium sized muscular and large elastic arteries. [3] Recent evidences suggest that even a moderate increase in CRP levels, such as those found in periodontitis patients, may predict a risk of atherosclerosis and cardiovascular diseases. The mechanism by which CRP participates in cardiovascular diseases is not clear; however, CRP may activate the complement system and may be involved in foam cell formation in atheromas. [4] Experimental studies have shown that CRP binds to ligands exposed in damaged tissues and then activates complement which may lead to complement mediated exacerbation of tissue injury. [5] There is an increasing evidence that chronic infections as well as inflammatory mechanisms play a major role in atherogenesis and cardiovascular diseases. [6] Several studies suggested an association between periodontal disease and atherosclerosis. [7] Direct and indirect host mediated effects of infectious agents may be responsible for the association between periodontitis and atherosclerosis. It is intriguing that among other infectious agents, periodontal pathogens such as Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Tannerella forsythensis, and  Prevotella intermedia Scientific Name Search ave been found in human atherosclerotic plaques. [8] Epidemiological studies have shown that levels of acute phase proteins including CRP are increased in otherwise healthy adults with poor periodontal status. [9] It has been hypothesized that any association between periodontitis and cardiovascular disease could be due to moderate increases in CRP reported in subjects with poor periodontal health. [10] In a study conducted by Beck, [11] it was observed that severe periodontitis was associated with 1.31 times odds of intima media thickness ≥ 1mm as compared with no periodontitis. The present study was undertaken to investigate the correlation between clinical parameters and serum levels of CRP in chronic periodontitis patients with or without atherosclerosis and healthy patients, to show a possible association between periodontitis and cardiovascular diseases.


   Materials and Methods Top


Fifteen chronic periodontitis patients with angiographically proven atherosclerosis in the age group of 30 - 55 years (mean age 44.56±0.11years) were selected from the general medicine ward of A. V. B. R. Hospital, Wardha. Atherosclerosis was defined as the intima media wall thickening > 1.2mm in carotid arteries and presence of calcified plaque in coronary and carotid arteries. There were 30 systemically healthy age matched patients; 15 of them with moderate to severe chronic periodontitis and 15 periodontally healthy patients (controls) were selected from department of periodontics, S. P. D. College, Wardha. Chronic periodontitis patients showed radiographic evidence of marginal alveolar bone loss ≥ 30%, affecting at least 50% of dentition and clinical attachment loss ≥ 4mm at a minimum of six sites. The following patients were excluded from the study:

  • Patients with a history of diabetes
  • History and/or presence of any other systemic infection.
  • Treatment with any medication known to affect the serum level of inflammatory markers (e.g. non-steroidal anti-inflammatory drugs)
  • Patients on any medication that could affect the manifestation of periodontal disease, such as chronic antibiotic use, phenytoin, cyclosporine, anti-inflammatory drugs, calcium channel blockers or corticosteroids
  • Smokers or users of any tobacco products
  • Patients treated by periodontal therapy in past six months
  • Pregnant females or lactating mothers


Prior to initiation, the purpose and design of study was explained to patients and an informed consent form was signed by every patient. Study protocol was approved by research and ethical committee of D.M.I.M.S, Wardha. The present study was a randomized, parallel design with a total of 45 patients in the age group of 30-55 years distributed into three groups. The first group included healthy individuals (controls, group A), second group included patients with chronic periodontitis only (group B), and third group included patients with chronic periodontitis and atherosclerosis (group C).

Periodontal disease status was determined using clinical and radiographic criteria. Clinical evaluation was based on full mouth plaque index (PI), [12] papillary bleeding index (PBI), [13] probing pocket depth (PPD) at six sites per tooth and clinical attachment level (CAL) at four sites per tooth. Radiographic alveolar bone level was assessed using standard orthopantomograph (O.P.G.).

If the presence of the alveolar bone from cementoenamel junction to root apex can be considered as about 100% alveolar bone present, alveolar bone level was quantified according to the existing alveolar bone level up to the root apex on the O.P.G. For example, if the alveolar bone level was at the level near coronal two-third, the existing bone level was considered to be 65-70 %. Similarly, if the alveolar bone level was near the mid-root region, the existing bone level was considered to be 50-55 %. Average alveolar bone level for each group was calculated by summation of alveolar bone level in each patient in the group divided by the total number of patients in the group.

For CRP level estimation of all patients, fasting blood samples were collected from each patient at the time of clinical examination in the plain bulb without any anticoagulant. Samples with the presence of fibrin were centrifuged before testing for separation of serum from plasma protein. CRP serum level of each patient was quantified using a commercial high sensitivity CRP-Turbilatex kit.

Statistical analysis

The mean and standard deviation (Mean±SD) values were calculated for all clinical parameters and C-reactive protein levels. The mean data were analyzed for the statistical significance by standard statistical method. Student's unpaired t-test was used to compare data of the three groups.


   Results Top


A total of 45 patients in the age group of 30-55 years participated in the study and were distributed into three groups. The first group (group A) served as a control group with 15 healthy individuals (nine male and six female) with a mean age of 39.56±0.07 years. Group B consisted of 15 chronic periodontitis patients (nine male and six female) and a mean age of 40.12±0.07 years. The third group consisted of 15 chronic periodontitis and atherosclerosis patients (seven males and eight females) with a mean age of 44.56±0.11 years. The demographic data is summarized in [Table 1].
Table 1 :Demographic characteristics of the patients


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Group A (control group) showed mean PI score of 0.091±0.07, mean PBI score of 0.87±0.11, mean PPD 1.76±0.13 mm, mean CAL 1.76±0.13 mm, mean radiographic marginal bone level 85 - 90% (89.66±2.47) and mean serum CRP levels 0.94±0.18 mg/L [Table 1]. Patients in this group showed good oral hygiene and satisfactory gingival condition.

Group B (Chronic Periodontitis [CP] only) showed mean PI score of 2. 41±0.91, mean PBI score of 2.26±0.15, mean PPD 5.11±0.37 mm, mean CAL 5.47±0.38 mm, mean radiographic marginal bone level 40 - 45% (43.50±4.98) and mean serum CRP levels 4.36±0.53 mg/L [Table 2]. The mean PI, PBI, PPD, CAL, radiographic marginal bone levels and serum CRP were compared between group A and group B using student's unpaired t - test. There were statistically significant differences in PI (1.22±0.05), PBI (1.39±0.05), PPD (3.34±0.10), CAL (3.70±0.10), radiographic marginal bone level (-46.16±1.43) and serum CRP levels (3.41±0.14) [Table 2].
Table 2 :Comparison of clinical parameters, radiographic bone level and serum CRP levels between different groups (Mean±SD)


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Group C (chronic periodontitis and atherosclerosis [CP+ATH]) showed mean PI score of 2.42±0.27, mean PBI score of 2.37±0.25, mean PPD 5.30±0.71 mm, mean CAL 5.67±0.79 mm, mean radiographic marginal bone level 35 - 40% (39.16±5.56) and mean serum CRP levels 8.02±1.23 mg/L [Table 2]. The mean PI, PBI, PPD, CAL, radiographic marginal bone levels and serum CRP were compared between group A and group C using student's unpaired t - test. There were statistically significant differences in PI (1.50±0.07), PBI (1.50±0.07), PPD (3.53±0.18), CAL (3.90±0.20), radiographic marginal bone level (-50.50±1.57) and serum CRP levels (7.07±0.32) [Table 2].

Results showed significant and positive correlations among all clinical parameters, radiographic marginal bone level and serum CRP levels.


   Discussion Top


Several cross sectional and longitudinal epidemiological studies are consistent in reporting that periodontitis patients are at higher risk for cardiovascular diseases including coronary artery diseases and stroke. The association is hypothesized to be linked to direct effects of periodontal pathogens or indirect host mediated effects triggered by infection. [14],[15] Systemic inflammatory host responses in periodontitis are suggested to be one of the possible underlying mechanisms of this relationship. [15] CRP and other acute phase molecules possess a wide variety of functions, including pro-inflammatory properties, activation of complement factors, neutralization of invasive pathogens, stimulation of repair, and regeneration of a variety of tissues. CRP represents an emerging and reliable marker of acute phase response to infectious burdens and/or inflammation. [16]

Several recent studies have emphasized that even moderately elevated CRP serum levels are predictors of increased risk of cardiovascular disease among apparently healthy individuals. [17] Chronic bacterial infections such as periodontitis are one of the established risk factors for moderately elevated CRP. [18] Previous studies [19],[20] have demonstrated that CRP levels are higher in periodontitis patients than in periodontally healthy subjects and that serum CRP levels are higher in patients with more severe periodontitis.

In the present study, values of CRP in patients with periodontal disease were compared with healthy controls. A very sensitive method (Turbidimetric analysis) was used to detect CRP (compared to other methods). The detection limit is 0.80 mg/L compared to 3.0 mg/L as reported minimum detectable concentration of turbidimetric analysis.

Recently, Salzberg et al, [21] reported that patients with aggressive periodontitis had elevated serum concentrations of CRP. Similar to their findings, results of the present study showed that serum CRP levels were higher in periodontitis patients with or without atherosclerosis than in periodontally healthy subjects. These results suggest a positive correlation between severity of periodontal disease and CRP level. Previous investigations have reported similar results. In two recent epidemiological studies, Slade et al, [18] and Wu et al, [15] showed a significant correlation between periodontal status and prevalence of elevated CRP levels. Fredriksson et al[22] and Ebersole et al, [19] reported higher CRP serum concentrations in periodontitis patients in comparison with controls. The latter study reported about 9 mg/L, roughly twice of what was observed in the present study. This discrepancy could be caused by investigation of more severe periodontitis cases in their study. In addition to chronic infections, CRP serum concentrations are reported to be positively correlated with age, smoking, body mass index (BMI) or lipid parameters. [23],[24] Therefore, these potential confounding parameters were excluded in the present study.

The results of the present study confirmed the outcomes of recent investigations which reported an elevation of CRP levels in periodontitis patients. Recently, Buhlin et al, [25] reported significant association between periodontitis and high levels of C-reactive protein (CRP) [odds ratio - 4.0). Based on the results of their study, Buhlin et al, [25] concluded that periodontitis is associated with increased levels of CRP. A strong relationship between increased serum CRP and presence of chronic periodontitis with cardiovascular disease is demonstrated in the present study as well. CRP levels were significantly higher in chronic periodontitis patients with cardiovascular disease group when compared to chronic periodontitis group. These findings point to an association between periodontal infection and cardiovascular disease. Several underlying mechanisms for these observations are possible.

Periodontal diseases are infections characterized by inflammation and destruction of the supporting tissues of affected teeth. [26] Gram negative anaerobes are present in large numbers in subgingival plaque in periodontal pockets. Low levels of bacteremia, endotoxins derived from gram negative microorganisms and other bacterial components may provide a stimulus for systemic inflammatory responses such as increased production of CRP due to activation of the cascade of inflammatory cytokine production by monocytes and other cells in the periodontal tissue and elsewhere. [27] In a very recent study, CRP proved to be the strongest and more significant predictor of the risk of future cardiovascular events amongst several plasma variables. [28]

The results presented in this study suggest that elevated CRP values in periodontitis patients with or without cardiovascular diseases could contribute at least in part to the increased risk for cardiovascular disease associated with elevated CRP levels in these patients. Further studies are required to determine the effects of antimicrobial periodontal therapy on systemic inflammatory mediators and the increased risk for cardiovascular diseases. The study also had several limitations. Firstly, small sample size limited the statistical analysis of the study. Also, microbial assay was not performed; so the effect of bacterial endotoxins on cytokine mediated CRP production could not be assessed.


   Conclusions Top


From the analysis of the results, and within the limitations of the study, it can be concluded that chronic periodontitis patients, both with and without atherosclerosis, showed significantly greater serum CRP levels compared to healthy controls and chronic periodontitis group with atherosclerosis showed almost double fold increase in serum CRP levels compared to chronic periodontitis without atherosclerosis group. Chronic periodontitis should be considered a significant risk factor for developing atherosclerotic lesions and therefore should be treated accordingly.

 
   References Top

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Correspondence Address:
Vikas Deo
Department of Periodontics and Implantology, Sharad Pawar Dental College, Deemed University, Sawangi (Meghe), Wardha - 442 001, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-9290.70787

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    Tables

  [Table 1], [Table 2]

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