CRP and Periodontal Disease - Final Part

CRP and Periodontal Disease - Final Part

Periodontal disease especially in form of chronic periodontitis forms a chronic source of inflammation in any subject. The increased CRP during the periodontal infection can have a dual effect i.e a local and a systemic effect. The local inflammation in the periodontal structure along with the bacterial toxins could drive the CRP levels higher in the local tissues. The role or CRP in the local periodontal environment is quite unclear at this moment, however its role in stimulating the tissue factor and in turning on the humoral immunity may play role in altering the balance between health and disease[1, 2]. The recent invitro and invivo studies regarding CRP causing increased nitric oxide (NO) production[3], affecting the monocyte adhesion[4] and in expression of the adhesion molecules like intercellular adhesion molecules (ICAM) and vascular adhesion molecule (VCAM) support the hypothesis that CRP plays a pro-inflammatory role[5].
I hypothesize that in presence of periodontal disease the subgingival bacteria and its toxins increases the level of the various proteinases, cytokines (Interleukin 6 (IL6) is known to regulate CRP) and acute phase proteins. Increase in acute phase protein of which CRP in specific could act as a proinflammatory factor by expressing the adhesion molecules, and NO production, causing a vicious cycle to build up. Its atherosclerotic effects of CRP could occur in the local vessels which could decrease the total blood flow in the already diseased area. The known affect of CRP in complement binding and humoral response along with its above mentioned actions could exacerbate the already persistent inflammation and thus acting as a cofactor, alter the course of the periodontal disease. (Figure1)[9]

[ Adapted from: Paquette, journal of contemporary dental practice 1999;1: 1-8]

The increase in the CRP during the periodontal infection is seen to emerge as a risk factor with results of various clinical trials associating it with cardiovascular disease and preterm delivery. A recent studyfound that the periodontitis may increase the CRP levels in pregnant women and it could mediate the association of periodontitis with advance pregnancy outcomes[6]. The relationship between cardiovascular disease and periodontitis has been extensively researched in recent times. It is proposed from these studies that the periodontal infection and subsequent release of the proteinases ( matrix metalloprotienases 9) and cytokines (IL6, TNFα) and acute phase proteins ( CRP being one of them) can systemically affect the events like platelet aggregation, thrombus formation and atherogenesis and thus increase the risk for atherosclerosis, coronary heart disease and stroke. A study by Ebersole,[7] showed that periodontal debridement reduced the serum level of CRP and another study by Ridker,[8] have showed that lower serum levels of CRP is associated with reduced risk of myocardial infraction. These studies indirectly support the hypothesis that periodontal treatment can potentially reduce the likelihood of systemic disease[9].
Data regarding CRP and its affect on periodontal disease is insufficient and calls for more studies. However further research is needed to understand the association between periodontal disease, inflammation and its range of effect on the systemic health.

…….So is my own personal view.
All comments, criticism and discussions on the above topic is welcome

1.Saran de Ferranti, Nadir Rifai, C-reactive protein and cardiovascular disease: a review of risk prediction and interventions. Clinical Chimica Acta 2000; 317: 1-15

2.G.M. Hirschfield and M.B. Pepys, C-reactive protein and cardiovascular disease: new insights from an old molecule. Q J Med 2003; 96: 793 – 807.

3.Clapp BR, Inflammation and endothelial function: direct vascular effects of human C-reactive protein on nitric oxide bioavailability, Circulation. 2005;111(12):1530-6.

4.Woollard KJ, Direct modulatory effect of C-reactive protein on primary human monocyte adhesion to human endothelial cells. Clin Exp Immunol. 2002 ;130(2):256-62.

5.Vincenzo Pasceri, MD Direct Proinflammatory Effect of C-Reactive Protein on Human Endothelial Cells, Circulation. 2000;102:2165.

6.Waranuch Pitiphat, Periodontitis and Plasma C-Reactive Protein During Pregnancy, Journal of Periodontology 2006, Vol. 77, No. 5, Pages 821-825

7.Ebersole JL, et al. Systemic acute-phase reactants, C-reactive protein and haptoglobin, in adult periodontitis. Clin Exp Immunol 1997;107: 347-352.

8.Ridker PM, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Eng J Med 1997;336: 973-979.

9.Paquette DW, et al. The concept of “risk” and the emerging discipline of periodontal medicine, The journal of contemporary dental practice 1999;1: 1-8

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