Journal List > J Korean Acad Periodontol > v.39(Suppl) > 1049816

J Korean Acad Periodontol. 2009 Dec;39(4):391-398. Korean.
Published online December 31, 2009.  https://doi.org/10.5051/jkape.2009.39.4.391
Copyright © 2009 Korean Academy of Periodontology
The expressions of C-reactive protein and macrophage colony-stimulating factor in gingival tissue of human chronic periodontitis with hypertension
Chul-Woo Kim,1 Jin-Woo Park,1 Jo-Young Suh,1 Je-Yoel Cho,2 and Jae-Mok Lee1
1Department of Periodontology, School of Dentistry, Kyungpook National University, Daegu, Korea.
2Department of Biochemistry, School of Dentistry, Kyungpook National University, Daegu, Korea.

Correspondence: Dr. Jae-Mok Lee. Department of Periodontology, School of Dentistry, Kyungpook national University, 188-1, Samduk-dong 2ga, Jung-gu Daegu, 700-412, Korea. Email: leejm@knu.ac.kr , Tel: 82-53-600-7511, Fax: 82-53-427-3263
Received October 15, 2009; Accepted November 16, 2009.

Abstract

Purpose

The purpose of this study was to quantify and compare the expressions of CRP and M-CSF in the gingival tissues of the patients with chronic periodontitis associated to hypertension.

Methods

Gingival tissue samples were obtained during periodontal surgery or tooth extraction. Clinically healthy gingival tissue samples from systemically healthy 12 patients were categorized as group 1 (n=12). Inflammatory gingival tissue samples from patients with chronic periodontitis were categorized as group 2 (n=12). Inflammatory gingival tissue samples from patients with chronic periodontitis associated with hypertension were categorized as group 3 (n=12). Tissue samples were prepared and analyzed by Western blotting. The quantification of CRP and M-CSF were performed using a densitometer and statistically analyzed by one-way ANOVA followed by Tukey test.

Results

There were significant differences between group 1 and group 2 and between group 1 and group 3 in both CRP and M-CSF. The differences between group 2 and group 3 were not statistically significant in both proteins. However, the expression levels of CRP and M-CSF in hypertensive inflammatory gingiva showed increased tendency compared to non-hypertensive inflammatory gingiva.

Conclusions

It is suggested that CRP and M-CSF might be used as inflammatory and bone resorption markers in periodontal diseased tissue. It is assumed that hypertension may be associated with the progression of periodontal inflammation and alveolar bone resorption.

Keywords: chronic periodontitis; C-reactive protein; hypertension; macrophage colony-stimulating factor

Figures


Figure 1
CRP Western analysis showing 4 representative samples in each group. CRP levels were quantified on the basis of β-actin levels. CRP corresponding to molecular weight 27 kDa was shown to be expressed in all samples including healthy gingiva, and the expression levels of CRP were increased in order of group 1, group 2 and group 3.

Group 1 : healthy gingiva from systemically healthy person, Group 2 : inflamed gingiva from patient with chronic periodontitis, Group 3 : inflamed gingiva from patient with chronic periodontitis and hypertension.

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Figure 2
Graphics showing the average amounts (ratio of CRP/β-actin) and standard deviation of CRP level in groups 1, 2 and 3. In the inflamed gingiva (group 2 and 3), the levels of CRP were significantly increased as compared to group 1 (P<0.05). Group 1 : healthy gingiva from systemically healthy person. Group 2 : inflamed gingiva from patient with chronic periodontitis. Group 3 : inflamed gingiva from patient with chronic periodontitis and hypertension.

+significant difference between group 1 and group 2 (P<0.05). *significant difference between group 1 and group 3 (P<0.05).

Click for larger image


Figure 3
M-CSF Western analysis showing 4 representative samples in each group. M-CSF levels were quantified on the basis of β-actin levels. M-CSF corresponding to molecular weight 18.5 kDa was shown to be expressed in all samples including healthy gingiva, and the expression levels of M-CSF were increased in order of group 1, group 2 and group 3. Group 1 : healthy gingiva from systemically healthy person. Group 2 : inflamed gingiva from patient with chronic periodontitis. Group 3 : inflamed gingiva from patient with chronic periodontitis and hypertension.
Click for larger image


Figure 4
Graphics showing the average amounts (ratio of M-CSF/β-actin) and standard deviation of M-CSF level in groups 1, 2 and 3. In the inflamed gingiva (group 2 and 3), the levels of M-CSF were significantly increased as compared to group 1 (P<0.05). Group 1 : healthy gingiva from systemically healthy person. Group 2 : inflamed gingiva from patient with chronic periodontitis. Group 3 : inflamed gingiva from patient with chronic periodontitis and hypertension.

+significant difference between group 1 and group 2 (P<0.05). *significant difference between group 1 and group 3 (P<0.05).

Click for larger image

Tables


Table 1
Patient Characteristics
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Table 2
Normalized CRP expressions by CRP/β-actin
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Table 3
Normalized M-CSF expressions by M-CSF/β-actin
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References
1. Shapira L, Soskolne WA, Sela MN, Offenacher S, Barak V. The secretion of PFE2, IL-1β, IL-6 and TNF-α by adherent mononuclear cells from early onset periodontitis patients. J Periodontol 1994;65:139–146.
2. Hernichel-Gorbach E, Kornman KS, Holt SC, et al. Host responses in patients with generalized refractory periodontitis. J Periodontol 1994;65:8–16.
3. Page RC. The role of inflammatory mediators in the pathogenesis of periodontal disease. J Periodont Res 1991;26:230–242.
4. Liu D, Xu JK, Figliomeni L, et al. Expression of RANKL and OPG mRNA in periodontal disease: Possible involvement in bone destruction. Int J Mol Med 2003;11:17–21.
5. Crotti T, Smith MD, Hirsch R, et al. Receptor activator NF kappaB ligand (RANKL) and osteoprotegerin (OPG) protein expression in periodontitis. J Periodont Res 2003;38:380–387.
6. Suda T, Takahashi N, Martin TJ. Modulation of osteoclast differentiation. Endocr Rev 1992;13:6–80.
7. Lacey DL, Timms E, Tan HL, et al. Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation. Cell 1998;93:165–167.
8. Katagiri T, Takahashi N. Regulatory mechanism of osteoblast and osteoclast differentiation. Oral Diseases 2000;8:147–159.
9. Cochran DL. Inflammation and bone loss in periodontal disease. J Periodontol 2008 suppl:1569–1576.
10. Masato K, Masahide M, Motokawa M, et al. VEGF and M-CSF levels in periodotal tissue during tooth movement. Biomed Res 2008;29:181–187.
11. Steel D, Whitehead AS. The major acute phase reactants: C-reactive protein, serum amyloid P component and serum amyloid A protein. Immunol Today 1994;15:81–88.
12. Baumann H, Gauldie J. The acute phase response. Immunol Today 1994;15:74–80.
13. Buhin K, Gustafsson A, Pockley AG, Frostegard J, Klinge B. Risk factors for cardiovascular disease in patients with periodontitis. Eur Heart J 2003;24:2099–2107.
14. Vigushin DM, Pepsy MB, Hawkins PN. Metabolic and scintigraphic studies of radioiodinated human C-reactive protein in health and diseases. J Clin Invest 1993;91:1351–1357.
15. Yeh ETH, Willerson JT. Coming of Age of C-reactive protein using Inflammation markers in cardiology. Circulation 2003;107:370–371.
16. Loos BG, Craandijk J, Hoek FJ, Wertheim-van Dillen P, van der Velden U. Elevation of systemic markers related to cardiovascular diseases in the peripheral blood of periodontitis patients. J Periodontol 2000;71:1528–1534.
17. Slade GD, Offenbacher S, Beck JD, Heiss G, Pankow JS. Acute phase inflammatory response to periodontal disease in the US population. J Dent Res 2000;79:49–57.
18. Scannapieco FA, Bush RB, Paju S. Associations between periodontal diseases and risk for atherosclerosis, cardiovascular disease, and stroke. Ann Periodontol 2003;8:38–53.
19. Destefano F, Anda RF, Kahn HS, Williamson DF, Russell CR. Dental disease and risk of coronary heart disease and mortality. BMJ 1993;306:688–691.
20. Albandar JM, Strekfus CF, Adesanya MR, Winn DM. Cigar, pipe, and cigarette smoking as risk factors for periodontal diseases and tooth loss. J Periodontol 2000;71:1874–1881.
21. Susin C, Oppermann RV, Haugejorden O, Albandar JM. Periodontal attachment loss attributable to cigarette smoking in an urban Brazilian population. J Clin Periodontol 2004;31:951–958.
22. Emrich LJ, Shlossman M, Genco RJ. Periodontal disease in non-insulin-dependent diabetes mellitus. J Periodontol 1991;62:123–131.
23. Bridges RB, Anderso JW, Saxe SR, Greogrory K, Bridge SR. Periodontal status of diabetic and non-diabetic men: effects of smoking, glycemic control, and socioeconomic factors. J Periodontol 1996;67:1185–1192.
24. Mühlemann HR, Son SH. Gingival sulcus bleeding-a leading symptom in initial gingivitis. Helv Odontol Acta 1971;15:107–113.
25. Kim DH, Park JW, Lee JM, et al. The comparison of MMP-2, MMP-9 and tumor necrosis factor-α expressions in human gingiva with chronic periodontitis with or without associated to type 2 diabetes mellitus. J Korean Aca Periodontol 2006;36:409–426.
26. Cho JY, Xing S, Liu X, Buckwalter TLF, et al. Expression and activity of human Na+/I- symporter in human glioma cells by adenovirus-mediated gene delivary. Gene Therapy 2000;7:740–749.
27. Frederiksson MI, Figueredo CMS, Gustafsson A, Bergstrom KG, Asman BE. Effect of periodontitis and smoking on blood leukocytes and acute-phase proteins. J Periodontol 1999;70:1355–1360.
28. Ebersole JL, Machen RL, Steffen MJ, Willmann DE. systemic acute phase reactants, C-reactive protein and haptoglobin in adult periodontitis. Clin Exp Immunol 1997;107:347–352.
29. Beck JD, Slade G, Offenbacher S. Oral disease, cardiovascular disease and systemic inflammation. J Periodontol 2000;23:110–120.
30. Noack B, Genco RJ, Trevisan M, et al. Periodontal infections contribute to elevate systemic C-reactive protein level. J Periodontol 2001;72:1221–1227.
31. Matilla K, Vesanen M, Valtonen V, et al. Effect of treating periodontitis on C-reactive protein levels: A pilot study. BMC Infect Dis 2002;2:30–32.
32. Ide M, Mcpartin D, Coward PY, et al. Effect of treatment of chronic periodontitis on levels of serum markers of acute-phase inflammatory and vascular responses. J Clin Periodontol 2003;30:334–340.
33. Tussanee Y, Kanokporn L, Prasit P. Human periodontal ligament cells secret macrophage colony-stimulating factor in response to tumor necrosis factor-alpha in vitro. J periodontol 2006;77:955–962.
34. Roberts FA, McCaffery KA, Michalek SM. Profile of cytokine mRNA expression in chronic adult periodontitis. J Dent Res 1997;76:1833–1839.
35. Sudha A, Charu SC, Nicholas PP, et al. Regulation of periodontal ligament cell functions by interleukin-1 beta. Infect Immun 1998;66:932–937.
36. Castelli WA, Diaz-Perez R, Nasjleti CE, Caffesse RG. Effect of renovascular hypertension of the morphology of oral blood vessels. Oral Surg Oral Med Oral Pathol 1978;46:576–582.
37. Perlstein MI, Bissada NF. Influence of obesity and hypertension on the severity of periodontitis in rats. Oral Surg Oral Med Oral Pathol 1977;4:707–719.
38. Angeli F, Verdecchia P, Pelligrino C, et al. Association between periodontal diseases and left ventricle mass in essential hypertension. Hypertension 2003;41:488–492.
39. Ridker PM, Buring JE, Cook NR, Rifai N. C-reactive protein, the metabolic syndrome, and risk of incident cardiovascular events: an 8-year follow up of 1419 initially healthy American women. Circulation 2003;107:391–397.
40. Lakoski SG, Cushman M, Palmas W, et al. The relationship between blood pressure and C-reactive protein in the Multi-Ethnic study of Atherosclerosis (MESA). J Am Coll Cardiol 2005;46:1869–1874.