悬液芯片系统检测冠心病和牙周炎病人血清和龈沟液细胞因子水平
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摘要
[目的]
近几年研究表明，细菌和病毒感染引起的炎症反应与冠心病发病有一定关系，其中牙周炎是重要的组成部分。细胞因子是重要的调节细胞和体液炎症反应的蛋白，血清和龈沟液中某些细胞因子的浓度常作为冠心病和牙周病活动性指标，与治疗有密切的关系。本文应用悬液芯片仪检测血清和龈沟液细胞因子水平，分析牙周炎和冠心病的相关性。
[方法]
共选择40名受检者，分成4组，分别为健康对照组(H)、牙周炎组(P)、冠心病组(C)、冠心病合并牙周炎组(P／C)。对所有受检者进行牙周检查，记录牙周袋深度，松动度等指标，并采取血清和龈沟液标本，应用Bio-Plex悬液芯片仪检测血清和龈沟液中细胞因子IL-1β、MCP-1、VEGF和PDGF水平。
[结果]
P组、C组、P／C组的血清和龈沟液中IL-1β水平明显高于H组(P＜0.05)；
P组、C组、P／C组的血清MCP-1水平明显高于H组(P＜0.05)，而龈沟液水平未体现出差异；P组、C组、P／C组的血清VEGF的浓度低于H组，而龈沟液中VEGF的浓度高于正常组；龈沟液和血清中PDGF的浓度在各组之间没有统计学意义上的差异。
[结论]
牙周病和冠心病之间可能通过血清和龈沟液中细胞因子水平的变化，相互影响疾病的发展变化过程，其中IL-1β和MCP-1在二种疾病的发生发展中发挥了关键作用，这二种细胞因子水平变化可作为反映牙周病和冠心病病变活跃性变化的重要标记物。
[Objective]
In the recent years, some reports raised the hypothesis that the incidence and progression of CHD was associated with chronic infections, including periodontal inflammation. Oral inflammation maybe a risk factor of CHD. Cytokines are important cell signalling proteins and mediate a wide range of physiological responses. The level of cytokines in serum and gingival crevical fluid were regarded as markers that contribute to elucidating novel mechanisms of periodontitis and CHD. They provided useful information for the diagnosis and treatment of the two diseases.
To study shared etiological factors between CHD and periodontitis, we identified and quantified four kinds of cytokines (IL-1β, MCP-1, VEGF and PDGF) in serum and gingival crevicular fluid (GCF) by Suspension Array System.
[Methods]
40 subjects were divided into 4 groups, one of which suffered from periodontitis but without CHD (P), and the second group was made of 10 CHD patients with no periodontitis(C), while the third was 10 patients suffering from periodontitis and CHD(P/C) and the fourth was healthy volunteers(H). All of them underwent a comprehensive periodontal examination, such as pocket probing depth and tooth mobility et al. GCF was collected from all individuals, and blood samples were withdrawn on the time of GCF sampling. The four kinds of Cytokines' levels in GCF and serum samples were detected by Bio-Plex Suspension Assay System.
[Results]
The IL-1β level in serum and GCF from all patients (including P group, C group, PC group) was higher than healthy subjects (P<0.05). And so was observed for MCP-1 level in serum, however, the level of MCP-1 in GCF had no difference between patients and healthy volunteers. The VEGF concentration in serum of P group, C group, PC group was lower than H group, on the contrary, the VEGF concentration in GCF of the patients was higher than H group. There were no significant differences of the level of PDGF in serum and GCF among four groups
[Conclusions]
It was concluded that PD and CHD had effect on each other's progress depending on the changing level of cytokines. Furthermore, elevated levels of IL-1β and MCP-1 in serum and GCF could serve as a reliable marker that reflected the inflammatory activity of PD and CHD.
近几年研究表明，细菌和病毒感染引起的炎症反应与冠心病发病有一定关系，其中牙周炎是重要的组成部分。细胞因子是重要的调节细胞和体液炎症反应的蛋白，血清和龈沟液中某些细胞因子的浓度常作为冠心病和牙周病活动性指标，与治疗有密切的关系。本文应用悬液芯片仪检测血清和龈沟液细胞因子水平，分析牙周炎和冠心病的相关性。
[方法]
共选择40名受检者，分成4组，分别为健康对照组(H)、牙周炎组(P)、冠心病组(C)、冠心病合并牙周炎组(P／C)。对所有受检者进行牙周检查，记录牙周袋深度，松动度等指标，并采取血清和龈沟液标本，应用Bio-Plex悬液芯片仪检测血清和龈沟液中细胞因子IL-1β、MCP-1、VEGF和PDGF水平。
[结果]
P组、C组、P／C组的血清和龈沟液中IL-1β水平明显高于H组(P＜0.05)；
P组、C组、P／C组的血清MCP-1水平明显高于H组(P＜0.05)，而龈沟液水平未体现出差异；P组、C组、P／C组的血清VEGF的浓度低于H组，而龈沟液中VEGF的浓度高于正常组；龈沟液和血清中PDGF的浓度在各组之间没有统计学意义上的差异。
[结论]
牙周病和冠心病之间可能通过血清和龈沟液中细胞因子水平的变化，相互影响疾病的发展变化过程，其中IL-1β和MCP-1在二种疾病的发生发展中发挥了关键作用，这二种细胞因子水平变化可作为反映牙周病和冠心病病变活跃性变化的重要标记物。
[Objective]
In the recent years, some reports raised the hypothesis that the incidence and progression of CHD was associated with chronic infections, including periodontal inflammation. Oral inflammation maybe a risk factor of CHD. Cytokines are important cell signalling proteins and mediate a wide range of physiological responses. The level of cytokines in serum and gingival crevical fluid were regarded as markers that contribute to elucidating novel mechanisms of periodontitis and CHD. They provided useful information for the diagnosis and treatment of the two diseases.
To study shared etiological factors between CHD and periodontitis, we identified and quantified four kinds of cytokines (IL-1β, MCP-1, VEGF and PDGF) in serum and gingival crevicular fluid (GCF) by Suspension Array System.
[Methods]
40 subjects were divided into 4 groups, one of which suffered from periodontitis but without CHD (P), and the second group was made of 10 CHD patients with no periodontitis(C), while the third was 10 patients suffering from periodontitis and CHD(P/C) and the fourth was healthy volunteers(H). All of them underwent a comprehensive periodontal examination, such as pocket probing depth and tooth mobility et al. GCF was collected from all individuals, and blood samples were withdrawn on the time of GCF sampling. The four kinds of Cytokines' levels in GCF and serum samples were detected by Bio-Plex Suspension Assay System.
[Results]
The IL-1β level in serum and GCF from all patients (including P group, C group, PC group) was higher than healthy subjects (P<0.05). And so was observed for MCP-1 level in serum, however, the level of MCP-1 in GCF had no difference between patients and healthy volunteers. The VEGF concentration in serum of P group, C group, PC group was lower than H group, on the contrary, the VEGF concentration in GCF of the patients was higher than H group. There were no significant differences of the level of PDGF in serum and GCF among four groups
[Conclusions]
It was concluded that PD and CHD had effect on each other's progress depending on the changing level of cytokines. Furthermore, elevated levels of IL-1β and MCP-1 in serum and GCF could serve as a reliable marker that reflected the inflammatory activity of PD and CHD.
引文
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1、 孙少宣，潘可凤，主编．美容牙医学[M]．第2版．北京：科学出版社，2003．42．
2、 徐晓岚．Ceram·X duo美容修复前牙243颗随访观察．南通大学学报(医学版)
2. Ellis,RW. Infection and coronary heart disease. J.Med.Microbiol.1997, 46:535-539.
3. Saadeddin SM, Habbab MA, Ferns GA. Markers of inflammation and coronary artery disease. Med Sci Monit. 2002, 8(1): 5-12.
4. Behle JH, Papapanou PN.Periodontal infections and atherosclerotic vascular disease: an update. Int Dent J. 2006,56(4 Suppl 1):256-62.
5. Griffiths GS. Formation, collection and significance of gingival crevice fluid. Periodontol 2000. 2003;31:32-42.
6. Jeffrey L, Ebersole. Humoral immune responses in gingival crevice fluid: local and systemic implications. Periodontology 2000. 2003,31: 135-166.
7. M. Mogia, J. Otogotob, N. Ota.Interleukin-1β, interleukin-6, β 2-microglob- ulin, and transforming growth factor- α in gingival crevicular fluid from human periodontal disease. Archives of Oral Biology 1999,44:535-539.
8. Eberhard JJ, Reimers N, Dommisch H, Hacker J, Freitag S, Acil Y, Albers HK, &Jepsen SS. The effect of the topical administration of bioactive glass on inflammatory markers of human experimental gingivitis. Biomaterials. 2005, 26: 1545-51.
9. Spahr A, Klein E, Khuseyinova N,et al.Periodontal infections and coronary heart disease: role of periodontal bacteria and importance of total pathogen burden in the Coronary Event and Periodontal Disease (CORODONT) study. Arch Intern Med. 2006,13;166(5):554-9.5
10. Loos BG, Craandijk J, & Hoek FJ. Elevation of systemic markers related to cardiovascular diseases in the peripheral blood of periodontitis patients. Journal of Periodontology. 2000,71: 1528-34
11. Slade GD, Offenbacher S, Beck JD, Heiss G, & Pankow JS. Acute-phase inflammatory response to periodontal disease in the US population. Journal of Dental Research. 2000,79: 49-57
12. D'Aiuto F, Parkar M, Andreaou G, Brett PM, Ready D, & Tonetti MS. Periodontitis and atherogenesis: causal association or simple coincidence?. Journal of Clinical Periodontology. 2004, 31: 402-411.
13. Libby P, Egan D, Skarlattos S. Roles of infectious agents in atherosclerosis and restenosis: an assessment of the evidence and need for future research. Circulation 1997, 96:4095 - 4103.
14. M, Van Dyke TE, Vita JA. Periodontal disease is associated with brachial artery endothelial dysfunction and systemic inflammation. Arterioscler Thromb Vasc Biol. 2003, 23:1245 - 1249.
15. Huynh-Ba G, Lang NP, Tonetti MS, Salvi GE.The association of the composite IL-1 genotype with periodontitis progression and/or treatment outcomes: a systematic review. J Clin Periodontol. 2007, 34 (4):305-17.
16. Hoogeveen RC, Morrison A, Boerwinkle E. Plasma MCP-1 level and risk for peripheral arterial disease and incident coronary heart disease: Atherosclerosis Risk in Communities study. Atherosclerosis. 2005,183 (2):301-7.
17. Cui B, Huang L, Song YM.The relationship between circulating endothelial progenitor cells and the risk factors of CHD as well as the severity of coronary lesions, and its clinical significance. Zhonghua Xin Xue Guan Bing Za Zhi. 2005, 33(9):785-8.
18. Czarkowska-Paczek B, Bartlomiejczyk I, Przybylski J. The serum levels of growth factors: PDGF, TGF-BETA and VEGF are increased after strenuous physical exercise. J Physiol Pharmacol. 2006, 57(2): 189-97.
19. De Nardin E. The role of inflammatory and immunological mediators in periodontitis and cardiovascular disease. Ann Periodontol. 2001,6 (1):30-40.
20. Palmer RM, Wilson RF, Hasan AS, & Scott DA, Mechanisms of action of environmental factors--tobacco smoking. Journal of Clinical Periodontology. 2005; 32(Suppl 6): 180-95
21. Zheng P, Chen H, Shi S, et al. Periodontal parameters and platelet-activating factor levels in serum and gingival crevicular fluid in a Chinese population. J Clin Periodontol. 2006, 33(11):797-802.
22. Zhang YM, Zhong LJ, He BX.Study on the correlation between coronary heart disease and chronic periodontitis. Zhonghua Liu Xing Bing Xue Za Zhi. 2006, 27(3):256-9.
23. Yong-Hee P. Chun, Kyoung-Ryul, J. Chun et al. Biological foundation for periodontitis as a potential risk factor for atherosclerosis. J Periodont Res. 2005,40:87-95.
24. Binder TA, Goodson JM, & Socransky SS. Gingival fluid levels of acid and alkaline phosphatase. Journal of periodontal research. 1987; 22: 14-9.
25. Pei Zheng, Hui Chen, Sailang Shi,et al. Periodontal parameters and platelet-activating factor levels in serum and gingival crevicular fluid in a Chinese population. Joumal of Clinical Periodontology. 2006,33:797-802.
26. Lamster IB, Oshrain RL, Celenti R, Levine K, & Fine JB. Correlation analysis for clinical and gingival crevicular fluid parameters at anatomically related gingival sites. Journal of Clinical Periodontology. 1991，18：272-277．
27． 周以均，袁乃梅，陈铁楼．牙周炎患者龈沟液和龈组织PGE2水平相关性的研究．实用口腔医学杂志．1994，10：160-2．
28. Paul R. Knight, Arun Sreekumar, Javed Siddiqui et al. development of a sensitive microarray immunoassay and comparison with standard enzyme-linked immunoassay for cytokine analysis. Shock. 2004, 21:26-30.
29. de Jager W, Velthuis H, et al. Simultaneous Detection of 15 Human Cytokines in a Single Sample of Stimulated Peripheral Blood Mononuclear Cells。 Clin Diagn Lab Immunol. 2003, 10(1): 133-9.
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2、 徐晓岚．Ceram·X duo美容修复前牙243颗随访观察．南通大学学报(医学版)