Assessment of serum levels of monocyte chemoattractant protein 1 (MCP 1) in patients with periodontitis and atherosclerotic cardiovascular disease
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Abstract
Background: Monocyte chemotactic protein-1 (MCP-1) is a chemokine expressed by inflammatory and endothelial cells. It has a crucial role in initiating, regulating, and mobilizing monocytes to active sites of periodontal inflammation. Its expression is also elevated in response to pro-inflammatory stimuli and tissue injury, both of which are linked to atherosclerotic lesions. Aim of the study: To determine the serum level of MCP-1 in patients with periodontitis and atherosclerotic cardiovascular disease in comparison to healthy control and evaluate the biomarker's correlations with periodontal parameters. methods: This study enrolled 88 subjects, both males and females, ranging in age from 36-66 years old, and divided into four groups: 1ST group with atherosclerotic cardiovascular disease (ASCVD) without periodontal disease (25 patients), 2nd group with periodontitis and systemically healthy, (25 patients),3rdgroup having both ASCVD and periodontitis (25 patients), and the 4th is the control group without any systemic disease and with good oral hygiene (13 subjects). The clinical periodontal parameters plaque index (PL I), Bleeding on probing (BOP), Probing Pocket depth (PPD) and clinical attachment level (CAL) were used to evaluate periodontal health status. Atherosclerotic cardiovascular disease patients were chosen after clinical examination by specialists and diagnoses confirmed with catheterization. Following clinical assessment, 5ml of venous blood was drawn from each participant MCP-1 levels in the blood were then measured using enzyme-linked-immunosorbent assay (ELISA). Results: According to the findings of this study, the mean values of PLI and BOP were higher in periodontitis group and athero+periodontitis group than in athero group and control group, PPD and CAL mean values were greater in athero+periodontitis group than in periodontitis group. The serum level of MCP-1 was higher in athero+periodontitis group than in athero, periodontitis and control groups. Regarding the correlations between MCP-1 and clinical periodontal parameters. In periodontitis group there was a positive correlation with PPD and CAL and there was a positive correlation with CAL in athero+periodontitis. Conclusion: This study revealed that periodontitis with higher MCP-1 level may be linked to an increased risk of atherosclerosis.
Received date: 10-01-2022
Accepted date: 26-02-2022
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References
Peres MA, Macpherson LM, Weyant RJ, Daly B, Venturelli R, Mathur MR, et al. Oral diseases: Glob. Public Health. The Lancet. 2019;394(10194):249-60. DOI: https://doi.org/10.1016/S0140-6736(19)31146-8
Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med. 2006;3(11):e442. DOI: https://doi.org/10.1371/journal.pmed.0030442
Zardawi F, Gul S, Abdulkareem A, Sha A, Yates J. Association between periodontal disease and atherosclerotic cardiovascular diseases: revisited. FRONT CARDIOVASC MED . 2020;7. DOI: https://doi.org/10.3389/fcvm.2020.625579
Peacock ME, Carson RE. Frequency of self‐reported medical conditions in periodontal patients. J. Periodontol. 1995;66(11):1004-7. DOI: https://doi.org/10.1902/jop.1995.66.11.1004
Hujoel PP, Drangsholt M, Spiekerman C, DeRouen TA. Periodontal disease and coronary heart disease risk. Jama. 2000;284(11):1406-10. DOI: https://doi.org/10.1001/jama.284.11.1406
Reyes L, Herrera D, Kozarov E, Roldán S, Progulske‐Fox A. Periodontal bacterial invasion and infection: contribution to atherosclerotic pathology. J. Clin. Periodontol. 2013;40:S30-S50. DOI: https://doi.org/10.1111/jcpe.12079
Schenkein HA, Loos BG. Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases. J. Periodontol. 2013;84:S51-S69. DOI: https://doi.org/10.1902/jop.2013.134006
Tonetti MS, Van Dyke TE, workshop* wgotjEA. Periodontitis and atherosclerotic cardiovascular disease: consensus report of the Joint EFP/AAPWorkshop on Periodontitis and Systemic Diseases. J. Periodontol. 2013;84:S24-S9. DOI: https://doi.org/10.1902/jop.2013.1340019
Deshmane SL, Kremlev S, Amini S, Sawaya BE. Monocyte chemoattractant protein-1 (MCP-1): an overview. J. Interferon Cytokine Res. 2009;29(6):313-26. DOI: https://doi.org/10.1089/jir.2008.0027
Conti I, Rollins BJ, editors. CCL2 (monocyte chemoattractant protein-1) and cancer. Semin. Cancer Biol; 2004: Elsevier. DOI: https://doi.org/10.1016/j.semcancer.2003.10.009
Gilbert J, Lekstrom-Himes J, Donaldson D, Lee Y, Hu M, Xu J, et al. Effect of CC chemokine receptor 2 CCR2 blockade on serum C-reactive protein in individuals at atherosclerotic risk and with a single nucleotide polymorphism of the monocyte chemoattractant protein-1 promoter region. Am. J. Cardiol. 2011;107(6):906-11. DOI: https://doi.org/10.1016/j.amjcard.2010.11.005
Silva T, Garlet G, Fukada S, Silva J, Cunha F. Chemokines in oral inflammatory diseases: apical periodontitis and periodontal disease. J. Dent. Res. 2007;86(4):306-19. DOI: https://doi.org/10.1177/154405910708600403
Tonetti MS, Greenwell H, Kornman KS. Staging and grading of periodontitis: Framework and proposal of a new classification and case definition. J. Periodontol. 2018;89:S159-S72. DOI: https://doi.org/10.1002/JPER.18-0006
Chapple IL, Mealey BL, Van Dyke TE, Bartold PM, Dommisch H, Eickholz P, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri‐Implant Diseases and Conditions. J. Periodontol. 2018;89:S74-S84.
O'Leary TJ, Drake RB, Naylor JE. The plaque control record. J. Periodontol. 1972;43(1):38-. DOI: https://doi.org/10.1902/jop.1972.43.1.38
Koo TK, Li MY. A guideline of selecting and reporting intraclass correlation coefficients for reliability research. J Chiropr Med. 2016;15(2):155-63. DOI: https://doi.org/10.1016/j.jcm.2016.02.012
Buhlin K, Mäntylä P, Paju S, Peltola JS, Nieminen MS, Sinisalo J, et al. Periodontitis is associated with angiographically verified coronary artery disease. J. Clin. Periodontol. 2011;38(11):1007-14. DOI: https://doi.org/10.1111/j.1600-051X.2011.01775.x
López‐Jornet P, Berná‐Mestre J, Berná‐Serna J, Camacho‐Alonso F, Fernandez‐Millan S, Reus‐Pintado M. Measurement of atherosclerosis markers in patients with periodontitis: A case‐control study. J. Periodontol. 2012;83(6):690-8. DOI: https://doi.org/10.1902/jop.2011.110412
Vražić D, Miovski Z, Strozzi M, Puhar I, Badovinac A, Božić D, et al. Periodontal disease and its association with angiographically verified coronary artery disease. Acta Stomatol Croat. 2015;49(1):14-20. DOI: https://doi.org/10.15644/asc49/1/2
Androsz-Kowalska O, Jankowski K, Rymarczyk Z, Kowalski J, Pruszczyk P, Górska R. Correlation between clinical parameters of periodontal disease and mean platelet volume in patients with coronary artery disease: a pilot study. Kardiol Pol. 2013;71(6):600-5. DOI: https://doi.org/10.5603/KP.2013.0124
Zhu H, Lin X, Zheng P, Chen H. Inflammatory cytokine levels in patients with periodontitis and/or coronary heart disease. Int J Clin Exp Pathol. 2015;8(2):2214.
Lira‐Junior R, Figueredo CM, Bouskela E, Fischer RG. Severe chronic periodontitis is associated with endothelial and microvascular dysfunctions: a pilot study. J. Periodontol. 2014;85(12):1648-57. DOI: https://doi.org/10.1902/jop.2014.140189
Bartova J, Sommerova P, Lyuya-Mi Y, Mysak J, Prochazkova J, Duskova J, et al. Periodontitis as a risk factor of atherosclerosis. J. Immunol. Res. 2014;2014. DOI: https://doi.org/10.1155/2014/636893
Baker PJ. The role of immune responses in bone loss during periodontal disease. Microbes Infect. 2000;2(10):1181-92. DOI: https://doi.org/10.1016/S1286-4579(00)01272-7
Maeno Y, Kashiwagi A, Nishio Y, Takahara N, Kikkawa R. IDL can stimulate atherogenic gene expression in cultured human vascular endothelial cells. Diabetes Res Clin Pract . 2000;48(2):127-38. DOI: https://doi.org/10.1016/S0168-8227(99)00147-3
Dwivedi A, Änggård EE, Carrier MJ. Oxidized LDL-mediated monocyte adhesion to endothelial cells does not involve NFκB. Biochem. Biophys. Res. Commun. 2001;284(1):239-44. DOI: https://doi.org/10.1006/bbrc.2001.4955
Pradeep A, Daisy H, Hadge P. Serum levels of monocyte chemoattractant protein-1 in periodontal health and disease. Cytokine. 2009;47(2):77-81. DOI: https://doi.org/10.1016/j.cyto.2009.05.012
Gupta M, Chaturvedi R, Jain A. Role of monocyte chemoattractant protein-1 (MCP-1) as an immune-diagnostic biomarker in the pathogenesis of chronic periodontal disease. Cytokine. 2013;61(3):892-7. DOI: https://doi.org/10.1016/j.cyto.2012.12.012
Babu DS, Poornodaya S, Sai KA, Anumala D, Reddy DS, Reddy NR. Estimation of CCL2/MCP-1 levels in serum and gingival crevicular fluid in periodontal health, disease and after treatment–A clinico biochemical study. J. Orofac. Sci. 2017;9(2):85. DOI: https://doi.org/10.4103/jofs.jofs_113_17
Kinane DF, Lappin DF. Clinical, pathological and immunological aspects of periodontal disease. Acta Odontol. Scand. 2001;59(3):154-60. DOI: https://doi.org/10.1080/000163501750266747
Graves DT, Cochran D. The contribution of interleukin‐1 and tumor necrosis factor to periodontal tissue destruction. J. Periodontol. 2003;74(3):391-401. DOI: https://doi.org/10.1902/jop.2003.74.3.391
Kim MS, Day CJ, Selinger CI, Magno CL, Stephens SR, Morrison NA. MCP-1-induced human osteoclast-like cells are tartrate-resistant acid phosphatase, NFATc1, and calcitonin receptor-positive but require receptor activator of NFκB ligand for bone resorption. J. Biol. Chem. 2006;281(2):1274-85. DOI: https://doi.org/10.1074/jbc.M510156200
Kim MS, Magno CL, Day CJ, Morrison NA. Induction of chemokines and chemokine receptors CCR2b and CCR4 in authentic human osteoclasts differentiated with RANKL and osteoclast like cells differentiated by MCP‐1 and RANTES. J. Cell. Biochem. 2006;97(3):512-8. DOI: https://doi.org/10.1002/jcb.20649