DOENCA PERIODONTAL COMO FATOR DE RISCO PARA DOENÇA CARDIOVASCULAR: REVISÃO DE LITERATURA
Palavras-chave:
inflamação, citocinas, lipoproteínas de bactérias, polimorfonucleares, doença periodontal
Resumo
Introdução: estudos recentes têm demonstrado que existe uma associação entre doença periodontal e as doenças cardiovasculares devido a inflamação sistêmica crônica que aquela gera no indivíduo. Objetivos: compilar artigos científicos que confirmem essa associação. Métodos: utilizou se a base dados PUBMed para pesquisa dos artigos, e foram encontrados um total de 551 publicações nos últimos 5 anos e foram eleitos 14 artigos. Resultados: mostram que níveis de citocinas inflamatórias foram maiores após a indução da doença periodontal, o que pode contribuir para uma disfunção endotelial. Também demonstraram que, a ativação de polimorfonucleares é maior em pacientes com doença periodontal o que indica efeito inflamatório sistêmico, a partir de uma inflamação local. E por fim, que o processo inflamatório desencadeado por lipopolissacarídeos de bactérias, eleva a gravidade da periodontite, a magnitude da inflamação e induzem formação de placa aterosclerótica. Conclusão: a doença periodontal promove inflamação sistêmica de forma crônica, capaz de interferir no sistema cardiovascular. Portanto, deve ser abordada como fator de risco para doenças cardiovasculares.
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Referências
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7. DELANGE, N, et al. Periodontal disease and its connection to systemic biomarkers of cardiovascular disease in young American Indian/Alaskan natives. J Periodontol. 2018; 89: 219– 227. https://doi.org/10.1002/JPER.17-0319
8. EULER, G.J. et al. Interleukin-6 in neutrophils from peripheral blood and inflammatory periradicular tissues. Journal Of Endodontics, [S.L.], v. 24, n. 7, p. 480-484, jul. 1998. Elsevier BV. http://dx.doi.org/10.1016/s0099-2399(98)80051-4.
9. FINE N, et al. Periodontal Inflammation Primes the Systemic Innate Immune Response. Journal of Dental Research. 2021;100(3):318-325. doi:10.1177/0022034520963710
10. FONG, I.W. Emerging relations between infectious and coronary artery disease and atherosclerosis. Can. Med. Assoc. J., Ottawa, v.163, n.1, p.49-53, 2000. Supplement.
11. GARLET, G.P., et al. (2010), Regulatory T cells attenuate experimental periodontitis progression in mice. Journal of Clinical Periodontology, 37: 591-600. https://doi.org/10.1111/j.1600-051X.2010.01586.x
12. GARRIDO, M. et al; Elevated Systemic Inflammatory Burden and Cardiovascular Risk in Young Adults with Endodontic Apical Lesions. Journal Of Endodontics, [S.L.], v. 45, n. 2, p. 111-115, fev. 2019. Elsevier BV. http://dx.doi.org/10.1016/j.joen.2018.11.014.
13. GHARBI A., et al. Biochemical parameters and oxidative stress markers in Tunisian patients with periodontal disease. BMC Oral Health. 2019 Oct 22;19(1):225. doi: 10.1186/s12903-019-0912-4. PMID: 31640685; PMCID: PMC6805394.
14. GRUDYANOV, A. I.; TKACHEVA, O. N.; AVRAAMOVA, T. V.. Correlation of chronic periodontal disease and cardiovascular disease. Stomatologiya, [S.L.], v. 96, n. 1, p. 4, 2017. Media Sphere Publishing Group. http://dx.doi.org/10.17116/stomat20179614-7.
15. HARVEY, J D.. Periodontal Microbiology. Dental Clinics Of North America, [S.L.], v. 61, n. 2, p. 253-269, abr. 2017. Elsevier BV. http://dx.doi.org/10.1016/j.cden.2016.11.005.
16. HILLMAN G.; HILLMAN, B.; GEURTSEN, W. Immunohistological determination of interleukin-1â in inflamed human gingival epithelium. Arch Oral Biol., 40(4), 353-359, 1994.
17. HUJOEL, P.P. et al. Periodontal disease and coronary heart disease risk. JAMA: The Journal of the American Medical Association, Chicago, v.284, n.11, p.1406-1410, 2000.
18. KINANE, D., STATHOPOULOU, P. & PAPAPANOU, P. Periodontal diseases. Nat Rev Dis Primers 3, 17038 (2017). https://doi.org/10.1038/nrdp.2017.38
19. KØLLGAARD T, et al. (2017) Cholesterol crystals enhance TLR2- and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis. PLOS ONE 12(2): e0172773. https://doi.org/10.1371/journal.pone.0172773
20. KÖSE, O, et al. Biochemical and histopathologic analysis of the effects of periodontitis on left ventricular heart tissues of rats. J Periodont Res 2017; 52: 176– 185. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. https://doi.org/10.1111/jre.12380
21. LINDHE, J. Tratado de peridontia e Implantodontia Oral. Rio de Janeiro: Guanabara Koogan, 1999.
22. LU, H.-K., et al. (2006), Identification of the osteoprotegerin/receptor activator of nuclear factor-kappa B ligand system in gingival crevicular fluid and tissue of patients with chronic periodontitis. Journal of Periodontal Research, 41: 354-360. https://doi.org/10.1111/j.1600-0765.2006.00883.x
23. MARTINEZ-HERRERA, M, et al. Chronic periodontitis impairs polymorphonuclear leucocyte–endothelium cell interactions and oxidative stress in humans. J Clin Periodontol. 2018; 45: 1429– 1439. https://doi.org/10.1111/jcpe.13027
24. NAKAYAMA, M.; OHARA, N.. Molecular mechanisms of Porphyromonas gingivalis -host cell interaction on periodontal diseases. Japanese Dental Science Review, [S.L.], v. 53, n. 4, p. 134-140, nov. 2017. Elsevier BV. http://dx.doi.org/10.1016/j.jdsr.2017.06.001.
25. PAPAPANOU, P.N. and SUSIN, C. (2017), Periodontitis epidemiology: is periodontitis under-recognized, over-diagnosed, or both?. Periodontol 2000, 75: 45-51. https://doi.org/10.1111/prd.12200
26. PETERSEN, P.E. and OGAWA, H. (2012), The global burden of periodontal disease: towards integration with chronic disease prevention and control. Periodontology 2000, 60: 15-39. https://doi.org/10.1111/j.1600-0757.2011.00425.x
27. PIZZICANNELLA, J, et al. Endothelial committed oral stem cells as modelling in the relationship between periodontal and cardiovascular disease. J Cell Physiol. 2018; 233: 6734– 6747. https://doi.org/10.1002/jcp.26515
28. RAMIRES JAF, CÉSAR LAM, FERREIRA JMF. Insuficiência coronariana crônica. Rev Bras Med. 2003; 60(7): 415–28.
29. SAITO A; SOJAR H.T; GENCO R.J. Interleukin-1 gene expression and protein tyrosine kinase activities induced by surface protein components of Porphyromonas gingivalis: role of tyrosine kinases in signal transduction. Oral Microbiol Immunol., v.12, p. 135-140, 1997.
30. SILVA, Grazielle Caroline; et al . Experimental Periodontal Disease Triggers Coronary Endothelial Dysfunction in Middle-Aged Rats: preventive effect of a prebiotic β-glucan. The Journals Of Gerontology: Series A, [S.L.], v. 76, n. 8, p. 1398-1406, 3 mar. 2021. Oxford University Press (OUP). http://dx.doi.org/10.1093/gerona/glab066.
31. SMALL DM. George Lyman Duff memorial lecture. Progression and regression of atherosclerotic lesions. Insights from lipid physical biochemistry. Arteriosclerosis. 1988;8: 103–129. pmid:3348756
32. STELZEL, M., et al (2002), Detection of Porphyromonas gingivalis DNA in Aortic Tissue by PCR. Journal of Periodontology, 73: 868-870. https://doi.org/10.1902/jop.2002.73.8.868
33. SUAREZ, L.J. et al. Relative proportions of T-cell subpopulations and cytokines that mediate and regulate the adaptive immune response in patients with aggressive periodontitis. J. Periodontol., Chicago, v.75, n.9, p.1209-1215, 2004.
34. SUH, J.S., et al. Periodontitis-induced systemic inflammation exacerbates atherosclerosis partly via endothelial–mesenchymal transition in mice. Int J Oral Sci 11, 21 (2019). https://doi.org/10.1038/s41368-019-0054-1
35. WANG, C.-Y., TANI-ISHII, N. and STASHENKO, P. (1997), Bone-resorptive cytokine gene expression in periapical lesions in the rat. Oral Microbiology and Immunology, 12: 65-71. https://doi.org/10.1111/j.1399-302X.1997.tb00619.x
2. BECK, J.D. and OFFENBACHER, S. (2002), Relationships Among Clinical Measures of Periodontal Disease and Their Associations With Systemic Markers. Annals of Periodontology, 7: 79-89. https://doi.org/10.1902/annals.2002.7.1.79
3. BECK, J.D. et al. Periodontal disease and cardiovascular disease. J. Periodontol., Chicago, v.67, n.10, p.1123-1137, 1996. Supplement.
4. BOYAPATI R., et al. Mapping the link between cardiac biomarkers and chronic periodontitis: A clinico-biochemical study. J Indian Soc Periodontol. Jul-Ago 2020;24(4):309-315. doi: 10.4103/jisp.jisp 417 19. Epub 2020 Jul 1. PMID: 32831502; PMCID: PMC7418541.
5. ÇALAPKORUR, MU, et al. Association of peripheral arterial disease with periodontal disease: analysis of inflammatory cytokines and an acute phase protein in gingival crevicular fluid and serum. J Periodont Res 2017; 52: 532– 539. © 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. https://doi.org/10.1111/jre.12419
6. CHAPPLE, ILC, et al. Primary prevention of periodontitis: managing gingivitis. J Clin Periodontol 2015; 42 (Suppl. 16): S71– S76. doi: 10.1111/jcpe.12366.
7. DELANGE, N, et al. Periodontal disease and its connection to systemic biomarkers of cardiovascular disease in young American Indian/Alaskan natives. J Periodontol. 2018; 89: 219– 227. https://doi.org/10.1002/JPER.17-0319
8. EULER, G.J. et al. Interleukin-6 in neutrophils from peripheral blood and inflammatory periradicular tissues. Journal Of Endodontics, [S.L.], v. 24, n. 7, p. 480-484, jul. 1998. Elsevier BV. http://dx.doi.org/10.1016/s0099-2399(98)80051-4.
9. FINE N, et al. Periodontal Inflammation Primes the Systemic Innate Immune Response. Journal of Dental Research. 2021;100(3):318-325. doi:10.1177/0022034520963710
10. FONG, I.W. Emerging relations between infectious and coronary artery disease and atherosclerosis. Can. Med. Assoc. J., Ottawa, v.163, n.1, p.49-53, 2000. Supplement.
11. GARLET, G.P., et al. (2010), Regulatory T cells attenuate experimental periodontitis progression in mice. Journal of Clinical Periodontology, 37: 591-600. https://doi.org/10.1111/j.1600-051X.2010.01586.x
12. GARRIDO, M. et al; Elevated Systemic Inflammatory Burden and Cardiovascular Risk in Young Adults with Endodontic Apical Lesions. Journal Of Endodontics, [S.L.], v. 45, n. 2, p. 111-115, fev. 2019. Elsevier BV. http://dx.doi.org/10.1016/j.joen.2018.11.014.
13. GHARBI A., et al. Biochemical parameters and oxidative stress markers in Tunisian patients with periodontal disease. BMC Oral Health. 2019 Oct 22;19(1):225. doi: 10.1186/s12903-019-0912-4. PMID: 31640685; PMCID: PMC6805394.
14. GRUDYANOV, A. I.; TKACHEVA, O. N.; AVRAAMOVA, T. V.. Correlation of chronic periodontal disease and cardiovascular disease. Stomatologiya, [S.L.], v. 96, n. 1, p. 4, 2017. Media Sphere Publishing Group. http://dx.doi.org/10.17116/stomat20179614-7.
15. HARVEY, J D.. Periodontal Microbiology. Dental Clinics Of North America, [S.L.], v. 61, n. 2, p. 253-269, abr. 2017. Elsevier BV. http://dx.doi.org/10.1016/j.cden.2016.11.005.
16. HILLMAN G.; HILLMAN, B.; GEURTSEN, W. Immunohistological determination of interleukin-1â in inflamed human gingival epithelium. Arch Oral Biol., 40(4), 353-359, 1994.
17. HUJOEL, P.P. et al. Periodontal disease and coronary heart disease risk. JAMA: The Journal of the American Medical Association, Chicago, v.284, n.11, p.1406-1410, 2000.
18. KINANE, D., STATHOPOULOU, P. & PAPAPANOU, P. Periodontal diseases. Nat Rev Dis Primers 3, 17038 (2017). https://doi.org/10.1038/nrdp.2017.38
19. KØLLGAARD T, et al. (2017) Cholesterol crystals enhance TLR2- and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis. PLOS ONE 12(2): e0172773. https://doi.org/10.1371/journal.pone.0172773
20. KÖSE, O, et al. Biochemical and histopathologic analysis of the effects of periodontitis on left ventricular heart tissues of rats. J Periodont Res 2017; 52: 176– 185. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. https://doi.org/10.1111/jre.12380
21. LINDHE, J. Tratado de peridontia e Implantodontia Oral. Rio de Janeiro: Guanabara Koogan, 1999.
22. LU, H.-K., et al. (2006), Identification of the osteoprotegerin/receptor activator of nuclear factor-kappa B ligand system in gingival crevicular fluid and tissue of patients with chronic periodontitis. Journal of Periodontal Research, 41: 354-360. https://doi.org/10.1111/j.1600-0765.2006.00883.x
23. MARTINEZ-HERRERA, M, et al. Chronic periodontitis impairs polymorphonuclear leucocyte–endothelium cell interactions and oxidative stress in humans. J Clin Periodontol. 2018; 45: 1429– 1439. https://doi.org/10.1111/jcpe.13027
24. NAKAYAMA, M.; OHARA, N.. Molecular mechanisms of Porphyromonas gingivalis -host cell interaction on periodontal diseases. Japanese Dental Science Review, [S.L.], v. 53, n. 4, p. 134-140, nov. 2017. Elsevier BV. http://dx.doi.org/10.1016/j.jdsr.2017.06.001.
25. PAPAPANOU, P.N. and SUSIN, C. (2017), Periodontitis epidemiology: is periodontitis under-recognized, over-diagnosed, or both?. Periodontol 2000, 75: 45-51. https://doi.org/10.1111/prd.12200
26. PETERSEN, P.E. and OGAWA, H. (2012), The global burden of periodontal disease: towards integration with chronic disease prevention and control. Periodontology 2000, 60: 15-39. https://doi.org/10.1111/j.1600-0757.2011.00425.x
27. PIZZICANNELLA, J, et al. Endothelial committed oral stem cells as modelling in the relationship between periodontal and cardiovascular disease. J Cell Physiol. 2018; 233: 6734– 6747. https://doi.org/10.1002/jcp.26515
28. RAMIRES JAF, CÉSAR LAM, FERREIRA JMF. Insuficiência coronariana crônica. Rev Bras Med. 2003; 60(7): 415–28.
29. SAITO A; SOJAR H.T; GENCO R.J. Interleukin-1 gene expression and protein tyrosine kinase activities induced by surface protein components of Porphyromonas gingivalis: role of tyrosine kinases in signal transduction. Oral Microbiol Immunol., v.12, p. 135-140, 1997.
30. SILVA, Grazielle Caroline; et al . Experimental Periodontal Disease Triggers Coronary Endothelial Dysfunction in Middle-Aged Rats: preventive effect of a prebiotic β-glucan. The Journals Of Gerontology: Series A, [S.L.], v. 76, n. 8, p. 1398-1406, 3 mar. 2021. Oxford University Press (OUP). http://dx.doi.org/10.1093/gerona/glab066.
31. SMALL DM. George Lyman Duff memorial lecture. Progression and regression of atherosclerotic lesions. Insights from lipid physical biochemistry. Arteriosclerosis. 1988;8: 103–129. pmid:3348756
32. STELZEL, M., et al (2002), Detection of Porphyromonas gingivalis DNA in Aortic Tissue by PCR. Journal of Periodontology, 73: 868-870. https://doi.org/10.1902/jop.2002.73.8.868
33. SUAREZ, L.J. et al. Relative proportions of T-cell subpopulations and cytokines that mediate and regulate the adaptive immune response in patients with aggressive periodontitis. J. Periodontol., Chicago, v.75, n.9, p.1209-1215, 2004.
34. SUH, J.S., et al. Periodontitis-induced systemic inflammation exacerbates atherosclerosis partly via endothelial–mesenchymal transition in mice. Int J Oral Sci 11, 21 (2019). https://doi.org/10.1038/s41368-019-0054-1
35. WANG, C.-Y., TANI-ISHII, N. and STASHENKO, P. (1997), Bone-resorptive cytokine gene expression in periapical lesions in the rat. Oral Microbiology and Immunology, 12: 65-71. https://doi.org/10.1111/j.1399-302X.1997.tb00619.x
Publicado
2023-08-12
Como Citar
1.
Schneider DF, Hernandes L, Fiorotto AP. DOENCA PERIODONTAL COMO FATOR DE RISCO PARA DOENÇA CARDIOVASCULAR: REVISÃO DE LITERATURA. arqmudi [Internet]. 12º de agosto de 2023 [citado 6º de setembro de 2025];27(2):28-9. Disponível em: https://periodicos.uem.br/ojs/index.php/ArqMudi/article/view/67688
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Artigo de Revisão em Morfofisiologia
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