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Endodontik Tıp: Apikal Periodontitis Kardiyovasküler Hastalıklara Predispozan Etken Olabilir mi?

Year 2023, Volume: 5 Issue: 2, 133 - 138, 28.08.2023

Abstract

Apikal periodontitis (AP), pulpa dokusunda gelişen polimikrobiyal enfeksiyon nedeniyle periradiküler alanda gelişen akut veya kronik inflamatuar lezyon olarak bilinir. Kök kanal tedavisi sırasında enfektif doku, irrigasyon solüsyonları veya dolgu maddelerinin periapikal alana taşırılmasıyla da oluşabilen, görülme sıklığı oldukça yüksek bir patolojidir. Mikrobiyal faktörlerle konakçı immun yanıtı arasındaki etkileşim periradiküler dokuların iltihaplanması ve mineralize dokuların rezorpsiyonuyla sonuçlanır. Apikal periodontitiste görülen inflamasyon sürecinin, sistemik etkileri konusunda araştırmalar yapan endodontik tıp kavramı doğmuştur. Milattan önceki yıllara kadar dayanan endodontik tıp, endodonti bilimini pulpa ve periapikal doku patolojilerinin lokal incelenmesi ve tedavisinin ötesine taşımış; odontojenik enfeksiyonların romatoid artrit, diabet, kalp hastalıkları gibi çeşitli sistemik hastalıklarla ilişkisi incelenmiştir. İnflamatuar mediatör salınımının yoğun olduğu kronik enfeksiyonda bakterilerin metastatik yolla lokalize kalmayabileceği, uzak dokulardaki patolojiyi destekleyebileceği düşünülmektedir. Dünyada mortalite ve morbidite oranı en yüksek hastalıklar arasında üst sıralarda yer alan kardiyovasküler hastalıkların major risk faktörlerinin yanında koagulasyon eğilimini arttıran faktörler ve inflamasyon göstergeleri (fibrinojen, CRP, Cu, Fe, IL-6, TNF-α gibi) eklenmiştir. Tedavi edilmemiş enfekte kök kanalları ve apikal periodontitiste yükseldiği tespit edilen bu değerlerin, genel sağlığı etkileyebileceği düşünülmektedir. Endodontik enfeksiyonun sistemik bir hastalığa sebep olabileceği gibi sistemik hastalığın da endodontik enfeksiyonun patogenezinde rol alabileceği ve ayrıca endodontik tedavi görmüş dişlerin iyileşme sürecini de etkileyebileceği öne sürülmüştür. Bu derlemenin amacı; güncel araştırmalar ışığında kronik inflamasyona neden olan apikal periodontitis ile kardiyovasküler hastalıklar arasındaki ilişkinin araştırılmasıdır.

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References

  • 1. Ørstavik D, Pitt FT. Apical periodontitis: microbial infection and host responses. In: Ørstavik D, Pitt FT, editors. Essential Endodontology. Prevention and Treatment of Apical Periodontitis, 2nd ed. London, UK: Wiley-Blackwell;2007:179–91.
  • 2. Nair PNR. Pathogenesis of apical periodontitis and the causes of endodontic failures. Crit Rev Oral Biol Med. 2004;15:348-81.
  • 3. Martinho FC, Chiesa WMM, Leite FRM, Cirelli JA, Gomes BPFA. Correlation between clini-cal/radiographic features and inflammatory cytokine networks produced by macrophages stimulated with endodontic content. J Endod. 2012;38:740-5.
  • 4. Endo M, Martinho FC, Zaia AA, Ferraz CCR, Almeida JFA, Gomes BPFA. Quantification of cultivable bacte-ria and endotoxin in post-treatment apical periodonti-tis before and after chemo-mechanical preparation. Eur J Clin Microbiol Infect Dis. 2012;31:2575-83.
  • 5. Hong CY, Lin SK, Kok SH, Cheng SJ, Lee MS, Wang TM, et al. The role of lipopolysaccharide in infectious bo-ne resorption of periapical lesion. J Oral Pathol Med. 2004; 33:162-9.
  • 6. Wicken A, Knox KW. Lipoteichoic Acids: A New Class of Bacterial Antigen: Membrane lipoteichoic acids can function as surface antigens of gram-positive bac-teria. Science. 1975;187:1161-7.
  • 7. Martinho FC, Chiesa WMM, Leite FRM, Cirelli JA, Gomes BPFA. Antigenic activity of bacterial endodon-tic contents from primary root canal infection with periapical lesions against macrophage in the release of interleukin-1β and tumor necrosis factor α. J En-dod. 2010;36: 1467-74.
  • 8. Barbosa-Ribeiro M, De-Jesus-Soares A, Zaia AA, Fer-raz CCR, Almedia JFA, Gomes BPFA. Quantification of lipoteichoic acid contents and cultivable bacteria at the different phases of the endodontic retreatment. J Endod. 2016;42: 552-6.
  • 9. Zhao L, Chen J, Cheng L, Wang X, Du J, Wang F, et al. Effects of E nterococcus faecalis lipoteichoic acid on receptor activator of nuclear factor‐κ B ligand and os-teoprotegerin expression in periodontal ligament fib-roblasts. Int Endod J. 2014;47:163-72.
  • 10. Bhakdi S, Klonisch T, Nuber P, Fischer W. Stimula-tion of monokine production by lipoteichoic acids. Infect Immun. 1991;59:4614-20.
  • 11. Henderson B and MJC Wilson. Cytokine induction by bacteria: beyond lipopolysaccharide. Cytokine. 1996;8: 269-82.
  • 12. Baumgartner JC, Siquera JF, Sedgley CM, Kishen A. Microbiology of endodontic disease. Ingle’s endodon-tics. 2008;6:221-308.
  • 13. Orstavik D. Essential endodontology: prevention and treatment of apical periodontitis. John Wiley & Sons. 2020.
  • 14. Pallasch TJ, Wahl MJ. Focal infection: new age or ancient history? Endod Topics. 2003;4:32-45.
  • 15. Roth GA, Abate D, Abate KH, Abay SM, Abbafati CN, Abbasi N. Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 co-untries and territories, 1980–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018; 392:1736-88.
  • 16. Koletsi D, Iliadi A, Tzanetakis GN, Vavuranakis M, Eliades T. Cardiovascular disease and chronic endo-dontic infection. Is there an association? A systema-tic review and meta-analysis. Int J Environ Res Public Health. 202118:9111
  • 17. Stöllberger C and J Finsterer. Role of infectious and immune factors in coronary and cerebrovascular ar-teriosclerosis. Clin Vaccine Immunol. 2002;9: 207-15.
  • 18. Cominacini L, Rigoni A, Pasini FA, Garbin U, Davoli A, Campagnola M, et al. The binding of oxidized low density lipoprotein (ox-LDL) to ox-LDL receptor-1 reduces the intracellular concentration of nitric oxide in endothelial cells through an increased production of superoxide. J Biol Chem. 2001;276:13750-5.
  • 19. Yılmaz G. Atorvastatin kullanan dislipidemi hastala-rında tedavi öncesi ve 3 ay sonrası serum Paraokso-naz-1 ve okside LDL düzeyleri (Uzmanlık Tezi), Tak-sim eğitim ve araştırma Hastanesi, İstanbul. 2008.
  • 20. Rafferty B, Jönsson D, Kalachikov S, Demmer RT, Nowygrod R, Elkind MS, Bush H Jr, Kozarov E. Im-pact of monocytic cells on recovery of uncultivable bacteria from atherosclerotic lesions. J Intern Med. 2011;270: 273-80.
  • 21. Tomás I, Diz P, Tobías A, Scully C, Donos N. Perio-dontal health status and bacteraemia from daily oral activities: systematic review/meta-analysis. J Clin Periodontol. 2012;39: 213–28.
  • 22. Lockhart PB, Bolger AF, Papapanou PN, Osinbowale O, Trevisan M, Levison ME, et al. Periodontal disease and atherosclerotic vascular disease: does the evi-dence support an independent association? A scienti-fic statement from the American Heart Association. Circulation. 2012; 125:2520-44.
  • 23. Fouad AFJ, Diabetes mellitus as a modulating factor of endodontic infections. J Dent Educ. 2003;67: 459-67.
  • 24. Khalighinejad N, Aminoshariae MR, Aminoshariae A, Kulild JC, Mickel A, Fouad AF, Association between systemic diseases and apical periodontitis. J Endod. 2016; 42:1427-34.
  • 25. Caplan D, Chasen JB, Krall EA, Cai J, Kang S, Garcia RI, et al., Lesions of endodontic origin and risk of coro-nary heart disease. J Dent Res. 2006;85:996-1000.
  • 26. Wang C-H, Chueh L-H, Chen S-C, Feng Y-C, Hsiao CK, Chiang C-P. Impact of diabetes mellitus, hypertension, and coronary artery disease on tooth extraction after nonsurgical endodontic treatment. J Endod. 2011;37:1-5.
  • 27. Willershausen B, Kasaj A, Willerhausen I, Zahorka D, Briseño B, Blettner M, et al. Association between chronic dental infection and acute myocardial infarc-tion. J Endod. 2009;35:626-30.
  • 28. Cotti E, Dessì C, Piras A, Flore G, Deidda M, Madeddu C, et al. Association of endodontic infection with de-tection of an initial lesion to the cardiovascular sys-tem. J Endod. 2011;37:1624-9.
  • 29. Rôças IN, Siqueira JF Jr. Root canal microbiota of teeth with chronic apical periodontitis. J Clin Micro-biol 2008; 46:3599-606
  • 30. Siqueira JF Jr, Rôças IN, Alves FR, Silva MG. Bacteria in the apical root canal of teeth with primary apical periodontitis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009;107:721-6
  • 31. Liljestrand J, Mäntylä P, Paju S, Buhlin K, Kopra KAE, Persson GR, et al. Association of endodontic lesions with coronary artery disease. J Dent Res. 2016;95:1358-65.
  • 32. Costa THR, de Figueiredo Neto JA, de Oliveira AMF, de Figueiredo Lopes e Maia M, de Almeida AL, Asso-ciation between chronic apical periodontitis and co-ronary artery disease. J Endod. 2014;40:164-7.
  • 33. Rashmi N, Galhotra V, Goel P, Rajguru JP, Jha SK, Kul-karni K. Assessment of C-reactive Proteins, Cytokines, and Plasma Protein Levels in Hypertensive Patients with Apical Periodontitis. J Contemp Dent Pract. 2017; 18:516-21.
  • 34. Elbim C, Lizard G. Flow cytometric investigation of neutrophil oxidative burst and apoptosis in physio-logical and pathological situations. Cytom., : j. Int Soc Anal Cytol. 2009;75:475-81.
  • 35. Spiteller G. Is lipid peroxidation of polyunsaturated acids the only source of free radicals that induce aging and age-related diseases? Rejuvenation Res. 2010;13: 91-103.
  • 36. Shao D, Oka S, Brady CD, Haendeler J, Eaton P, Sados-hima J. Redox modification of cell signaling in the cardiovascular system. J Mol Cell Cardiol. 2012;52:550-8.
  • 37. Ghoti H, Fibach E, Merkel D, Perez-Avraham G, Grisa-riu S, Rachmilewitz E. Changes in parameters of oxi-dative stress and free iron biomarkers during treat-ment with deferasirox in iron-overloaded patients with myelodysplastic syndromes. Haematologica. 2010;95:1433.
  • 38. Kamboj SS, Sandhir R. Protective effect of N-acetylcysteine supplementation on mitochondrial oxidative stress and mitochondrial enzymes in ce-rebral cortex of streptozotocin-treated diabetic rats. Mitochondrion. 2011;11:214-22.
  • 39. Steeves CH, Potrykus J, Barnet DA, Bearne SL. Oxida-tive stress response in the opportunistic oral patho-gen Fusobacterium nucleatum. Proteomics. 2011;11: 2027-37.
  • 40. Inchingolo F, Marelli M, Annibali S, Cristalli MP, Dipalma G, Inchingolo AD, et al. Influence of endo-dontic treatment on systemic oxidative stress. Int J Med Sci. 2013; 11:1-6.
  • 41. Chauhan N, Mittal S, Tewari S, Sen J, Laller K. Associa-tion of apical periodontitis with cardiovascular dise-ase via noninvasive assessment of endothelial func-tion and subclinical atherosclerosis J Endod. 2019;45:681-90.
  • 42. Azuma MM, Gomes-Filho JE, de Barros Morais Car-doso C, Pipa CB, Narciso LG, Bomfim SR, et al. Omega 3 fatty acids reduce the triglyceride levels in rats with apical periodontitis. Braz Dent J. 2018;29:173-8.
  • 43. Conti LC, Segura-Egea JJ, Cardoso CBM, Benetti F, Azuma MM, Oliveira PHC, et al. Relationship between apical periodontitis and atherosclerosis in rats: lipid profile and histological study. Int Endod J. 2020;53:1387-97.
  • 44. Barcelos RCS, Rosa HZ, Roversi K, dos Santos Tibúr-cio-Machado C, Inchaki PT, Burger ME, et al. Apical periodontitis induces changes on oxidative stress pa-rameters and increases Na(+)/K(+)-ATPase activity in adult rats. Arch Oral Biol. 2020;118:104849.
  • 45. Fredrik F. Epidemiological aspects on apical periodon-titis. Studies based on the Prospective Population Study of Women in Göteborg and the Population Study on Oral Health in Jönköping, Sweden. Inst of Odontology. Dept of Endodontology/Oral Diagnosis.; 2007;11-78
  • 46. Gomes MS, Hugo FN, Bilgert JB, Sant’Ana Filho M, Padilha DMP, Simonsick EM, et al. Apical periodonti-tis and incident cardiovascular events in the Baltimo-re Longitudinal Study of Ageing. Int Endod J. 2016;49: 334-42.

Endodontic Medicine: Can Apical Periodontitis Be a Predisposing Factor to Cardiovascular Diseases?

Year 2023, Volume: 5 Issue: 2, 133 - 138, 28.08.2023

Abstract

Apical periodontitis (AP) is known as an acute or chronic inflammatory lesion developing in the periradicular area due to polymicrobial
infection in the pulp tissue. It is a pathology with a very high incidence, which can also occur when infected pulp tissue, dentin debris,
irrigation solutions or filling materials are carried over to the periapical area during root canal treatment. Endodontic medicine has moved
the science of endodontics beyond the local examination and treatment of pulp and periapical tissue pathologies; the relationship between
odontogenic infections and various systemic diseases such as rheumatoid arthritis, diabetes and heart diseases was investigated. It is
thought that in chronic infection where inflammatory mediator release is intense, bacteria may cause bacteremia via metastatic way and
support the pathology in distant tissues. It is suspected that chronic oral infections may have a predisposing effect on cardiovascular
diseases, which are among the diseases with the highest mortality and morbidity rates in the world. Inflammation indicators found to be
elevated in untreated infected root canals and apical periodontitis are thought to affect general health. It has been suggested that as
endodontic infection may cause a systemic disease, systemic disease may also play a role in the pathogenesis of endodontic infection and
may also affect the healing process of endodontically treated teeth.

Project Number

-

References

  • 1. Ørstavik D, Pitt FT. Apical periodontitis: microbial infection and host responses. In: Ørstavik D, Pitt FT, editors. Essential Endodontology. Prevention and Treatment of Apical Periodontitis, 2nd ed. London, UK: Wiley-Blackwell;2007:179–91.
  • 2. Nair PNR. Pathogenesis of apical periodontitis and the causes of endodontic failures. Crit Rev Oral Biol Med. 2004;15:348-81.
  • 3. Martinho FC, Chiesa WMM, Leite FRM, Cirelli JA, Gomes BPFA. Correlation between clini-cal/radiographic features and inflammatory cytokine networks produced by macrophages stimulated with endodontic content. J Endod. 2012;38:740-5.
  • 4. Endo M, Martinho FC, Zaia AA, Ferraz CCR, Almeida JFA, Gomes BPFA. Quantification of cultivable bacte-ria and endotoxin in post-treatment apical periodonti-tis before and after chemo-mechanical preparation. Eur J Clin Microbiol Infect Dis. 2012;31:2575-83.
  • 5. Hong CY, Lin SK, Kok SH, Cheng SJ, Lee MS, Wang TM, et al. The role of lipopolysaccharide in infectious bo-ne resorption of periapical lesion. J Oral Pathol Med. 2004; 33:162-9.
  • 6. Wicken A, Knox KW. Lipoteichoic Acids: A New Class of Bacterial Antigen: Membrane lipoteichoic acids can function as surface antigens of gram-positive bac-teria. Science. 1975;187:1161-7.
  • 7. Martinho FC, Chiesa WMM, Leite FRM, Cirelli JA, Gomes BPFA. Antigenic activity of bacterial endodon-tic contents from primary root canal infection with periapical lesions against macrophage in the release of interleukin-1β and tumor necrosis factor α. J En-dod. 2010;36: 1467-74.
  • 8. Barbosa-Ribeiro M, De-Jesus-Soares A, Zaia AA, Fer-raz CCR, Almedia JFA, Gomes BPFA. Quantification of lipoteichoic acid contents and cultivable bacteria at the different phases of the endodontic retreatment. J Endod. 2016;42: 552-6.
  • 9. Zhao L, Chen J, Cheng L, Wang X, Du J, Wang F, et al. Effects of E nterococcus faecalis lipoteichoic acid on receptor activator of nuclear factor‐κ B ligand and os-teoprotegerin expression in periodontal ligament fib-roblasts. Int Endod J. 2014;47:163-72.
  • 10. Bhakdi S, Klonisch T, Nuber P, Fischer W. Stimula-tion of monokine production by lipoteichoic acids. Infect Immun. 1991;59:4614-20.
  • 11. Henderson B and MJC Wilson. Cytokine induction by bacteria: beyond lipopolysaccharide. Cytokine. 1996;8: 269-82.
  • 12. Baumgartner JC, Siquera JF, Sedgley CM, Kishen A. Microbiology of endodontic disease. Ingle’s endodon-tics. 2008;6:221-308.
  • 13. Orstavik D. Essential endodontology: prevention and treatment of apical periodontitis. John Wiley & Sons. 2020.
  • 14. Pallasch TJ, Wahl MJ. Focal infection: new age or ancient history? Endod Topics. 2003;4:32-45.
  • 15. Roth GA, Abate D, Abate KH, Abay SM, Abbafati CN, Abbasi N. Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 co-untries and territories, 1980–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018; 392:1736-88.
  • 16. Koletsi D, Iliadi A, Tzanetakis GN, Vavuranakis M, Eliades T. Cardiovascular disease and chronic endo-dontic infection. Is there an association? A systema-tic review and meta-analysis. Int J Environ Res Public Health. 202118:9111
  • 17. Stöllberger C and J Finsterer. Role of infectious and immune factors in coronary and cerebrovascular ar-teriosclerosis. Clin Vaccine Immunol. 2002;9: 207-15.
  • 18. Cominacini L, Rigoni A, Pasini FA, Garbin U, Davoli A, Campagnola M, et al. The binding of oxidized low density lipoprotein (ox-LDL) to ox-LDL receptor-1 reduces the intracellular concentration of nitric oxide in endothelial cells through an increased production of superoxide. J Biol Chem. 2001;276:13750-5.
  • 19. Yılmaz G. Atorvastatin kullanan dislipidemi hastala-rında tedavi öncesi ve 3 ay sonrası serum Paraokso-naz-1 ve okside LDL düzeyleri (Uzmanlık Tezi), Tak-sim eğitim ve araştırma Hastanesi, İstanbul. 2008.
  • 20. Rafferty B, Jönsson D, Kalachikov S, Demmer RT, Nowygrod R, Elkind MS, Bush H Jr, Kozarov E. Im-pact of monocytic cells on recovery of uncultivable bacteria from atherosclerotic lesions. J Intern Med. 2011;270: 273-80.
  • 21. Tomás I, Diz P, Tobías A, Scully C, Donos N. Perio-dontal health status and bacteraemia from daily oral activities: systematic review/meta-analysis. J Clin Periodontol. 2012;39: 213–28.
  • 22. Lockhart PB, Bolger AF, Papapanou PN, Osinbowale O, Trevisan M, Levison ME, et al. Periodontal disease and atherosclerotic vascular disease: does the evi-dence support an independent association? A scienti-fic statement from the American Heart Association. Circulation. 2012; 125:2520-44.
  • 23. Fouad AFJ, Diabetes mellitus as a modulating factor of endodontic infections. J Dent Educ. 2003;67: 459-67.
  • 24. Khalighinejad N, Aminoshariae MR, Aminoshariae A, Kulild JC, Mickel A, Fouad AF, Association between systemic diseases and apical periodontitis. J Endod. 2016; 42:1427-34.
  • 25. Caplan D, Chasen JB, Krall EA, Cai J, Kang S, Garcia RI, et al., Lesions of endodontic origin and risk of coro-nary heart disease. J Dent Res. 2006;85:996-1000.
  • 26. Wang C-H, Chueh L-H, Chen S-C, Feng Y-C, Hsiao CK, Chiang C-P. Impact of diabetes mellitus, hypertension, and coronary artery disease on tooth extraction after nonsurgical endodontic treatment. J Endod. 2011;37:1-5.
  • 27. Willershausen B, Kasaj A, Willerhausen I, Zahorka D, Briseño B, Blettner M, et al. Association between chronic dental infection and acute myocardial infarc-tion. J Endod. 2009;35:626-30.
  • 28. Cotti E, Dessì C, Piras A, Flore G, Deidda M, Madeddu C, et al. Association of endodontic infection with de-tection of an initial lesion to the cardiovascular sys-tem. J Endod. 2011;37:1624-9.
  • 29. Rôças IN, Siqueira JF Jr. Root canal microbiota of teeth with chronic apical periodontitis. J Clin Micro-biol 2008; 46:3599-606
  • 30. Siqueira JF Jr, Rôças IN, Alves FR, Silva MG. Bacteria in the apical root canal of teeth with primary apical periodontitis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009;107:721-6
  • 31. Liljestrand J, Mäntylä P, Paju S, Buhlin K, Kopra KAE, Persson GR, et al. Association of endodontic lesions with coronary artery disease. J Dent Res. 2016;95:1358-65.
  • 32. Costa THR, de Figueiredo Neto JA, de Oliveira AMF, de Figueiredo Lopes e Maia M, de Almeida AL, Asso-ciation between chronic apical periodontitis and co-ronary artery disease. J Endod. 2014;40:164-7.
  • 33. Rashmi N, Galhotra V, Goel P, Rajguru JP, Jha SK, Kul-karni K. Assessment of C-reactive Proteins, Cytokines, and Plasma Protein Levels in Hypertensive Patients with Apical Periodontitis. J Contemp Dent Pract. 2017; 18:516-21.
  • 34. Elbim C, Lizard G. Flow cytometric investigation of neutrophil oxidative burst and apoptosis in physio-logical and pathological situations. Cytom., : j. Int Soc Anal Cytol. 2009;75:475-81.
  • 35. Spiteller G. Is lipid peroxidation of polyunsaturated acids the only source of free radicals that induce aging and age-related diseases? Rejuvenation Res. 2010;13: 91-103.
  • 36. Shao D, Oka S, Brady CD, Haendeler J, Eaton P, Sados-hima J. Redox modification of cell signaling in the cardiovascular system. J Mol Cell Cardiol. 2012;52:550-8.
  • 37. Ghoti H, Fibach E, Merkel D, Perez-Avraham G, Grisa-riu S, Rachmilewitz E. Changes in parameters of oxi-dative stress and free iron biomarkers during treat-ment with deferasirox in iron-overloaded patients with myelodysplastic syndromes. Haematologica. 2010;95:1433.
  • 38. Kamboj SS, Sandhir R. Protective effect of N-acetylcysteine supplementation on mitochondrial oxidative stress and mitochondrial enzymes in ce-rebral cortex of streptozotocin-treated diabetic rats. Mitochondrion. 2011;11:214-22.
  • 39. Steeves CH, Potrykus J, Barnet DA, Bearne SL. Oxida-tive stress response in the opportunistic oral patho-gen Fusobacterium nucleatum. Proteomics. 2011;11: 2027-37.
  • 40. Inchingolo F, Marelli M, Annibali S, Cristalli MP, Dipalma G, Inchingolo AD, et al. Influence of endo-dontic treatment on systemic oxidative stress. Int J Med Sci. 2013; 11:1-6.
  • 41. Chauhan N, Mittal S, Tewari S, Sen J, Laller K. Associa-tion of apical periodontitis with cardiovascular dise-ase via noninvasive assessment of endothelial func-tion and subclinical atherosclerosis J Endod. 2019;45:681-90.
  • 42. Azuma MM, Gomes-Filho JE, de Barros Morais Car-doso C, Pipa CB, Narciso LG, Bomfim SR, et al. Omega 3 fatty acids reduce the triglyceride levels in rats with apical periodontitis. Braz Dent J. 2018;29:173-8.
  • 43. Conti LC, Segura-Egea JJ, Cardoso CBM, Benetti F, Azuma MM, Oliveira PHC, et al. Relationship between apical periodontitis and atherosclerosis in rats: lipid profile and histological study. Int Endod J. 2020;53:1387-97.
  • 44. Barcelos RCS, Rosa HZ, Roversi K, dos Santos Tibúr-cio-Machado C, Inchaki PT, Burger ME, et al. Apical periodontitis induces changes on oxidative stress pa-rameters and increases Na(+)/K(+)-ATPase activity in adult rats. Arch Oral Biol. 2020;118:104849.
  • 45. Fredrik F. Epidemiological aspects on apical periodon-titis. Studies based on the Prospective Population Study of Women in Göteborg and the Population Study on Oral Health in Jönköping, Sweden. Inst of Odontology. Dept of Endodontology/Oral Diagnosis.; 2007;11-78
  • 46. Gomes MS, Hugo FN, Bilgert JB, Sant’Ana Filho M, Padilha DMP, Simonsick EM, et al. Apical periodonti-tis and incident cardiovascular events in the Baltimo-re Longitudinal Study of Ageing. Int Endod J. 2016;49: 334-42.
There are 46 citations in total.

Details

Primary Language Turkish
Subjects Dentistry
Journal Section REVİEW ARTICLE
Authors

Eray Ceylanoğlu 0000-0002-6170-8470

Dilek Hançerlioğulları 0000-0002-0404-1200

Project Number -
Publication Date August 28, 2023
Submission Date March 18, 2023
Acceptance Date July 3, 2023
Published in Issue Year 2023 Volume: 5 Issue: 2

Cite

Vancouver Ceylanoğlu E, Hançerlioğulları D. Endodontik Tıp: Apikal Periodontitis Kardiyovasküler Hastalıklara Predispozan Etken Olabilir mi?. NEU Dent J. 2023;5(2):133-8.