Evaluation the Relationship Between Periodontal Disease and Inflammatory Bowel Diseases by Emphasizing the Role of Cytokines

Year 2021, Volume: 10 Issue: 2, 143 - 149, 25.05.2021

Ayaz Enver Nurdan Özmeriç

Abstract

Periodontal disease is a local, chronic and inflammatory process that resulted from a complex interactions between biofilm and inflammatory immune response. Biofilm infections generally cause simultaneous activation of both natural and adaptive immune responses. Inflammatory bowel diseases characterized by chronic inflammation in the intestines with exacerbations and remissions. Although the etiopathogenesis is not fully known, it is suggested that the disease is caused by chronic immune-mediated intestinal damage as a result of the complex interaction of genetic susceptibility and endogenous and exogenous triggers. Cytokines take a place in many events including proliferation, growth, differentiation, hemostasis, regeneration, repair and inflammation. We aim in this review to evaluate the studies dealing with periodontal disease, inflammatory bowel diseases and their relation by emphasizing the role of cytokines.
Keywords: Cytokines; Inflammatory bowel diseases; Periodontal disease.

Keywords

Cytokines, Inflammatory Bowel Diseases, Periodontal Diseases

Supporting Institution

-

Project Number

-

Thanks

-

Periodontal Hastalık ve İnflamatuar Bağırsak Hastalıkları Arasındaki İlişkinin, Sitokinlerin Rolünü Vurgulayarak Değerlendirilmesi

Abstract

Periodontal hastalık, biyofilm ve inflamatuar immün yanıt arasındaki komplike etkileşimlerden kaynaklanan lokal, kronik ve inflamatuar yanıttır. Biyofilm enfeksiyonları genellikle hem doğal hem de kazanılmış immün yanıtlarında aktivasyonuna neden olur. Inflamatuar bağırsak hastalıkları, Aktivasyon ve remesyonla birlikte bağırsaklarda kronik inflamasyon ile karakterizedir. Etiyopatogenezi tam olarak bilinmemekle birlikte, hastalığa genetik yatkınlık ile endojen ve ekzojen tetikleyicilerin komplike etkileşiminin bir sonucu olarak kronik immün aracılı bağırsak hasarından kaynaklandığı ileri sürülmektedir. Sitokinler, proliferasyon, büyüme, farklılaşma, hemostaz, rejenerasyon, onarım ve inflamasyon gibi birçok olayda yer alır. Bu derlemede, sitokinlerin rolünü vurgulayarak periodontal hastalık, inflamatuar bağırsak hastalıkları ve bunların ilişkisini ele alan çalışmaları değerlendirmeyi amaçlamaktayız.
Anahtar Kelimeler: Sitokinler; Inflamatuar bağırsak hastalıkları; Periodontal hastalık.

Keywords

Sitokinler, Inflammatory Bowel Diseases, Periodontal Disease

Project Number

-

References

• Referans1 Hinrichs JE, Kotsakis G. Classification of Diseases and Conditions Affecting the Periodontium: In Carranza's Clinical Periodontology. Newman MG, Takei H, Klokkevold PR, Carranza FA, Eds. 12th ed. USA: Elsevier Health Sciences; 2012. p.45-67.
• Referans2 Mariotti A. Dental plaque-induced gingival diseases. Ann Periodontol. 1999;4:7-19.
• Referans3 Caton JG, Armitage G, Berglundh T, Chapple IL, Jepsen S, S. Kornman K, et al. A new classification scheme for periodontal and peri‐implant diseases and conditions–Introduction and key changes from the 1999 classification. J Periodontol. 2018;1:S1-S8.
• Referans4 Zelkha SA, Freilich RW, Amar S. Periodontal innate immune mechanisms relevant to atherosclerosis and obesity. Periodontol 2000. 2010;54:207-21.
• Referans5 Schenekein H. Academy Reports- Pathogenesis of Periodontal Disease. J Periodontol. 1999;70:457–70.
• Referans 6 Page RC, Schroeder HE. Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab Invest. 1976;34:235–49.
• Referans 7 Page RC, Offenbacher S, Schroeder HE, Seymour GJ, Kornman KS. Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions. Periodontol 2000. 1997;14:216–48.
• Referans8 Kinane DF, Bartold PM. Clinical relevance of the host responses of periodontitis. Periodontol 2000. 2007;43:278-93.
• Referans9 Holt SC, Bramanti TE. Factors in virulence expression and their role in periodontal disease pathogenesis. Crit Rev Oral Biol Med. 1991;2:177-281.
• Referans10 Madianos PN, Bobetsis YA, Kinane DF. Generation of inflammatory stimuli: how bacteria set up inflammatory responses in the gingiva. Journal of Clinical Periodontol. 2005;6:57-71.
• Referans11 Akçam M. Çocukluk çağı inflamatuar barsak hastalıkları. Türkiye Klinikleri J Pediatr Sci. 2012;8:56-60.
• Referans12 Kliegman, R, Nelson, WE. Nelson textbook of pediatrics. 18th ed. Philadelphia: Saunders; 2007.
• Referans13 Geissler, C, Powers HJ, Garrow JS. Human nutrition. 11th ed. Edinburgh; New York: Elsevier/Churchill Livingstone; 2005.
• Referans14 Gasche C, Scholmerich J, Brynskov J, D'Haens G, Hanauer GB, Irvine EJ, et al. A simple classification of Crohn's disease: report of the Working Party for the World Congresses of Gastroenterology, Vienna 1998. Inflamm Bowel Dis. 2000;6:8-15.
• Referans15 Silverberg MS, Satsangi J, Ahmad T, Arnott IDR, Bernstein CN, Brant SR, Caprilli R, et al. Toward an integrated clinical, molecular and serological classification of inflammatory bowel disease: report of a Working Party of the 2005 Montreal World Congress of Gastroenterology. Can J Gastroenterol. 2005;19A:5A-36A.
• Referans16 Walker, W.A. Pediatric gastrointestinal disease : pathophysiology, diagnosis, management. 5rd ed. Hamilton, Ont.;Lewiston, NY: B.C. Decker; 2008.
• Referans17 Gollop JH, Phillips SF, Melton LJ, Zinsmeister AR. Epidemiologic aspects of Crohn’s disease: a population based study in Olmsted County, Minnesota, 1943-1982. Gut.1988;29:49-56.
• Referans18 Tozun N, Atug O, Imeryuz N, Hamzaoglu HO, Tiftikci A, Parlak E. Clinical characteristics of inflammatory bowel disease in Turkey: a multicenter epidemiologic survey. J Clin Gastroenterol. 2009;43:51-7.
• Referans19 Gahl WA, Brantly M, Kaiser-Kupfer MI, Iwata F, Hazelwood S, Shotelersuk V, et al. Genetic defects and clinical characteristics of patients with a form of oculocutaneous albinism (Hermansky Pudlak syndrome). N Engl J Med. 1998;30;338:1258-64.
• Referans20 Roe TF, Coates TD, Thomas DW, Miller JH, Gilsanz V. Brief report: Treatment of chronic inflammatory bowel disease in glycogen storage disease type Ib with colony stimulating factors. N Engl J Med. 1992;18;326:1666-9.
• Referans21 Seymour GJ, Gemmell E. Cytokines in periodontal disease: where to from here?. Acta Odontol Scand. 2001;59:167-73.
• Referans22 Shapira L, Wilensky A, Kinane DF. Effect of genetic variability on the inflammatory response to periodontal infection. J Clin Periodontol. 2005;6:72-86.
• Referans23 Munro CL, Grap MJ, Jablonski R, Boyle A. Oral health measurement in nursing research: state of the science. Biol Res Nurs. 2006;8:35-42.
• Referans24 Giannobile WV, Beikler T, Kinney JS, Ramseier CA, Morelli T, Wong DT. Saliva as a diagnostic tool for periodontal disease: current state and future directions. Periodontol 2000. 2009;50:52-64.
• Referans25 Jaedicke KM, Taylor JJ, Preshaw PM. Validation and quality control of ELISAs for the use with human saliva samples. J Immunol Methods. 2012;30;377:62-5.
• Referans26 Jaedicke KM, Preshaw PM, Taylor JJ. Salivary cytokines as biomarkers of periodontal diseases. Periodontol 2000. 2016;70:164-83.
• Referans27 Siew NgC, Shi HY, Hamidi N, Underwood FE, Tang W, Benchimol El, et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: a systematic review of population-based studies. Lancet. 2018;23;390:2769-2778.
• Referans28 Kinane, DF, Stathopoulou PG, Papapanou PN. Periodontal diseases. Nat Rev Dis Primers. 2017;22;3:17038.
• Referans29 Nesse W, Abbas F, Van Der Ploeg I, Spijkervet FKL, Dijkstra PU, Vissink A. Periodontal inflamed surface area: quantifying inflammatory burden. J Clin Periodontol. 2008;35:668-73.
• Referans30 Pietropaoli D, Del Pinto R, Corridoni D, Rodriguez-Palacios A, Di Stefano G, Monaco A, et al. Occurence of spontaneous periodontal disease in the SAMP1-Yitc murine model of Crohn disease. J Periodontol. 2014;85:1799-805.
• Referans31 Agossa K, Dendooven A, Dubuquoy L, Gower-Rousseau C, Delcourt-Debruyne E, Capron M. Periodontal manifestations of inflammatory bowel disease: Emerging epidemiologic and biologic evidence. J. Periodontal Res. 2017;52, 313–324.
• Referans32 Khan SA, Kong EF, Meiller TF, Jabra-Rizk MA. Periodontal Diseases: Bug Induced, Host Promoted. PLoS Pathog. 2015 Jul 30;11(7):e1004952.
• Referans33 Menegat JSB, Lira-Junior R, Siqueira MA, Brito F, Carvalho AT, Fischer RG, et al. Cytokine expression in gingival and intestinal tissues of patients with periodontitis and inflammatory bowel disease: An exploratory study. Arch Oral Biol. 2016;66:141-6.
• Referans34 Koutsochristou V, Zellos A, Dimakou K, Panayotou I, Siahanidou S, Roma-Giannikou E, et al. Dental Caries and Periodontal Diseases in Children and Adolescents with Inflammatory Bowel Disease: A case-Control Study. Inflamm Bowel Dis. 2015:21:1839-46.
• Referans35 Figueredo CM, Brito F, Barros FC, Menegat JSB, Pedreira RR, Fischer RG, et al. Expression of cytokines in the gingival crevicular fluid and serum from patients with inflammatory bowel disease and untreated chronic periodontitis. J Periodont Res. 2011;46:141–146.
• Referans36 Brito F, Zaltman C, Carvalho ATP, Fischer RG, Persson R, Gustafsson A, et al. Subgingival microflora in inflammatory bowel disease patients with untreated periodontitis. Eur J Gastroenterol Hepatol. 2013;25:239.45.
• Referans37 Schulz S, Reichert S, Streetz K, Trautwein C, Reichert Y, Glaser C, et al. Tumor necrosis factor and oral inflammation in patient with Crohn disease. J Periodontol. 2014;85:1424,31.
• Referans38 Stein JM, Lammert F, Zimmer V, Granzow M, Reichert S, Schulz S, et al. Clinical periodontal and microbiologic parameters in patients with Crohns disease with consideration of the CARD15 genotype. J Periodontal. 2010;81:535-545.
• Referans39 Chu CQ, Wittmer S, Dalton DK. Failure to suppress the expansion of the activated CD4 T cell population in interferon gamma-defificient mice leads to exacerbation of experimental autoimmune encephalomyelitis. J Exp Med. 2000;3;192:123-8.
• Referans40 Zhang GX, Gran B, Yu S, Li J, Siglienti I, Chen X, et al. Induction of experimental autoimmune encephalomyelitis in IL-12 receptor-beta 2-defificient mice: IL-12 responsiveness is not required in the pathogenesis of inflflammatory demyelination in the central nervous system. J Immunol. 2003;15;170:2153-60.
• Referans41 Brito F, de Barros FC, Zaltman C, Carvalho ATP, Carneiro AJV, Fischer RG, et al. Prevalence of periodontitis and DMFT index in patients with Crohn’s disease and ulceratice colitis. J Clin Periodontol. 2008 Jun;35(6):555-60.
• Referans42 Kelsen J, Bittinger K, Pauly-Hubbard H, Posivak L, Grunberg S, Baldassano R, et al. Alteration of the subgingival microbiota in pediatric Crohn’s disese studied longitudinally in discovery and validation cohorts. Inflamm Bowel Dis. 2015;21:2797-805.
• Referans43 Andersen KM, Selvig KA, Leknes KN, Altered healing following mucogingival surgery in a patient with Crohns disease: a literature review and case report. J Periodontol. 2003;74:537-46.
• Referans44 Habashneh RA, Khader YS, Alhumouz MK, Jadallah K, Ajlouni Y. The association between inflammatory bowel disease and periodontitis among Jordanians: a case control study. J Periodontal Res. 2012;47:293-8.
• Referans45 Vavricka SR, Manser CN, Hediger S, Vögelin M, Scharl M, Biedermann L, et al. Periodontitis and gingivitis in inflammatory bowel disease: a case control study. 2013;19:2768-77.
• Referans46 Figueredo CM, Martins AP, Lira-Junior R, Menegat JB, Carvalho AT, Fischer RG, et al. Activity of inflammatory bowel disease influences the expression of cytokines in gingival tissue. Cytokine. 2017;95:1-6.
• Referans47 Bunte K, Beikler T. Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases. Int J Mol Sci. 2019;10;20:3394.
• Referans48 She Y, Kong X, Ge Y, Liu1 Z, Chen J, Jiang J, et al. Periodontitis and inflammatory bowel disease: a meta-analysis. BMC Oral Health. 2020;12;20:67.
• Referans49 Cotti E, Mezzena S, Schirru E, Ottonello O, Mura M,  Ideo F, et al. Healing of Apical Periodontitis in Patients with Inflammatory Bowel Diseases and under Anti–tumor Necrosis Factor Alpha Therapy. J Endod. 2018;44:1777-1782.
• Referans50 Ben Lagha A, Grenier D, Tea polyphenols inhibit the activation of NF-κB and the secretion of cytokines and matrix metalloproteinases by macrophages stimulated with Fusobacterium nucleatum. Sci Rep. 2016;3;6:34520.