Diyabet ve Kök Kanal Enfeksiyonlarının İlişkisi

Yıl 2023, , 77 - 83, 29.08.2023

Sevinç Aktemur Türker , Füsun Cömert

https://doi.org/10.21306/dishekimligi.1292997

Öz

Giriş: Endodontik enfeksiyonlar, periapikal dokuların enfeksiyonu olarak tanımlanmaktadır. Kök kanalında bulunan mikroorganizmaların ya da bu mikroorganizmaların toksinlerinin, enzimlerinin ve metabolitik ürünlerinin kök dışına (periapekse) invazyonu sonucu sert doku rezorpsiyonu ve periodontal ligamentin yıkım ile karakterize periapikal lezyon (apikal periododontitis) gelişmektedir. Son yıllarda yapılan çalışmalarda oral/periodontal enfeksiyon ve inflamasyonun çeşitli sistemik hastalıkların ve durumların gelişimini ve şiddetini etkileyen birer risk faktörü olduğu bildirilmiştir. Diyabet oral enfeksiyonlardan etkilenen yaygın görülen bu sistemik hastalıklardan biridir. Diyabetin oral ve periodontal sağlık ile ilgili olan ilişkisi literatürde geniş bir şekilde araştırılmıştır. Fakat periodontal enfeksiyonlara benzer özelliklere sahip endodontik enfeksiyonların diyabetik hastalarda izlediği patogenez, ilerleme ve iyileşme süreci henüz kesin olarak belirlenmemiştir.
Sonuç: Diyabetin endodontik enfeksiyonlarla olan ilişkisini bilmek, kök kanal tedavisinin teşhis, tedavi ve takibinde büyük önem taşımaktadır.

Anahtar Kelimeler

Diabetes Mellitus, Kök kanal enfeksiyonları, Mikroorganizmalar

Relationship between Diabetes Mellitus and Root Canal Infections

Öz

Objective: Endodontic infections are defined as infections of the periapical tissues. Periapical lesion (apical periododontitis), characterized by the hard tissue resorption and destruction of the periodontal ligament, develops as a result of invasion of the microorganisms in the root canal or their toxins, enzymes and metabolite products out of the root (periapex). In recent studies, it has been reported that oral/periodontal infection and inflammation are risk factors that affect the development and severity of various systemic diseases and conditions. Diabetes mellitus (DM) is one of these common systemic diseases affected by oral infections. The relationship of diabetes with oral and periodontal health has been extensively studied in the literature. However, the pathogenesis, progression and healing process of endodontic infections, which have similar features to periodontal infections, in diabetic patients have not been determined yet.
Conclusion: Knowing the relationship between DM and endodontic infections is of great importance in the diagnosis, treatment and follow-up of root canal treatment.

Anahtar Kelimeler

Diabetes Mellitus, Root canal infections, Microorganisms

Kaynakça

• 1. Sedrez-Porto JA, Rosa WL, da Silva AF, Münchow E1. Siqueira JF Jr Microbiology of apical periodontitis. In: Essential endodontology. Ørstavik D, Pitt Ford T, editors. Oxford, UK: Blackwell Munksgaard Ltd, 2008; 135–1962.
• 2. American Diabetes A. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2013;36 Suppl 1(Suppl 1):67-74.
• 3. Sano T, Matsuura T, Ozaki K, Narama I. Dental caries and caries-related periodontitis in type 2 diabetic mice. Vet Pathol. 2011 ;48(2):506-12.
• 4. Fouad AF. Diabetes mellitus as a modulating factor of endodontic infections. J Dent Educ. 2003;67(4):459-67.
• 5. Iwama A, Morimoto T, Tsuji M et al. Increased number of anaerobic bacteria in the infected root canal in type 2 diabetic rats. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006; 101(5):681-6.
• 6. Bender IB, Bender AB. Diabetes mellitus and the dental pulp. J Endod. 2003; 29(6):383-9.
• 7. Lima SM, Grisi DC, Kogawa EM et al. Diabetes mellitus and inflammatory pulpal and periapical disease: a review. Int Endod J. 2013; 46(8):700-9.
• 8. Garber SE, Shabahang S, Escher AP, Torabinejad M. The effect of hyperglycemia on pulpal healing in rats. J Endod. 2009; 35(1):60-2.
• 9. Cai W, Ramdas M, Zhu L, Chen X, Striker GE, Vlassara H. Oral advanced glycation endproducts (AGEs) promote insulin resistance and diabetes by depleting the antioxidant defenses AGE receptor-1 and sirtuin 1. Proc Natl Acad Sci USA. 2012; 109(39):15888-93.
• 10. Tanaka K, Yamaguchi T, Kaji H, Kanazawa I, Sugimoto T. Advanced glycation end products suppress osteoblastic differentiation of stromal cells by activating endoplasmic reticulum stress. Biochem Biophys Res Commun. 2013; 438(3):463-7.
• 11. Li DX, Deng TZ, Lv J, Ke J. Advanced glycation end products (AGEs) and their receptor (RAGE) induce apoptosis of periodontal ligament fibroblasts. Braz J Med Biol Res. 2014; 47(12):1036-43.
• 12. Wang YD, Wang L, Li DJ, Wang WJ. Dehydroepiandrosterone inhibited the bone resorption through the upregulation of OPG/RANKL. Cell Mol Immunol. 2006; 3(1):41-5.
• 13. Britto LR, Katz J, Guelmann M, Heft M. Periradicular radiographic assessment in diabetic and control individuals. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2003; 96(4):449-52.
• 14. Catanzaro O, Dziubecki D, Lauria LC, Ceron CM, Rodriguez RR. Diabetes and its effects on dental pulp. J Oral Sci. 2006; 48(4):195-9.
• 15. Aldoss A, Alghofaily M, Alsalleeh F. Bacterial quantity and interleukin-17 expression in necrotic teeth with apical periodontitis from type II diabetic patients. Int Endod J. 2023 ;56(7):881-95.
• 16. Lopez-Lopez J, Jane-Salas E, Estrugo-Devesa A, Velasco-Ortega E, Martin-Gonzalez J, Segura-Egea JJ. Periapical and endodontic status of type 2 diabetic patients in Catalonia, Spain: a cross-sectional study. J Endod. 2011; 37(5):598-601.
• 17. Bender IB, Seltzer S, Freedland J. The Relationship of Systemic Diseases to Endodontic Failures and Treatment Procedures. Oral Surg Oral Med Oral Pathol. 1963;16:1102-15.
• 18. Wittrant Y, Gorin Y, Woodruff K, Horn D, Abboud HE, Mohan S, et al. High d(+)glucose concentration inhibits RANKL-induced osteoclastogenesis. Bone. 2008; 42(6):1122-30.
• 19. Dienelt A, zur Nieden NI. Hyperglycemia impairs skeletogenesis from embryonic stem cells by affecting osteoblast and osteoclast differentiation. Stem Cells Dev. 2011; 20(3):465-74.
• 20. Hussain MJ, Peakman M, Gallati H, et al. Elevated serum levels of macrophage-derived cytokines precede and accompany the onset of IDDM. Diabetologia. 1996; 39(1):60-9.
• 21. Liu L, Zhang C, Hu Y, Peng B. Protective effect of metformin on periapical lesions in rats by decreasing the ratio of receptor activator of nuclear factor kappa B ligand/osteoprotegerin. J Endod. 2012; 38(7):943-7.
• 22. Cintra LT, Samuel RO, Facundo AC et al. Relationships between oral infections and blood glucose concentrations or HbA1c levels in normal and diabetic rats. Int Endod J. 2014; 47(3):228-37.
• 23. Segura-Egea JJ, Jimenez-Pinzon A, Rios-Santos JV, Velasco-Ortega E, Cisneros-Cabello R, Poyato-Ferrera M. High prevalence of apical periodontitis amongst type 2 diabetic patients. Int Endod J. 2005; 38(8):564-9.
• 24. Wang S, Wang X, Bai F, Shi X, Zhou T, Li F. Effect of endodontic treatment on clinical outcome in type 2 diabetic patients with apical periodontitis. Heliyon. 2023: 22;9(3):e13914.
• 25. Segura-Egea JJ, Martin-Gonzalez J, Castellanos-Cosano L. Endodontic medicine: connections between apical periodontitis and systemic diseases. Int Endod J. 2015; 48(10):933-51.
• 26. Siqueira JF, Jr., Rocas IN. A critical analysis of research methods and experimental models to study the root canal microbiome. Int Endod J. 2022; 55 Suppl 1:46-71.
• 27. Xu X, He J, Xue J et al. Oral cavity contains distinct niches with dynamic microbial communities. Environ Microbiol. 2015; 17(3):699-710.
• 28. Mason MR, Nagaraja HN, Camerlengo T, Joshi V, Kumar PS. Deep sequencing identifies ethnicity-specific bacterial signatures in the oral microbiome. PLoS One. 2013; 8(10):e77287.
• 29. Belstrom D, Holmstrup P, Nielsen CH et al. Bacterial profiles of saliva in relation to diet, lifestyle factors, and socioeconomic status. J Oral Microbiol. 2014;1-6.
• 30. Li J, Quinque D, Horz HP et al. Comparative analysis of the human saliva microbiome from different climate zones: Alaska, Germany, and Africa. BMC Microbiol. 2014; 14:316.
• 31. Graves DT, Correa JD, Silva TA. The Oral Microbiota Is Modified by Systemic Diseases. J Dent Res. 2019; 98(2):148-56.
• 32. Shillitoe E, Weinstock R, Kim T et al. The oral microflora in obesity and type-2 diabetes. J Oral Microbiol. 2012;4.
• 33. Vázquez-Ramos VR, Pérez-Serrano RM, García-Solís P. et al. Root canal microbiota as an augmented reservoir of antimicrobial resistance genes in type 2 diabetes mellitus patients. J Appl Oral Sci. 2023: 3;30:e20220362.
• 34. Pickup JC. Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes. Diabetes Care. 2004; 27(3):813-23.
• 35. Fouad AF, Barry J, Caimano M et al. PCR-based identification of bacteria associated with endodontic infections. J Clin Microbiol. 2002; 40(9):3223-31.
• 36. Fouad AF, Kum KY, Clawson ML et al. Molecular characterization of the presence of Eubacterium spp and Streptococcus spp in endodontic infections. Oral Microbiol Immunol. 2003; 18(4):249-55.
• 37. Mohammadi F, Javaheri MR, Nekoeian S, Dehghan P. Identification of Candida species in the oral cavity of diabetic patients. Curr Med Mycol. 2016; 2(2):1-7.
• 38. Zomorodian K, Kavoosi F, Pishdad GR et al. Prevalence of oral Candida colonization in patients with diabetes mellitus. J Mycol Med. 2016; 26(2):103-10.
• 39. De la Torre-Luna R, Dominguez-Perez RA, Guillen-Nepita AL et al. Prevalence of Candida albicans in primary endodontic infections associated with a higher frequency of apical periodontitis in type two diabetes mellitus patients. Eur J Clin Microbiol Infect Dis. 2020; 39(1):131-8.
• 40. Gomes CC, Guimaraes LS, Pinto LCC, Camargo G, Valente MIB, Sarquis MIM. Investigations of the prevalence and virulence of Candida albicans in periodontal and endodontic lesions in diabetic and normoglycemic patients. J Appl Oral Sci. 2017; 25(3):274-81.
• 41. Delamaire M, Maugendre D, Moreno M, Le Goff MC, Allannic H, Genetet B. Impaired leucocyte functions in diabetic patients. Diabet Med. 1997; 14(1):29-34.
• 42. Iacopino AM. Periodontitis and diabetes interrelationships: role of inflammation. Ann Periodontol. 2001; 6(1):125-37.
• 43. Salvi GE, Carollo-Bittel B, Lang NP. Effects of diabetes mellitus on periodontal and peri-implant conditions: update on associations and risks. J Clin Periodontol. 2008; 35(8 Suppl):398-409.
• 44. Fouad A, Barry J, Russo J, Radolf J, Zhu Q. Periapical lesion progression with controlled microbial inoculation in a type I diabetic mouse model. J Endod. 2002; 28(1):8-16.
• 45. Iwama A, Nishigaki N, Nakamura K, Imaizumi I, Shibata N, Yamasaki M, et al. The effect of high sugar intake on the development of periradicular lesions in rats with type 2 diabetes. J Dent Res. 2003; 82(4):322-5.
• 46. Armada-Dias L, Breda J, Provenzano JC, Breitenbach M, Rocas I, Gahyva SM, et al. Development of periradicular lesions in normal and diabetic rats. J Appl Oral Sci. 2006; 14(5):371-5.
• 47. Fouad AF, Burleson J. The effect of diabetes mellitus on endodontic treatment outcome: data from an electronic patient record. J Am Dent Assoc. 2003; 134(1):43-51; quiz 117-8.
• 48. Ferreira MM, Carrilho E, Carrilho F. Diabetes mellitus e sua influência no sucesso do tratamento endodôntico: um estudo clínico retrospetivo [Diabetes mellitus and its influence on the success of endodontic treatment: a retrospective clinical study]. Acta Med Port. 2014; 27(1):15-22.