Warning: mkdir(): Permission denied in /home/virtual/lib/view_data.php on line 81

Warning: fopen(upload/ip_log/ip_log_2024-12.txt): failed to open stream: No such file or directory in /home/virtual/lib/view_data.php on line 83

Warning: fwrite() expects parameter 1 to be resource, boolean given in /home/virtual/lib/view_data.php on line 84
The role of Type 2 Diabetes as a predisposing risk factor on the pulpo-periapical pathogenesis: review article


Your browser does not support the NLM PubReader view.

Go to this page to see a list of supporting browsers.

The role of Type 2 Diabetes as a predisposing risk factor on the pulpo-periapical pathogenesis: review article

Article information

Restor Dent Endod. 2009;34(3):169-176
Publication date (electronic) : 2009 May 31
doi : https://doi.org/10.5395/JKACD.2009.34.3.169
Jin-Hee Kim1, Kwang-shik Bae2, Deog-Gyu Seo3, Sung-Tae Hong4, Yoon Lee5, Sam-Pyo Hong6, Kee-Yeon Kum2
1School of Dentistry, Seoul National University, Korea.
2Department of Conservative Dentistry, Dental Research Institute, BK 21 Program, Seoul National University, Korea.
3Department of Conservative Dentistry, Yonsei University, Korea.
4Department of Conservative Dentistry, Seoul National University, Korea.
5Department of Conservative Dentistry, Wonkwnag University, Korea.
6Department of Oral Pathology, Dental Research Institute, BK 21 Program, Seoul National University, Korea.
Corresponding Author: Kee-Yeon Kum. Department of Conservative Dentistry, Dental Research Institute, School of Dentistry, Seoul National University, 28-2 Yeongun-dong, Chongro-gu, Seoul, Korea 110-749. Tel: +82-2-2072-2656, Fax: +82-2-764-3514, kum6139@snu.ac.kr
Received 2008 December 19; Revised 2009 January 19; Accepted 2009 January 21.

Abstract

Diabetes Mellitus (DM) is a syndrome accompanied with the abnormal secretion or function of insulin, a hormone that plays a vital role in controlling the blood glucose level (BGL). Type 1and 2 DM are most common form and the prevalence of the latter is recently increasing. The aim of this article was to assess whether Type 2 DM could act as a predisposing risk factor on the pulpo-periapical pathogenesis. Previous literature on the pathologic changes of blood vessels in DM was thoroughly reviewed. Furthermore, a histopathologic analysis of artificially-induced periapical specimens obtained from Type 2 diabetic and DM-resistant rats was compared. Histopathologic results demonstrate that the size of periapical bone destruction was larger and the degree of pulpal inflammation was more severe in diabetic rats, indicating that Type 2 DM itself can be a predisposing risk factor that makes the host more susceptible to pulpal infection. The possible reasons may be that in diabetic state the lumen of pulpal blood vessels are thickened by atheromatous deposits, and microcirculation is hindered. The function of polymorphonuclear leukocyte is also impaired and the migration of immune cells is blocked, leading to increased chance of pulpal infection. Also, lack of collateral circulation of pulpal blood vessels makes the pulp more susceptible to infection. These decrease the regeneration capacity of pulpal cells or tissues, delaying the healing process. Therefore, when restorative treatment is needed in Type 2 DM patients, dentists should minimize irritation to the pulpal tissue un der control of BGL.

Keywords: Atheromatous deposits; BGL; collateral circulation; histopathologic analysis; pulpo-periapical pathogenesis; Type 2 DM

References

1. Diabetes 2000. 09. 04. Newsweek;
2. Bender IB. Diabetes and the dental pulp. J Endod 2003. 29383–389.
3. Soskolne WA, Klinger A. The relationship between periodontal diseases and diabetes: an overview. Ann Periodontol 2001. 691–98.
4. Ilgüy M, et al. Dental lesions in adult diabetic patients. N Y State Dent J 2007. 7358–60.
5. Mealey BL. Impact of advances in diabetes care on dental treatment of the diabetic patient. Compend Contin Educ Dent 1998. 1941–58.
6. Campbell J, et al. Pancreatic islet ultrastructure, serum and pancreatic immunoreactive insulin in somatotrophic and mestasomatrophic diabetes in dogs. J Submicrosc Cytol 1981. 13599–608.
7. Yoon JW. The role of viruses and environmental factors in the induction of diabetes. Curr Top Microbiol Immunol 1990. 16495–123.
8. Witko-Sarsat V, Deschamps-Latscha B. Neutrophil -derived oxidants and proteinases as immuno-modulating mediators in inflammation. Mediators Inflamm 1994. 3257–273.
9. Schmid-Schonbein GW, et al. In : Meiselman HJ, Liehtman MA, La Celle PL, eds. Viskoelastic deformation of white cells. Theory and analysis. White cell mechanics: basic science and clinical aspects 1984. New York: Alan R. Liss, Inc.; 19–51.
10. Krell V, et al. Light and electron microscopic findings. J Endod 1994. 20469–473.
11. Vlassara H. Recent progress in advanced glycation end products and diabetic complications. Diabetes 1997. 46Suppl 2. S19–S25.
12. Cai H, Harrison DG. Endothelial dysfunction in cardiovascular disease. the role of oxidant stress. Circ Res 2000. 87840–844.
13. Sen CK, Packer L. Antixoidant and redox regulation of gene transcription. FASEB J 1996. 10709–720.
14. Matsubara T, Ziff M. Increased superoxide anion release from human endothelial cells in response to cytokines. J Immunol 1986. 1373295–3298.
15. Li PF, et al. Reactive oxygen species induce apoptosis of vascular smooth muscle cell. FEBS Lett 1997. 404249–252.
16. Griendling KK, et al. Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. Circ Res 1994. 741141–1148.
17. Zalba G, et al. Vascular NADH/NADPH oxidase is involved in enhanced superoxide production in spontaneously hypertensive rats. Hypertension 2000. 351055–1061.
18. Chun KJ, et al. Mechanism of Impaired Endothelium-dependent Vasodilation in Otsuka Long-Evans Tokushima Fatty (OLETF) Rats. J Korean Diabetes Assoc 2002. 2646–56.
19. Iijima R, et al. Novel biological function of sialic acid(N-acetylneuraminic acid) as a hydrogen peroxide scavenger. FEBS Lett 2004. 561163–166.
20. Iijima R, et al. Characterization of the reaction between sialic acid(N-acetylneuraminic acid) and hydrogen peroxide. Biol Pharm Bull 2007. 30580–582.
21. Russell B. The dental pulp in diabetes mellitus. Acta Pathol Microbiol Scand 1967. 70319–332.
22. Bissada NF, Sharawy AM. Histologic study of gingival and pulpal vascular changes in human diabetics. Egypt Dent J 1970. 16283–296.
23. Fouad AF. Diabetes mellitus as a modulating factor of endodontic infections. J Dent Educ 2003. 67459–467.
24. Suchitra U, et al. In search of endodontic pathogens. Kathmandu Univ Med J (KUMJ) 2006. 4525–529.
25. Robinson HBG, Boling LR. Anochoretic effect in pulpitis. J Am Dent Assoc 1968. 28268.
26. Catanzaro O, et al. Diabetes and its effects on dental pulp. J Oral Sci 2006. 48195–199.
27. Kawashima N, et al. Effect of NOS inhibitor on cytokine and COX2 expression in rat pulpitis. J Dent Res 2005. 84762–767.
28. Deguchi S, et al. role of lipopolysaccharide. J Periodontal Res 1990. 25293–299.
29. Bhoola KD, et al. kallikreins, kininogens, and kininases. Pharmacol Rev 1992. 441–80.
30. Tiffany CW, Burch RM. Bradykinin stimulates tumor necrosis factor and interleukin-1 released from macrophages. FEBS Lett 1989. 247189–192.
31. Bhoola KD. Translocation of the neutrophil kinin moiety and changes in the regulation of kinin receptors in inflammation. Immunopharmacology 1996. 33247–256.
32. Weiss SJ. Tissue destruction by neutrophils. N Engl J Med 1989. 320365–376.
33. Vlassara H. Recent progress in advanced glycation end products and diabetic complications. Diabetes 1997. 46S19–S25.
34. Fouad AF, et al. PCR-based identification of bacteria associated with endodontic infections. J Clin Microbiol 2002. 403223–3231.
35. Kum KY, Fouad AF. PCR-based identification of Eubacterium spp. and Eggerthella denta in endodontic infection. J Korean Acad Conserv Dent 2003. 28241–248.
36. Fouad AF, Kum KY, Zhu Q. Molecular characteristics of the presence of Eubacterium spp. and Streptococcus spp. in endodontic infections. Oral Microbiol Immunol 2003. 18249–255.
37. Sbordone L, et al. Periodontal status and selected cultivable anaerobic microflora of insulin-dependent juvenile diabetics. J Periodontol 1995. 66452–461.
38. Sbordone L, et al. a 3-year longitudinal study. J Periodontol 1998. 69120–128.
39. Ay S, et al. Assessment of mandibular bone mineral density in patients with Type 2 diabetes mellitus. Dentomaxillofac Radiol 2005. 34327–331.
40. Kohsaka T, et al. Periapical lesions in rats with streptozotocin-induced diabetes. J Endod 1996. 22418–421.
41. Iwama A, et al. The effect of high sugar intake on the development of periradicular lesions in rats with Type 2 diabetes. J Dent Res 2003. 82322–325.
42. Ward DT, et al. Functional, molecular, and biochemical characterization of streptozotocin-induced diabetes. J Am Soc Nephrol 2001. 12779–790.
43. Schneider L, Schedl H. Diabetes and intestinal calcium absorption in rat. Am J Physiol 1972. 2231319–1323.
44. Soskolne WA, et al, . The relationship between periodontal diseases and diabetes: an overview. Ann Periodontol 2001. 691–98.

Article information Continued

Copyright © 2009 The Korean Academy of Conservative Dentistry
(open-access) :

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Figure 1

Figure 1

Obliterative endarteritis in the artery of Type 2 DM(OLEFT) rat(×100).

Figure 2

Figure 2

Histopathological analysis of block specimens including mandibular first molars and periapical bone. In the OLEFT (A, Type 2 DM rat) group, there were lots of inflammatory cells such like macrophages, lymphocytes, and plasma cells in the large periapical lesion of the mesio-buccal roots (A). In the LETO (B, DM-resistant rat) group, there was relatively small apical lesion with inflammatory cells and apoptotic bodies(×100, unpublished data).