Restorative Dentistry and Endodontics

The Korean Academy of Conservative Dentistry (대한치과보존학회)
권호 표지
DOI QR코드

DOI QR Code

THE ROLE OF TYPE 2 DIABETES AS A PREDISPOSING RISK FACTOR ON THE PULPO-PERIAPICAL PATHOGENESIS: REVIEW ARTICLE

치수 치근단 병소의 전구 위험요인으로서의 제 2 형 당뇨의 역할에 관한 소고

  • Kim, Jin-Hee (School of Dentistry, Seoul National University) ;
  • Bae, Kwang-Shik (Department of Conservative Dentistry, Seoul National University) ;
  • Seo, Deog-Gyu (Department of Conservative Dentistry, Yonsei University) ;
  • Hong, Sung-Tae (Department of Conservative Dentistry, Seoul National University) ;
  • Lee, Yoon (Department of Conservative Dentistry, Wonkwang University) ;
  • Hong, Sam-Pyo (Department of Oral Pathology, Seoul National University) ;
  • Kum, Kee-Yeon (Department of Conservative Dentistry, Seoul National University)
  • 김진희 (치의학전문대학원 서울대학교) ;
  • 배광식 (치과보존과학교실 서울대학교) ;
  • 서덕규 (치과보존과학교실 연세대학교) ;
  • 홍성태 (치과보존과학교실 서울대학교) ;
  • 이윤 (치과보존과학교실 원광대학교) ;
  • 홍삼표 (구강병리학교실 서울대학교) ;
  • 금기연 (치과보존과학교실 서울대학교)
  • Published : 2009.05.31
Download PDF
⟨ Previous Next ⟩

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 land 2 DM are most common form and the prevalence of the latter is recently increasing, The aim of this article was to assess whet her 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 w as larger and the degree of pulpal inflammation was more severe in diabetic rats, indicating that Type 2 D M 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 impair ed 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.

당뇨(Diabetes Mellitus)란 혈당을 조절하는 인슐린의 분비나 기능에 장애를 야기하는 질환으로 인슐린 의존성 여부에 따라 제 1 형과 제 2 형으로 분류된다. 본 종설은 최근 증가 추세에 있는 제 2 형 당뇨가 치수 치근단 병소의 병인 과정에 전구 위험요인으로 작용할 수 있는지를 평가 하고자 문헌고찰을 통해 당뇨의 병인 과정에서 특징적으로 나타나는 혈관 합병증에 관해 알아보고, 부가적으로 제 2 형 당뇨 쥐 모델에서 인위적인 치수 감염 후 얻은 치근단 조직의 조직병리학적 분석을 시행하였다. 조직학적 관찰 결과 제 2 형 당뇨 쥐에서 대조군에 비해 치수 치근단 병소의 크기가 증가하였고, 치수 염증 반응도 심하게 나타난 것으로 보아 당뇨 자체가 숙주를 감염에 취약한 상태로 만드는 전구 위험요소로 작용하였음을 알 수 있었다. 이러한 이유로는 첫째, 당뇨 시 전반적으로 나타나는 혈관 내 죽상 침착(atheromatous deposits)에 의해 혈관내벽의 두께가 두꺼워져 미세 순환의 장애는 물론 탐식 세포의 기능 저하, 면역 세포의 혈류 이동이 차단되어 치수 감염 시 쉽게 치근단 병소로 이환될 가능성이 높고, 둘째 치수 혈관에서 특징인 측부 순환(collateral circulation)의 부재에 따른 살균성 다형핵 백혈구의 활동 억제를 포함한 미세 혈관계의 취약성으로 인해 치수 조직의 재생능이 저하되어 추가적인 감염원의 공격에 대한 방어 및 치유 저하를 더욱 심화시키기 때문인 것으로 사료된다. 따라서 제 2 형 당뇨 환자의 수복치료 시 치과의사는 당뇨조절 하에서 치수 조직의 자극을 최소화하기 위한 세심한 처치가 필요하다.

Keywords

References

  1. Diabetes. Newsweek, September 4, 2000
  2. Bender IB. Diabetes and the dental pulp. J Endod 29:383-389, 2003 https://doi.org/10.1097/00004770-200306000-00001
  3. Soskolne WA and Klinger A. The relationship between periodontal diseases and diabetes: an overview. Ann Periodontol 91:263-270, 2001
  4. Mehmet I et al. Dental lesions in adult diabetic patients. NY State Dent J 73:58-60, 2007
  5. Mealey BL. Impact of advances in diabetes care on dental treatment of the diabetic patient. Compend Contin Educ Dent 19:41-58, 1998
  6. Campbell J at al. Pancreatic islet ultrastructure, serum and pancreatic immunoreactive insulin in somatotrophic and mestasomatrophic diabetes in dogs. J Submicrosc Cytol 13:599-608, 1981
  7. Yoon JW. The role of viruses and environmental factors in the induction of diabetes. Curr Top Microbiol Immunol 164:95-123, 1990
  8. Witko-Sarsat V and Deschamps-Latscha B. Neutrophil-derived oxidants and proteinases as immuno-modulating mediators in inflammation. Med Inflamm 3:257-273, 1994 https://doi.org/10.1155/S0962935194000360
  9. Schmid-Schonbein GW. et al. Viskoelastic deformation of white cells. Theory and analysis. In: Meiselman HJ, Liehtman MA, La Celle PL, eds. White cell mechanics: basic science and clinical aspects. New York: Alan R. Liss, Inc., p.19-51, 1984
  10. Keith V, et al. Vasculature of the Dental pulp of atherosclerotic monkeys: Light and electron microscopic findings. J Endod 20:469-473, 1994 https://doi.org/10.1016/S0099-2399(06)80041-5
  11. Vlassara H. Recent progress in advanced glycation end products and diabetic complications. Diabetes 46(Suppl 2):S19-25, 1997 https://doi.org/10.2337/diab.46.2.S19
  12. Cai H and Harrison DG. Endothelial dysfunction in cardiovascular disease. the role of oxidant stress. Circ Res 87:840-844, 2000 https://doi.org/10.1161/01.RES.87.10.840
  13. Sen CK and Packer L. Antixoidant and redox regulation of gene transcription. FASEB J 10:709-720, 1997
  14. Matsubrara T and Ziff M. Increased superoxide anion release from human endothelial cells in response to cytokines. J Immunol 137:3296-3298, 1986
  15. Li PF et al. Reactive oxygen species induce apoptosis of vascular smooth muscle cell. FEBS Lett 404:249-252, 1997 https://doi.org/10.1016/S0014-5793(97)00093-8
  16. Griengling KK et al. Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. Circ Res 74:1141-1148, 1994 https://doi.org/10.1161/01.RES.74.6.1141
  17. Zalba G et al. Vascular NADH/NADPH oxidase is involved in enhanced superoxide production in spontaneously hypertensive rats. Hypertension 35:1055-1061, 2000 https://doi.org/10.1161/01.HYP.35.5.1055
  18. 김인주 등. 제 2 형 당뇨병 모델 쥐에서 내피세포 의존성 혈관이완 장애의 기전. 혈관세포연구회, 대한당뇨병학회. Biowave 6:243-249, 2002
  19. Iijima R et al. Novel biological function of sialic acid(N-acetylneuraminic acid) as a hydrogen peroxide scavenger. FEBS Lett. 561:163-166, 2004 https://doi.org/10.1016/S0014-5793(04)00164-4
  20. Iijima R et al. Characterization of the reaction between sialic acid(N-acetylneuraminic acid) and hydrogen peroxide. Biol Pharm Bull 30:580-582, 2007 https://doi.org/10.1248/bpb.30.580
  21. Russell B. The dental pulp in diabetes mellitus. Acta Pathol Microbiol Scand. 70:319-320, 1967 https://doi.org/10.1111/j.1699-0463.1967.tb01299.x
  22. Bissada NF and Sharawy AM. Histologic study of gingival and pulpal vascular changes in human diabetics. Egyp Dent J 16:283-296, 1970
  23. Fouad AF. Diabetes mellitus as a modulating factor of endodontic infections. J Dent Edu 67:459-467, 2003
  24. Suchitra U et al. In search of endodontic pathogens. Kathmandu Univ Med J 4:525-529, 2006
  25. Robinson HBG and Boling LR. Anochoretic effect in pulpitis. J Am Dent Assoc 28:268, 1968
  26. Orlando C et al. Diabetes and its effects on dental pulp. J Oral Sci 48:195-199, 2006 https://doi.org/10.2334/josnusd.48.195
  27. Kawashima N. et al. Effect of NOS inhibitor on cytokine and COX2 expression in rat pulpitis. J Dent Res 84:762-767, 2005 https://doi.org/10.1177/154405910508400815
  28. Deguchi S et al. Neutrophil-mediated damage to human periodontal ligament-derived fibroblasts: role of lipopolysaccharide. J Periodontal Res 25:293-299, 1990 https://doi.org/10.1111/j.1600-0765.1990.tb00918.x
  29. Bhoola KD et al. Bioregulation of kinins: kallikreins, kininogens, and kininases. Pharmacol Rev 44:1-80, 1992
  30. Tiffany CW and Burch RM. Bradykinin stimulates tumor necrosis factor and interleukin-1 released from macrophages. FEBS Lett 247:189-192, 1989 https://doi.org/10.1016/0014-5793(89)81331-6
  31. Bhoola KD. Translocation of the neutrophil kinin moiety and changes in the regulation of kinin receptors in inflammation. Immunopharmacology 33:247-256, 1996 https://doi.org/10.1016/0162-3109(96)00067-7
  32. Weiss SJ. Tissue destruction by neutrophils. N Eng J Med 320: 365-376, 1989 https://doi.org/10.1056/NEJM198902093200606
  33. Vlassara H. Recent progress in advanced glycation end products and diabetic complications. Diabetes 46:S19-25, 1997 https://doi.org/10.2337/diabetes.46.1.19
  34. Fouad AF et al. PCR-based identification of bacteria in endodontic infections. J Clin Micro 40:1491-501, 2002
  35. Kum KY and Fouad AF. PCR-based identification of Eubacterium spp. and Eggerthella denta in endodontic infection. J Kor Acad Cons Dent 28; 241-248, 2003 https://doi.org/10.5395/JKACD.2003.28.3.241
  36. Fouad AF, Kum KY, Zhu Q. Molecular characteristics of the presence of Eubacterium spp. and Streptococcus spp. in endodontic infections. Oral Microbiol Immunol 28:241-248, 2003
  37. Sbordone L et al. Periodontal status and selected cultivable anaerobic microflora of insulin-dependent juvenile diabetics. J Periodontol 66:452-61, 1995 https://doi.org/10.1902/jop.1995.66.6.452
  38. Sbordone L et al. Periodontal status and subgingival microbiota of insulin-dependent juvenile diabetics: a 3-year longitudinal study. J Periodontol 69:120-8, 1998 https://doi.org/10.1902/jop.1998.69.2.120
  39. Ay S et al. Assessment of mandibular bone mineral density in patients with Type 2 diabetes mellitus. Dentomaxillofac Radiol 34:327-331, 2005 https://doi.org/10.1259/dmfr/52540810
  40. Toshiaki K et al. Periapical lesions in rats with streptozotocin-induced diabetes. J Endod 22:418-421, 1996 https://doi.org/10.1016/S0099-2399(96)80243-3
  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 82:322-325, 2003 https://doi.org/10.1177/154405910308200416
  42. Ward DT et al. Functional, molecular, and biochemical characterization of streptozotocin-induced diabetes. J Am Soc Nephrol 12:779-790, 2001
  43. Schneider L and Schedl H. Diabetes and intestinal calcium absorption in rat. Am J Physiol 223:1319-1323, 1972
  44. Soskolne WA and Klinger A. The relationship between periodontal diseases and diabetes: an overview. Ann Periodontol 91:263-270, 2001

Cited by

  1. Pulp necrosis following luxated injury to teeth in a patient with uncontrolled type II diabetes mellitus: a case report vol.37, pp.1, 2012, https://doi.org/10.5395/rde.2012.37.1.61