J Bacteriol Virol.  2016 Mar;46(1):52-56. 10.4167/jbv.2016.46.1.52.

Link between Periodontal Disease and Diabetes

• Na HS
• Chung J

• KMID: 2168744
• DOI: http://doi.org/10.4167/jbv.2016.46.1.52

Abstract

Diabetes mellitus (DM) is a complex disease with various systemic and oral complications including periodontitis. Periodontitis is a disease that leads to destruction of the soft and hard tissues of periodontium, which can result in periodontal bone loss and tooth loss. Although the etiology for periodontitis is bacterial plaque, the host immune response also mediates the destruction of periodontal tissues. DM is related to the development, progression and severity of periodontitis. There are several factors potentially contributing to the development of periodontitis in DM patients: 1) altered immune function, 2) hyperglycemia and advanced glycation end products, and 3) altered lipid metabolism. With limited number of studies, the potential mechanisms involved in the development of DM in periodontitis have also been suggested. DM clearly increases the risk of periodontitis and biological mechanisms have been illucidated. Less clear is the impact of periodontitis on the development of DM. It is possible that periodontitis may serve as initiators or propagators of insulin resistance in a way similar to obesity, thereby aggravating glycemic control.

Keyword

Periodontitis; Diabetes; Immune response; Advanced glycation end products; Lipid metabolism

MeSH Terms

Alveolar Bone Loss
Diabetes Mellitus
Glycosylation End Products, Advanced
Humans
Hyperglycemia
Insulin Resistance
Lipid Metabolism
Obesity
Periodontal Diseases*
Periodontitis
Periodontium
Tooth Loss
Glycosylation End Products, Advanced

Reference

1). Loe H. Periodontal disease. The sixth complication of diabetes mellitus. Diabetes Care. 1993; 16:329–34.

2). Kolb H, Mandrup-Poulsen T. The global diabetes epidemic as a consequence of lifestyle-induced low-grade inflammation. Diabetologia. 2010; 53:10–20.

3). Graves DT, Kayal RA. Diabetic complications and dysregulated innate immunity. Front Biosci. 2008; 13:1227–39.

4). Cortelli JR, Aquino DR, Cortelli SC, Fernandes CB, de Carvalho-Filho J, Franco GC, et al. Etiological analysis of initial colonization of periodontal pathogens in oral cavity. J Clin Microbiol. 2008; 46:1322–9.

5). Navarro-Sanchez AB, Faria-Almeida R, Bascones-Martinez A. Effect of non-surgical periodontal therapy on clinical and immunological response and glycaemic control in type 2 diabetic patients with moderate periodontitis. J Clin Periodontol. 2007; 34:835–43.

6). Gurav A, Jadhav V. Periodontitis and risk of diabetes mellitus. J Diabetes. 2011; 3:21–8.

7). Engebretson SP, Vossughi F, Hey-Hadavi J, Emingil G, Grbic JT. The influence of diabetes on gingival crevicular fluid beta-glucuronidase and interleukin-8. J Clin Periodontol. 2006; 33:784–90.

8). Karima M, Kantarci A, Ohira T, Hasturk H, Jones VL, Nam BH, et al. Enhanced superoxide release and elevated protein kinase C activity in neutrophils from diabetic patients: association with periodontitis. J Leukoc Biol. 2005; 78:862–70.

9). Salvi GE, Beck JD, Offenbacher S. PGE2, IL-1 beta, and TNF-alpha responses in diabetics as modifiers of periodontal disease expression. Ann Periodontol. 1998; 3:40–50.

10). Martinon F. Signaling by ROS drives inflammasome activation. Eur J Immunol. 2010; 40:616–9.

11). Feuerer M, Herrero L, Cipolletta D, Naaz A, Wong J, Nayer A, et al. Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters. Nat Med. 2009; 15:930–9.

12). Ribeiro FV, de Mendonca AC, Santos VR, Bastos MF, Figueiredo LC, Duarte PM. Cytokines and bone-related factors in systemically healthy patients with chronic periodontitis and patients with type 2 diabetes and chronic periodontitis. J Periodontol. 2011; 82:1187–96.

13). Duarte PM, Santos VR, Dos Santos FA, de Lima Pereira SA, Rodrigues DB, Napimoga MH. Role of smoking and type 2 diabetes in the immunobalance of advanced chronic periodontitis. J Periodontol. 2011; 82:429–38.

14). Pacios S, Kang J, Galicia J, Gluck K, Patel H, Ovaydi-Mandel A, et al. Diabetes aggravates periodontitis by limiting repair through enhanced inflammation. FASEB J. 2012; 26:1423–30.

15). Hotamisligil GS, Peraldi P, Budavari A, Ellis R, White MF, Spiegelman BM. IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. Science. 1996; 271:665–8.

16). Feingold KR, Doerrler W, Dinarello CA, Fiers W, Grunfeld C. Stimulation of lipolysis in cultured fat cells by tumor necrosis factor, interleukin-1, and the interferons is blocked by inhibition of prostaglandin synthesis. Endocrinology. 1992; 130:10–6.

17). Ryan ME, Carnu O, Kamer A. The influence of diabetes on the periodontal tissues. J Am Dent Assoc. 2003; 134:Spec No: 3. 4S–40S.

18). Yan SF, Ramasamy R, Schmidt AM. Receptor for AGE (RAGE) and its ligands-cast into leading roles in diabetes and the inflammatory response. J Mol Med (Berl). 2009; 87:235–47.

19). Lalla E, Lamster IB, Feit M, Huang L, Schmidt AM. A murine model of accelerated periodontal disease in diabetes. J Periodontal Res. 1998; 33:387–99.

20). Lalla E, Lamster IB, Feit M, Huang L, Spessot A, Qu W, et al. Blockade of RAGE suppresses periodontitis-associated bone loss in diabetic mice. J Clin Invest. 2000; 105:1117–24.

21). Rojo-Botello NR, Garcia-Hernandez AL, Moreno-Fierros L. Expression of toll-like receptors 2, 4 and 9 is increased in gingival tissue from patients with type 2 diabetes and chronic periodontitis. J Periodontal Res. 2012; 47:62–73.

22). Mealey BL, Oates TW. Diabetes mellitus and periodontal diseases. J Periodontol. 2006; 77:1289–303.

23). Goova MT, Li J, Kislinger T, Qu W, Lu Y, Bucciarelli LG, et al. Blockade of receptor for advanced glycation end-products restores effective wound healing in diabetic mice. Am J Pathol. 2001; 159:513–25.

24). Santana RB, Xu L, Chase HB, Amar S, Graves DT, Trackman PC. A role for advanced glycation end products in diminished bone healing in type 1 diabetes. Diabetes. 2003; 52:1502–10.

25). Hulbert AJ, Turner N, Storlien LH, Else PL. Dietary fats and membrane function: implications for metabolism and disease. Biol Rev Camb Philos Soc. 2005; 80:155–69.

26). Iacopino AM, Cutler CW. Pathophysiological relationships between periodontitis and systemic disease: recent concepts involving serum lipids. J Periodontol. 2000; 71:1375–84.

27). Feingold KR, Staprans I, Memon RA, Moser AH, Shigenaga JK, Doerrler W, et al. Endotoxin rapidly induces changes in lipid metabolism that produce hypertriglyceridemia: low doses stimulate hepatic triglyceride production while high doses inhibit clearance. J Lipid Res. 1992; 33:1765–76.

28). Simpson TC, Weldon JC, Worthington HV, Needleman I, Wild SH, Moles DR, et al. Treatment of periodontal disease for glycaemic control in people with diabetes mellitus. Cochrane Database Syst Rev. 2015; 11:CD004714.

29). D'Aiuto F, Nibali L, Parkar M, Patel K, Suvan J, Donos N. Oxidative stress, systemic inflammation, and severe periodontitis. J Dent Res. 2010; 89:1241–6.

30). Bastos AS, Graves DT, Loureiro AP, Rossa Junior C, Abdalla DS, Faulin Tdo E, et al. Lipid peroxidation is associated with the severity of periodontal disease and local inflammatory markers in patients with type 2 diabetes. J Clin Endocrinol Metab. 2012; 97:E1353–62.