ABB  Vol.3 No.6 A , October 2012
The influence of diabetes enhanced inflammation on cell apoptosis and periodontitis
ABSTRACT
Aim: Diabetes mellitus is a metabolic disorder leading to hyperglycemia and exhibiting altered fat and protein metabolism. Diabetes altered cellular microenvironment caused myriad untoward effects. Periodontitis is chronic inflammatory disease. Diabetes and periodontitis had higher prevalence in populations. The objective studied the relationship between diabetes and periodontitis associated with cell apoptosis and the influence of diabetes enhanced inflammation on apoptosis and periodontitis. Methods: This paper studied and analyzed the papers which published in the worldwide associated with the influence of diabetes enhanced inflammation on cell apoptosis and periodontitis, and reviewed the probably mechanism associated with apoptosis. Results: Diabetes induced hyperglycemia enhanced inflammation related to cell apoptosis. Periodontitis had a higher morbidity on diabetes patients. Periodontal intervention may be benefit to controlling the diabetes. The bidirectional efficiency happened between diabetes and periodontitis. Anti-apoptotic and anti-inflammation option can improve the therapeutic effects on diabetes and periodontitis. The finding included following several aspects. 1) Advanced glycation end products enhanced inflammatory response; 2) Hyperglycemia induced cell apoptosis; 3) inflammatory cytokines caused cell apoptosis; 4) Mutuality between cell apoptosis and periodontitis; 5) Diabetes induce periodontitis and bone loss; 6) Periodontitis induced insulin resistance. 7) TNFα induce prostaglandins elicited cell apoptosis; 8) periodontal therapies had effects on diabetes. Conclusion: Diabetes can enhance inflamemation leading to apoptosis and periodontitis. Effective periodontal therapy and control glucose may produce better effects on diabetes or periodontitis. Further research required to investigate the bidirectional mechanism between diabetes and periodontitis.

Cite this paper
Chen, T. , Xu, E. , Lu, H. , Xu, H. , Wang, S. , Zhao, H. and Liu, Y. (2012) The influence of diabetes enhanced inflammation on cell apoptosis and periodontitis. Advances in Bioscience and Biotechnology, 3, 712-719. doi: 10.4236/abb.2012.326092.
References
[1]   Rossini, A.A., Mordes, J.P. and Like, A.A. (1985) Immunology of insulin-dependent diabetes mellitus. Annu Rev Immunol, 3,289–320.

[2]   Kahn, B.B. and Flier, J.S. (2000) Obesity and insulin resistance. J Clin Invest, 106,473–481.

[3]   Alikhani, M., Alikhani, Z., Boyd, C., MacLellan, C.M., Raptis, M. and Liu, R. (2007) Advanced glycation end products stimulate osteoblast apoptosis via the MAP kinase and cytosolic apoptotic pathways. Bone, 40,345–353.

[4]   Santana, R.B., Xu, L., Chase, H.B., Amar, S., Graves, D.T. and Trackman, P.C. (2003) A role for advanced glycation end products in diminished bone healing in type 1 diabetes. Diabetes, 52,1502–1510.

[5]   Kanazawa, I., Yamaguchi, T., Yamamoto, M., Yamauchi, M., Kurioka, S. and Yano, S. (2009) Serum osteocalcin level is associated with glucose metabolism and atherosclerosis parameters in type 2 diabetes mellitus. J Clin Endocrinol Metab, 94,45–49.

[6]   Chen, T.L., Zhou, Y.J. and Wu, Z.F. (1994) Distributive and quantitative analysis of thromboxane B2 gingival with periodontal diseases by radioimmunoassay and immunohistochemistry. West China Journal of Stomatology, 12(4),241-243.

[7]   Chen, T.L., Zhou, Y.J. and Wu, Z.F. (1994) Quantitative and distributive analysis of 6-keto-prostaglandin F1α in gingival with periodontal diseases by radioimmunoassay and immunohistochemistry. Journal of Clinical Stomatology, 10(4),199-202.

[8]   Folsom, A.R., Rosamond, W.D. and Shahar, E. (1999) Prospective study of markers of hemostatic function with risk of ischemic stroke, the atherosclerosis risk in communities (ARIC) study investigators. Circulation, 100( 7), 736–742.

[9]   Favaro, E., Miceli, I. and Bussolati, B. (2008) Hyperglycemia induces apoptosis of human pancreatic islet endothelial cells: effects of pravastatin on the Akt survival pathway. American Journal of Pathology, 173( 2), 442–450.

[10]   Yang, Z., Mo, X. and Gong, Q. (2008) Critical effect of VEGF in the process of endothelial cell apoptosis induced by high glucose. Apoptosis, 13(11), 1331–1343.

[11]   Ho, F.M., Lin, W.W. and Chen, B.C. (2006) High glucose-induced apoptosis in human vascular endothelial cells is mediated through NF-κB and c-Jun NH2-terminal kinase pathway and prevented by PI3K/Akt/eNOS pathway. Cellular Signalling, 18( 3), 391–399.

[12]   Sheu, M.L., Ho, F.M. and Yang, R.S.(2005) High glucose induces human endothelial cell apoptosis through a phosphoinositide 3-kinase-regulated cyclooxygenase-2 pathway. Arteriosclerosis,Thrombosis, and Vascular Biology, 25( 3), 539–545.

[13]   Collin-Osdoby, P., Nickols, G.A. and Osdoby, P.(1995) Bone cell function, regulation and communication: a role for nitric oxide. J Cell Biochem, 57,399–408.

[14]   Charbonneau, A. and Marette, A. (2010) Inducible nitric oxide synthase induction underlies lipid-induced hepatic insulin resistance in mice: potential role of tyrosine nitration of insulin signaling proteins. Diabetes, 59, 861–871.

[15]   Chen, T.L., Zhou, Y.J., Wu, Z.F. and Jin, Y. (1995) Quantitative analysis of prostaglandin E2 in gingival with periodontal diseases by radioimmunoassay and immunohistochemistry. Chinese Journal of Conservative Dentistry ,5(3),141-143

[16]   Kluck, R.M., Bossy-Wetzel, E., Green, D.R. and Newmeyer, D.D. (1997) The release of cytochrome C from mitochondria: a primary site for Bcl- 2 regulation of apoptosis, Science, 275( 5303), 1132–1136.

[17]   Davidson, S.M. and Duchen, M.R. (2007) Endothelial mitochondria: contributing to vascular function and disease. Circulation Research, 100, 1128–1141.

[18]   Wicker, L.S., Todd, J.A., Peterson, L.B. (1995) Genetic control of autoimmune diabetes in the NOD mouse. Annu Rev Immunol, 13,179–200.

[19]   McKenzie, M.D., Dudek, N.L., Mariana, L. (2006) Perforin and Fas induced by IFN gamma and TNF alpha mediate beta cell death by OT-I CTL. Int Immunol, 18,837–846.

[20]   Larsen, C.M., Faulenbach, M., Vaag, A. (2007) Interleukin-1-receptor antagonist in type 2 diabetes mellitus. N Engl J Med, 356,1517–1526.

[21]   Alba-Loureiro, T.C., Munhoz, C.D., Martins, J.O. (2007) Neutrophil function and metabolism in individuals with diabetes mellitus. Braz J Med Biol Res, 40,1037–1044.

[22]   Otton, R., Soriano, F.G., Verlengia, R., Curi, R. (2004) Diabetes induces apoptosis in lymphocytes. J Endocrinol, 182,145–156.

[23]   Graves, D.T., Liu, R. and Alikhani, M. (2006) Diabetes-enhanced inflammation and apoptosis impact on periodontal pathology. Journal Dent Res, 85( 1), 15-21.

[24]   Chen, T.L. and WU, Z.F. (2011) The molecular mechanisms of apoptosis on the onset of periodontitis. Journal of Tongji University(Med Sci), 32(4), 116-119.

[25]   Williams, R. (1990) Periodontal disease. N Engl J Med, 322,373–382.

[26]   Herskind, A.M., Christensen, K., Norgaard-Andersen, K. and Andersen, J.F. (1992) Diabetes mellitus and healing of closed fractures. Diabetes Metab, 18,63–64.

[27]   Weinstein, R., Jilka, R., Parfitt, A. and Manolagas, S. (1998) Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects of bone. J Clin Invest, 102, 274–282.

[28]   Tuominen, J., Impivaara, O., Puukka, P. and Ronnenmaa, T. (1999) Bone mineral density in patients with type 1 and type 2 diabetes. Diabetes Care, 22, 1196–1200.

[29]   Ryan, M.E., Carnu, O. and Kamer, A. (2003) The influence of diabetes on the periodontal tissues. J Am Dent Assoc, 1, 34S–40S.

[30]   Lalla, E., Lamster, I.B., Feit, M., Huang, L., Spessot, A., Qu, W., Kislinger, T., Lu, Y., Stern, D.M. and Schmidt, A.M. (2000) Blockade of RAGE suppresses periodontitis associated alveolar bone loss in diabetic mice. J Clin Invest, 105, 1117–1124.

[31]   Soell, M., Hassan, M., Miliauskaite, A., Haikel, Y. and Selimovic, D. (2007) The oral cavity of elderly patients in diabetes. Diabetes Metab, 1, S10–S18.

[32]   Kurtis, B., Devlioglu, H., Taner, I., Balos, K. and Tekin, I. (1999) IL-6 levels in gingival crecicular fluid (GCF) from patients with non-insulin dependent diabetes mellitus (NIDDM), adult periodontitis and healthy subjects. J Oral Sci, 41,163–167.

[33]   Grossi, S.G. and Genco, R.J. (1998) Periodontal disease and diabetes mellitus: a two-way relationship. Ann Periodontol, 3,51–61.

[34]   Chen, T.L., Wang, S.F., Liu, G.Q., Zhang, X.H., Tang, D.H. and Wu, Z.F. (2012) Influence of periodontitis and nonsurgical periodontal intervention on atherosclerosis diseases . Advances in Bioscience and Biotechnology, 3, doi:10.4236/abb.2012.*****

[35]   Mealey, B.L. and Rose, L.F.(2008) Diabetes mellitus and inflammatory periodontal disease. Compendium, 29, 403–413.

[36]   Ritchie, C.S.( 2009) Mechanistic links between type 2 diabetes and periodontitis. J Dent, 37, 567–584.

[37]   Bluher, M., Fasshauer, M., Tonjes, A., Kratzsch, J., Schon, M.R., Paschke, R.( 2005) Association of interleukin-6, C-reactive protein, interleukin-10 and adiponectin plasma concentrations with measures of obesity, insulin sensitivity and glucose metabolism. Exp Clin Endocrinol Diabetes, 113, 534–537.

[38]   Southerland, J.H., Taylor, G.W. and Offenbacher, S.( 2005) Diabetes and periodontal infection: making the connection. Clin Diabetes, 23, 171–178.

[39]   Nelson, R.G., Shlossman, M., Budding, L.M., Pettitt, D.J., Saad, M.F., Genco, R.J. and Knowler, W.C. (1990) Periodontal disease and NIDDM in Pima Indians. Diabetes Care, 13, 836–844.

[40]   Nibali, L,D_Aiuto,F., Griffiths, G., Patel, K., Suvan, J. and Tonetti, M.S. (2007) Severe periodontitis is associated with systemic inflammation and a dysmetabolic status: a case–control study. J Clin Periodontol, 34, 931–937.

[41]   Shin, S.W., Seo, C.Y., Han, H., Han, J.Y., Jeong, J.S. and Kwak, J.Y. (2009) 15d-PGJ2 induces apoptosis by reactive oxygen species-mediated inactivation of Akt in leukemia and colorectal cancer cells and shows in vivo antitumor activity. Clin Cancer Res, 15,5414–5425.

[42]   Cornish, J., MacGibbon, A., Lin, J.M., Watson, M., Callon, K.E. and Tong, P.C. (2008) Modulation of osteoclastogenesis by fatty acids. Endocrinology, 149, 5688–5695.

[43]   Perez-Sayans, M., Somoza-Martin, J.M., Barros-Angueira, F., Rey, J.M. and Garcia-Garcia, A. (2010) RANK/RANKL/OPG role in distraction osteogenesis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 109,679–686.

[44]   van’t, Hof, R.J. and Ralston, S.H. (1997) Cytokine-induced nitric oxide inhibits bone resorption by inducing apoptosis of osteoclast progenitors and suppressing osteoclast activity. J Bone Miner Res, 12, 1797–1804.

[45]   Venugopal, S.K., Devaraj, S., Yuhanna, I., Shaul, P. and Jialal, I. (2002) Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells. Circulation, 106( 12), 1439–1441.

[46]   Behl, Y., Krothapalli, P., Desta, T., Roy, S. and Graves, D. T. (2009) FOXO1 plays an important role in enhanced microvascular cell apoptosis and microvascular cell loss in type 1 and type 2 diabetic rats. Diabetes, 58( 4), 917–925.

[47]   Venugopal, S.K., Devaraj, S. and Jialal, I. (2005) Effect of C-reactive protein on vascular cells: evidence for a proinflammatory, proatherogenic role. Current Opinion in Nephrology and Hypertension, 14( 1), 33–37.

[48]   Alexiewicz, J.M., Kumar, D., Smogorzewski, M., Klin, M. and Massry, S.G. (1995) Polymorphonuclear leukocytes in non-insulin dependent diabetes mellitus: abnormalities in metabolism and function. Annals of Internal Medicine, 123(12), 919–924.

[49]   Grossi, S.G., Zambon, J.J., Ho, A.W., Koch, G., Dunford, R.G., Machtel, E.E., Norderyd, O.M. and Genco, R.J.(1994) Assessment of risk for periodontal disease. I. Risk indicators for attachment loss. J Periodontol, 65, 260–267.

[50]   Sanchez, A.B.N., Almeida, R.F. and Martinez, A.B. (2007) Effects of non-surgical periodontal therapy on clinical and immunological response and glycemic control in type 2 diabetic patients with moderate periodontitis. J Clin Periodontol, 34, 835–843.

[51]   Lee, H.M., Golub, L.M., Chan, D., Leung, M., Schroeder, K., Wolff, M., Simon, M. and Crout, R.( 1997) α-proteinase inhibitor in gingival fluid of humans with adult periodontitis: serpinloytic inhibition by doxycycline. J Periodont Res, 32, 9–19.

[52]   Hsu,M.J., Chang, C.K., Chen, M.C., Chen, B.C., Ma, H.P. and Hong, C.Y. (2010) Apoptosis signal-regulating kinase 1 in peptidoglycan induced COX-2 expression in macrophages. J Leukoc Biol, 87,1069–1082.

[53]   Lalla, E., Kaplan, S., Yang, J., Roth, G.A., Papapanou, P.N. and Greenberg, S. (2007) Effect of periodontal therapy on serum C-reactive proteins, E-selectin, and tumour necrosis factor α secretion by peripheral blood-derived macrophages in diabetes. A pilot study. J Periodontal Res, 42, 274–282.

 
 
Top