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Journal of Diabetes Research
Volume 2016 (2016), Article ID 4840203, 10 pages
Research Article

Comparison of Experimental Diabetic Periodontitis Induced by Porphyromonas gingivalis in Mice

1State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, No. 14, 3rd Section S. Renmin Road, Chengdu, China
2Center for Dental Research, School of Dentistry, Loma Linda University, 11175 Campus Street, Loma Linda, CA, USA
3Shandong Provincial Key Laboratory of Oral Tissue Regeneration, School of Stomatology, Shandong University, 44-1 Wenhua W. Road, Jinan, China
4Department of Prosthodontics, The Affiliated Hospital of Stomatology, Guangxi Medical University, 10 Shuangyong Road, Nanning 530021, China

Received 9 June 2016; Accepted 2 November 2016

Academic Editor: Jose López-López

Copyright © 2016 Qi Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Periodontitis is one of the severe complications in diabetic patients and gingival epithelium plays an initial role on the onset and progression of this disease. However the potential mechanism is yet sufficiently understood. Meanwhile, the research on the correlational experimental animal models was also insufficient. Here, we established periodontitis with type 2 diabetes in db/db and Tallyho/JngJ (TH) mice and periodontitis with type 1 diabetes in streptozotocin induced diabetes C57BL/6J (STZ-C57) mice by oral infection of periodontal pathogen Porphyromonas gingivalis W50. We demonstrated that periodontal infected mice with high blood glucose levels showed dramatically more alveolar bone loss than their counterparts, in which infected db/db mice exhibited the most bone defects. No contrary impact could be observed between this periodontal infection and onset and severity of diabetes. The expressions of PTPN2 were inhibited whereas the expression of JAK1, STAT1, and STAT3 increased dramatically in gingival epithelia and the serum TNF-α also significantly increased in the mice with diabetic periodontitis. Our results indicated that the variations of inflammation-related protein expressions in gingival epithelia might lead to the phenotype differences in the mice with diabetic periodontitis.