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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<jats:italic>db\/db<\/jats:italic>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<jats:italic>Porphyromonas gingivalis<\/jats:italic>W50. We demonstrated that periodontal infected mice with high blood glucose levels showed dramatically more alveolar bone loss than their counterparts, in which infected<jats:italic>db\/db<\/jats:italic>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-<jats:italic>\u03b1<\/jats:italic>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.<\/jats:p>","DOI":"10.1155\/2016\/4840203","type":"journal-article","created":{"date-parts":[[2016,11,23]],"date-time":"2016-11-23T16:08:18Z","timestamp":1479917298000},"page":"1-10","source":"Crossref","is-referenced-by-count":17,"title":["Comparison of Experimental Diabetic Periodontitis Induced by<i>Porphyromonas gingivalis<\/i>in Mice"],"prefix":"10.1155","volume":"2016","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1588-9047","authenticated-orcid":true,"given":"Qi","family":"Wang","sequence":"first","affiliation":[{"name":"State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, No. 14, 3rd Section S. 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