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Although type 1 diabetes mellitus and type 2 diabetes mellitus have different etiologies, and their impact on bone is not identical, they share many of the same complications. Studies in animals and humans agree that both forms of diabetes increase inflammatory events in periodontal tissue, impair new bone formation, and increase expression of RANKL in response to bacterial challenge. High levels of glucose, reactive oxygen species, and advanced glycation end\u2010products are found in the periodontium of diabetic individuals and lead to increased activation of nuclear factor\u2010kappa B and expression of inflammatory cytokines such as tumor necrosis factor and interleukin\u20101. Studies in animals, moreover, suggest that there are multiple cell types in periodontal tissues that are affected by diabetes, including leukocytes, vascular cells, mesenchymal stem cells, periodontal ligament fibroblasts, osteoblasts, and osteocytes. The etiology of periodontal disease involves the host response to bacterial challenge that is affected by diabetes, which increases the expression of RANKL and reduces coupled bone formation. In addition, the inflammatory response also modifies the oral microbiota to render it more pathogenic, as demonstrated by increased inflammation and bone loss in animals where bacteria are transferred from diabetic donors to germ\u2010free hosts compared with transfer from normoglycemic donors. This approach has the advantage of not relying upon limited knowledge of the specific bacterial taxa to determine pathogenicity, and examines the overall impact of the microbiota rather than the presumed pathogenicity of a few bacterial groups. Thus, animal studies have provided new insights into pathogenic mechanisms that identify cause\u2010and\u2010effect relationships that are difficult to perform in human studies.<\/jats:p>","DOI":"10.1111\/prd.12318","type":"journal-article","created":{"date-parts":[[2019,12,18]],"date-time":"2019-12-18T05:57:25Z","timestamp":1576648645000},"page":"214-224","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":373,"title":["The impact of diabetes on periodontal diseases"],"prefix":"10.1111","volume":"82","author":[{"given":"Dana T.","family":"Graves","sequence":"first","affiliation":[{"name":"Department of Periodontics School of Dental Medicine University of Pennsylvania Philadelphia Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhenjiang","family":"Ding","sequence":"additional","affiliation":[{"name":"Department of Periodontics School of Dental Medicine University of Pennsylvania Philadelphia Pennsylvania USA"},{"name":"Department of Pediatric Dentistry School of Stomatology China Medical University Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yingming","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Periodontics School of Dental Medicine University of Pennsylvania Philadelphia Pennsylvania USA"},{"name":"State Key Laboratory of Oral Diseases and National Clinical Research Center for Oral Diseases Department of Preventive Dentistry West China School of Stomatology Sichuan University Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2019,12,18]]},"reference":[{"key":"e_1_2_10_2_1","volume-title":"IDF Diabetes Atlas","year":"2017"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s11892-018-1019-z"},{"issue":"2","key":"e_1_2_10_4_1","first-page":"63","article-title":"Diabetes and periodontal disease. 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