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Paradigms for bidirectional relationships between periodontitis and diabetes are discussed and opportunities for elaborating these models are considered.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Database searches were performed using MeSH terms, keywords, and title words. Studies were evaluated and summarized in a narrative review.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Periodontal microbiota appears unaltered by diabetes and there is little evidence that it may influence glycaemic control. Small\u2010scale clinical studies and experiments in animal models suggest that <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2, <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, <jats:styled-content style=\"fixed-case\">OPG<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">RANKL<\/jats:styled-content> may mediate periodontitis in diabetes. The <jats:styled-content style=\"fixed-case\">AGE<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">RAGE<\/jats:styled-content> axis is likely an important pathway of tissue destruction and impaired repair in diabetes\u2010associated periodontitis. A role for locally activated pro\u2010inflammatory factors in the periodontium, which subsequently impact on diabetes, remains speculative.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>There is substantial information on potential mechanistic pathways which support a close association between diabetes and periodontitis, but there is a real need for longitudinal clinical studies using larger patient groups, integrated with studies of animal models and cells\/tissues in vitro.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jcpe.12059","type":"journal-article","created":{"date-parts":[[2013,4,30]],"date-time":"2013-04-30T12:21:38Z","timestamp":1367324498000},"source":"Crossref","is-referenced-by-count":234,"title":["A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes"],"prefix":"10.1111","volume":"40","author":[{"given":"John J.","family":"Taylor","sequence":"first","affiliation":[{"name":"Centre for Oral Health Research and Institute of Cellular Medicine Newcastle University Newcastle upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip M.","family":"Preshaw","sequence":"additional","affiliation":[{"name":"Centre for Oral Health Research and Institute of Cellular Medicine Newcastle University Newcastle upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Evanthia","family":"Lalla","sequence":"additional","affiliation":[{"name":"Division of Periodontics Columbia University College of Dental Medicine New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,4,30]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.archoralbio.2012.06.007"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bone.2006.09.011"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-051X.2011.01764.x"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.55.02.06.db05-1201"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.283481"},{"key":"e_1_2_5_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellimm.2011.09.008"},{"key":"e_1_2_5_8_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI3042"},{"key":"e_1_2_5_9_1","doi-asserted-by":"publisher","DOI":"10.1902\/jop.2009.080385"},{"key":"e_1_2_5_10_1","first-page":"128","article-title":"Ex vivo lipopolysaccharide (LPS)\u2010induced TNF\u2010alpha, IL\u20101beta, IL\u20106 and PGE2 secretion in whole blood from Type 1 diabetes mellitus patients with or without aggressive periodontitis","volume":"14","author":"Araya A. 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