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An update on the evidence for pathogenic mechanisms that may link periodontitis and diabetes
Author(s) -
Polak David,
Shapira Lior
Publication year - 2018
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.12803
Subject(s) - periodontitis , diabetes mellitus , medicine , oral microbiome , periodontology , chronic periodontitis , microbiome , prediabetes , bioinformatics , type 2 diabetes , immunology , dentistry , disease , endocrinology , biology
Aim To provide an update of the review by Taylor ( Journal of Clinical Periodontology , 2013, 40, S113) regarding the scientific evidence of the biological association between periodontitis and diabetes. Methods Literature searches were performed using Me SH terms, keywords and title words and were published between 2012 and November 2016. All publications were screened for their relevance. The data from the articles were extracted and summarized in tables and a narrative review. Results Small‐scale molecular periodontal microbiome studies indicate a possible association between altered glucose metabolism in pre‐diabetes and diabetes and changes in the periodontal microbiome, with no evidence for casual relationships. Clinical and animal studies found elevated gingival levels of IL 1‐β, TNF ‐α, IL ‐6, RANKL / OPG and oxygen metabolites in poorly controlled diabetes. In addition, individuals with diabetes and periodontitis exhibit high levels of circulating TNF ‐α, CRP and mediators of oxidative stress, and successful periodontal treatment reduces their levels. Conclusions The elevated pro‐inflammatory factors in the gingiva of patients with poorly controlled diabetes suggest a biological pathway that may aggravate periodontitis. Some evidence suggests that the systemic inflammatory burden in periodontitis has the potential to affect diabetes control, but no studies addressed the impact of successful periodontal therapy on the pathophysiological mechanisms involved in systemic complications of diabetes.