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Cited by 398

The DOI matches its Crossref record; 131 of the 131 references it cites were found in a registry or an index.

The impact of diabetes on periodontal diseases

Graves, Dana T., Ding, Zhenjiang, Yang, Yingming·2020·Periodontology 2000
DOI 10.1111/prd.12318
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Abstract

The susceptibility and severity of periodontal diseases is made more severe by diabetes, with the impact on the disease process inversely proportional to the level of glycemic control. 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‐products are found in the periodontium of diabetic individuals and lead to increased activation of nuclear factor‐kappa B and expression of inflammatory cytokines such as tumor necrosis factor and interleukin‐1. 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‐free 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‐and‐effect relationships that are difficult to perform in human studies.

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Metadata

Authors
Graves, D. T., Ding, Z., & Yang, Y.
Venue
Periodontology 2000
Publisher
Wiley
Published
2019-12-18
Volume
82
Issue
1
Pages
214-224
ISSN
  • 0906-6713 (ISSN-L)
  • 1600-0757
DOI
10.1111/prd.12318
OpenAlex
W2994797447
Cited by
398
References
131
FWCI
25.78
Type
journal article
Language
en
Open access
closed

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