Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Jun 26;7(2):63-72.
doi: 10.1038/ijos.2015.2.

Diabetes mellitus related bone metabolism and periodontal disease

Ying-Ying Wu  1 , E Xiao  2 , Dana T Graves  3
Affiliations
Review

Diabetes mellitus related bone metabolism and periodontal disease

Ying-Ying Wu et al. Int J Oral Sci. .

Abstract

Diabetes mellitus and periodontal disease are chronic diseases affecting a large number of populations worldwide. Changed bone metabolism is one of the important long-term complications associated with diabetes mellitus. Alveolar bone loss is one of the main outcomes of periodontitis, and diabetes is among the primary risk factors for periodontal disease. In this review, we summarise the adverse effects of diabetes on the periodontium in periodontitis subjects, focusing on alveolar bone loss. Bone remodelling begins with osteoclasts resorbing bone, followed by new bone formation by osteoblasts in the resorption lacunae. Therefore, we discuss the potential mechanism of diabetes-enhanced bone loss in relation to osteoblasts and osteoclasts.

PubMed Disclaimer

Figures

Figure 1
Figure 1
A potential mechanism of diabetes-related alveolar bone loss in periodontal disease. Diabetes increases the RANKL/OPG ratios and enhances the expression level of AGEs, ROS and inflammatory mediators, which induce osteoblast apoptosis and osteoclastogenesis. This cascade of events contributes to both increased bone resorption and reduced reparative bone formation leading to greater alveolar bone loss in periodontal disease that is caused by bacterial pathogens. AGE, advanced glycation end product; IL, interleukin; OPG, osteoprotegerin; PDL, periodontal ligament; RANKL, receptor activator of nuclear factor kappa-B ligand; ROS, reactive oxygen species; TNF, tumor necrosis factor.
See this image and copyright information in PMC

References

    1. Bell GI, Polonsky KS. Diabetes mellitus and genetically programmed defects in beta-cell function. Nature 2001; 414(6865): 788–791. - PubMed
    1. Kahn SE. Clinical review 135: the importance of beta-cell failure in the development and progression of type 2 diabetes. J Clin Endocrinol Metab 2001; 86(9): 4047–4058. - PubMed
    1. Cavaghan MK, Ehrmann DA, Polonsky KS. Interactions between insulin resistance and insulin secretion in the development of glucose intolerance. J Clin Invest 2000; 106(3): 329–333. - PMC - PubMed
    1. Zimmet P, Alberti KG, Shaw J. Global and societal implications of the diabetes epidemic. Nature 2001; 414(6865): 782–787. - PubMed
    1. Kaul K, Tarr JM, Ahmad SI et al. Introduction to diabetes mellitus. Adv Exp Med Biol 2012; 771: 1–11. - PubMed

Publication types

MeSH terms