Diabetes is a risk factor for periodontitis, an inflammatory bone disorder and the greatest cause of tooth loss in adults. Diabetes has a significant impact on the gut microbiota; however, studies in the oral cavity have been inconclusive. By 16S rRNA sequencing, we show here that diabetes causes a shift in oral bacterial composition and, by transfer to germ-free mice, that the oral microbiota of diabetic mice is more pathogenic. Furthermore, treatment with IL-17 antibody decreases the pathogenicity of the oral microbiota in diabetic mice; when transferred to recipient germ-free mice, oral microbiota from IL-17-treated donors induced reduced neutrophil recruitment, reduced IL-6 and RANKL, and less bone resorption. Thus, diabetes-enhanced IL-17 alters the oral microbiota and renders it more pathogenic. Our findings provide a mechanistic basis to better understand how diabetes can increase the risk and severity of tooth loss. Diabetes increases periodontal disease, a major cause of tooth loss. Xiao et al. demonstrated, by transfer to germ-free mice, that oral microbiota from diabetic mice induced more periodontal inflammation and bone loss than microbiota from normal mice. Diabetes increased the pathogenicity of the oral microbiota through an IL-17-mediated mechanism.
|Journal||Cell Host and Microbe|
|State||Published - Jul 12 2017|
Bibliographical noteFunding Information:
This work was supported by grants R01DE017732 and R01DE021921 from the NIDCR and by assistance from the Center for Host-Bacteria Interactions, University of Pennsylvania School of Veterinary Medicine and the Imaging Core of the Penn Center for Musculoskeletal Diseases. We would like to thank Ana Misic, Dan Beiting, and Aurea Simon-Soro for helpful discussions. We also thank Somreeta Sharma, Lina Jawari, and Richa Pande for their assistance with histologic analysis.
© 2017 Elsevier Inc.
- bone loss
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