Long-term Hyperglycemia Naturally Induces Dental Caries But Not Periodontal Disease in Type-1 and Type-2 Diabetic Rodents

Periodontal disease (PD) in diabetic patients is described as the 6th complication of diabetes. We have previously shown that diabetes increases dental caries, and carious inflammation might have a strong effect on the adjacent periodontal tissue in diabetic rodent models. However, the possibility t...

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Veröffentlicht in:Diabetes (New York, N.Y.) N.Y.), 2017-11, Vol.66 (11), p.2868-2874
Hauptverfasser: Nakahara, Yutaka, Ozaki, Kiyokazu, Matsuura, Tetsuro
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Sprache:eng
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Zusammenfassung:Periodontal disease (PD) in diabetic patients is described as the 6th complication of diabetes. We have previously shown that diabetes increases dental caries, and carious inflammation might have a strong effect on the adjacent periodontal tissue in diabetic rodent models. However, the possibility that hyperglycemia may induce PD in diabetic animals could not be completely eliminated. The goal of this study was to confirm the presence of PD in diabetic animal models by preventing carious inflammation with fluoride administration. F344 rats injected with alloxan (type-1 diabetic model) and mice (type-2 diabetic model) were given either tap water alone or tap water containing fluoride. A cariostatic effect of fluoride was evident in the diabetic animals. Meanwhile, fluoride treatment drastically attenuated periodontal inflammation in addition to preventing dental caries. Furthermore, with fluoride treatment, periodontitis was notably nonexistent in the periodontal tissue surrounding the normal molars, whereas the caries-forming process was clearly observed in the teeth that were enveloped with persistent periodontitis, suggesting that enhanced periodontal inflammation might have been derived from the dental caries in the diabetic rodents rather than from the PD. In conclusion, long-term hyperglycemia naturally induces dental caries but not PD in type-1 and type-2 diabetic rodents.
ISSN:0012-1797
1939-327X
DOI:10.2337/DB17-0291