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Therapeutic potential for insulin on type 1 diabetes‐associated periodontitis: Analysis of experimental periodontitis in streptozotocin‐induced diabetic rats

AIMS/INTRODUCTION: The association between diabetes and periodontal disease is considered to be bidirectional. However, there is still controversy surrounding the relationship between periodontal disease and type 1 diabetes. We investigated whether insulin improves periodontitis without any local tr...

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Detalles Bibliográficos
Autores principales: Nishikawa, Toru, Suzuki, Yuki, Sawada, Noritaka, Kobayashi, Yasuko, Nakamura, Nobuhisa, Miyabe, Megumi, Miyajima, Shin‐ichi, Adachi, Kei, Minato, Tomomi, Mizutani, Makoto, Toriumi, Taku, Ohno, Norikazu, Kikuchi, Takeshi, Honda, Masaki, Noguchi, Toshihide, Mitani, Akio, Matsubara, Tatsuaki, Naruse, Keiko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7610127/
https://www.ncbi.nlm.nih.gov/pubmed/32302049
http://dx.doi.org/10.1111/jdi.13276
Descripción
Sumario:AIMS/INTRODUCTION: The association between diabetes and periodontal disease is considered to be bidirectional. However, there is still controversy surrounding the relationship between periodontal disease and type 1 diabetes. We investigated whether insulin improves periodontitis without any local treatments for periodontitis under type 1 diabetes conditions using the ligature‐induced experimental periodontitis model. MATERIALS AND METHODS: Type 1 diabetic rats were induced by streptozotocin injection. Experimental periodontitis was induced by ligature in normal and diabetic rats. Half of the diabetic rats were treated with insulin. Two weeks after the ligature, periodontitis was evaluated. RESULTS: Insulin treatment significantly improved inflammatory cell infiltration and inflammatory cytokine gene expression, leading to suppression of alveolar bone loss, in the periodontitis of diabetic rats. Insulin also suppressed the periodontitis‐increased nitric oxide synthase‐positive cells in periodontal tissue of the diabetic rats. Even without induction of periodontitis, diabetic rats showed decreased gingival blood flow and an increased number of nitric oxide synthase‐positive cells in the gingiva and alveolar bone loss compared with normal rats, all of which were ameliorated by insulin treatment. We further confirmed that insulin directly suppressed lipopolysaccharide‐induced inflammatory cytokine expressions in THP‐1 cells. CONCLUSIONS: There were abnormalities of periodontal tissue even without the induction of periodontitis in streptozotocin‐induced diabetic rats. Insulin treatment significantly ameliorated periodontitis without local periodontitis treatment in diabetic rats. These data suggest the therapeutic impacts of insulin on periodontitis in type 1 diabetes.