864-P: Effect of Imeglimin on Periodontitis in Streptozotocin-Induced Diabetic Rats
Introduction and Objective: Diabetes mellitus is known to be associated with a higher incidence and severity of periodontal disease, although the mechanism remains unclear. We and others previously demonstrated the involvement of increased oxidative stress, polyol pathway, and advanced glycation end...
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Published in | Diabetes (New York, N.Y.) Vol. 74; no. Supplement_1; p. 1 |
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Main Authors | , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
American Diabetes Association
20.06.2025
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Subjects | |
Online Access | Get full text |
ISSN | 0012-1797 1939-327X |
DOI | 10.2337/db25-864-P |
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Abstract | Introduction and Objective: Diabetes mellitus is known to be associated with a higher incidence and severity of periodontal disease, although the mechanism remains unclear. We and others previously demonstrated the involvement of increased oxidative stress, polyol pathway, and advanced glycation end products on periodontitis in subjects with diabetes like other chronic diabetic complications. Mitochondrial dysfunction is thought to be one of the common mechanisms of diabetic complications. To clarify the impacts of mitochondrial dysfunction on periodontitis in diabetes, we investigated the effect of imeglimin.
Methods: Diabetes was induced by intraperitoneal injection of streprozotocin(STZ) in six-week-old male Sprague-Dawley rats. 2 weeks after STZ administration, experimental periodontitis was induced by ligating nylon sutures around the cervical area of maxillary second molar teeth. Imeglimin was administered into Half of the diabetic rats for 2 weeks through an osmotic pump placed in the back skin. Two weeks after the induction of periodontitis, the rats were slaughtered, and maxillary periodontal tissues were collected and analyzed. Micro-CT analysis of maxillary alveolar bone was performed to evaluated alveolar bone loss.
Results: Imeglimin did not affect the blood glucose levels in diabetic rats. Periodontitis induced inflammatory cell infiltration of the gingiva.Periodontitis in diabetic rats showed increased inflammatory cell infiltration, increased gene expressions of TNF-α and iNOS in the gingiva, and increased alveolar bone resorption compared to that in normal rats. Administration of imeglimin significantly decreased the gene expressions of inflammatory cytokines and inflammatory cell infiltration in gingiva of diabetic rats. Imeglimin also significantly improved alveolar bone resorption in diabetic rats.
Conclusion: These results suggest that mitochondrial dysfunction may be involved in the mechanism of periodontal exacerbation in diabetes mellitus. |
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AbstractList | Introduction and Objective: Diabetes mellitus is known to be associated with a higher incidence and severity of periodontal disease, although the mechanism remains unclear. We and others previously demonstrated the involvement of increased oxidative stress, polyol pathway, and advanced glycation end products on periodontitis in subjects with diabetes like other chronic diabetic complications. Mitochondrial dysfunction is thought to be one of the common mechanisms of diabetic complications. To clarify the impacts of mitochondrial dysfunction on periodontitis in diabetes, we investigated the effect of imeglimin.
Methods: Diabetes was induced by intraperitoneal injection of streprozotocin(STZ) in six-week-old male Sprague-Dawley rats. 2 weeks after STZ administration, experimental periodontitis was induced by ligating nylon sutures around the cervical area of maxillary second molar teeth. Imeglimin was administered into Half of the diabetic rats for 2 weeks through an osmotic pump placed in the back skin. Two weeks after the induction of periodontitis, the rats were slaughtered, and maxillary periodontal tissues were collected and analyzed. Micro-CT analysis of maxillary alveolar bone was performed to evaluated alveolar bone loss.
Results: Imeglimin did not affect the blood glucose levels in diabetic rats. Periodontitis induced inflammatory cell infiltration of the gingiva.Periodontitis in diabetic rats showed increased inflammatory cell infiltration, increased gene expressions of TNF-α and iNOS in the gingiva, and increased alveolar bone resorption compared to that in normal rats. Administration of imeglimin significantly decreased the gene expressions of inflammatory cytokines and inflammatory cell infiltration in gingiva of diabetic rats. Imeglimin also significantly improved alveolar bone resorption in diabetic rats.
Conclusion: These results suggest that mitochondrial dysfunction may be involved in the mechanism of periodontal exacerbation in diabetes mellitus. Introduction and Objective: Diabetes mellitus is known to be associated with a higher incidence and severity of periodontal disease, although the mechanism remains unclear. We and others previously demonstrated the involvement of increased oxidative stress, polyol pathway, and advanced glycation end products on periodontitis in subjects with diabetes like other chronic diabetic complications. Mitochondrial dysfunction is thought to be one of the common mechanisms of diabetic complications. To clarify the impacts of mitochondrial dysfunction on periodontitis in diabetes, we investigated the effect of imeglimin. Methods: Diabetes was induced by intraperitoneal injection of streprozotocin(STZ) in six-week-old male Sprague-Dawley rats. 2 weeks after STZ administration, experimental periodontitis was induced by ligating nylon sutures around the cervical area of maxillary second molar teeth. Imeglimin was administered into Half of the diabetic rats for 2 weeks through an osmotic pump placed in the back skin. Two weeks after the induction of periodontitis, the rats were slaughtered, and maxillary periodontal tissues were collected and analyzed. Micro-CT analysis of maxillary alveolar bone was performed to evaluated alveolar bone loss. Results: Imeglimin did not affect the blood glucose levels in diabetic rats. Periodontitis induced inflammatory cell infiltration of the gingiva.Periodontitis in diabetic rats showed increased inflammatory cell infiltration, increased gene expressions of TNF-α and iNOS in the gingiva, and increased alveolar bone resorption compared to that in normal rats. Administration of imeglimin significantly decreased the gene expressions of inflammatory cytokines and inflammatory cell infiltration in gingiva of diabetic rats. Imeglimin also significantly improved alveolar bone resorption in diabetic rats. Conclusion: These results suggest that mitochondrial dysfunction may be involved in the mechanism of periodontal exacerbation in diabetes mellitus. |
Author | SASAJIMA, SACHIKO KONDO, SHUN MIYABE, MEGUMI SAIKI, TOMOKAZU NAKAMURA, NOBUHISA NARUSE, KEIKO SAWADA, NORITAKA MITANI, AKIO YAMAGUCHI, MASAYOSHI OZAKI, REINA KOJIMA, KENTO KATSUMATA, KOUDAI OHNO, TASUKU KIKUCHI, TAKESHI AIRI, HAYASHI MINATO, TOMOMI |
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SubjectTerms | Advanced glycosylation end products Alveolar bone Blood levels Bone loss Bone resorption Computed tomography Diabetes Diabetes mellitus Gingiva Gum disease Infiltration Inflammation Maxilla Mitochondria Nitric-oxide synthase Oxidative stress Periodontal diseases Periodontitis Root resorption Streptozocin Tumor necrosis factor-α |
Title | 864-P: Effect of Imeglimin on Periodontitis in Streptozotocin-Induced Diabetic Rats |
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