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 inDiabetes (New York, N.Y.) Vol. 74; no. Supplement_1; p. 1
Main Authors KONDO, SHUN, KOJIMA, KENTO, AIRI, HAYASHI, KATSUMATA, KOUDAI, NAKAMURA, NOBUHISA, MIYABE, MEGUMI, SASAJIMA, SACHIKO, OZAKI, REINA, YAMAGUCHI, MASAYOSHI, SAWADA, NORITAKA, MINATO, TOMOMI, SAIKI, TOMOKAZU, OHNO, TASUKU, KIKUCHI, TAKESHI, MITANI, AKIO, NARUSE, KEIKO
Format Journal Article
LanguageEnglish
Published New York American Diabetes Association 20.06.2025
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ISSN0012-1797
1939-327X
DOI10.2337/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.
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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Snippet Introduction and Objective: Diabetes mellitus is known to be associated with a higher incidence and severity of periodontal disease, although the mechanism...
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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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