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Updated: Feb 26, 2026

Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
Novel Method to Target Apical Periodontitis Worsened by Inflammatory Bowel Disease
M Nakano1, Y Tanaka2, M S Kyaw1
1Division of Operative Dentistry, Department of Ecological Dentistry, Tohoku University Graduate School of Dentistry, Seiryo-machi, Aoba-ku, Sendai, Miyagi, Japan.
Inflammatory bowel disease (IBD) worsens apical periodontitis (AP) and jawbone loss by increasing inflammation and neutrophils. Local delivery of tacrolimus using laser-induced cavitation effectively reduced bone destruction in this colitis+AP model.
Area of Science:
- Oral biology
- Immunology
- Gastroenterology
Background:
- Patients with inflammatory bowel disease (IBD) exhibit a higher prevalence of apical periodontitis (AP).
- The mechanisms driving accelerated jawbone destruction in patients with co-occurring IBD and AP are not well understood.
- IBD-associated systemic inflammation may impact local immune responses in the jawbone.
Purpose of the Study:
- To investigate the exacerbation of apical periodontitis (AP) and associated alveolar bone destruction in a model of colitis.
- To elucidate the role of inflammation and neutrophils in the combined condition.
- To evaluate the efficacy of targeted immunosuppressant delivery for treating exacerbated AP in the context of colitis.
Main Methods:
- Establishment of a colitis and apical periodontitis (AP) co-morbidity mouse model.
- Gene expression analysis to identify inflammatory and neutrophil-related pathways.
- Histological examination to assess local neutrophil infiltration in alveolar bone.
- Application of a laser-induced cavitation system for localized delivery of tacrolimus.
Main Results:
- The colitis+AP model demonstrated significantly exacerbated alveolar bone destruction compared to the AP-only model.
- Upregulation of inflammation and neutrophil-associated genes was observed in the colitis+AP model.
- Colitis induced increased neutrophil infiltration in alveolar bone, further amplified by root canal infection.
- Targeted local delivery of tacrolimus via laser-induced cavitation effectively suppressed alveolar bone loss in the colitis+AP model.
Conclusions:
- Systemic inflammation from IBD impairs local neutrophil function, leading to increased bone destruction and treatment-resistant AP.
- The interplay between IBD and AP involves heightened inflammatory responses and neutrophil activity.
- Laser-activated local administration of tacrolimus presents a promising therapeutic strategy for managing severe AP associated with IBD.
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