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Experimental colitis model demonstrates tissue damage from apical periodontitis and shows tacrolimus reduces bone loss.
Patients with inflammatory bowel disease (IBD) have a higher prevalence of apical periodontitis (AP), which is often associated with accelerated jawbone destruction. However, the mechanisms underlying this exacerbation remain unclear. In this study, we established a colitis+AP model and demonstrated that colitis exacerbates alveolar bone destruction. The upregulation of genes related to inflammation and neutrophils was also observed in the colitis+AP model compared with the AP-only model. In addition, colitis-induced local neutrophil infiltration was observed in the alveolar bone, which was further amplified by bacterial infection originating from the root canal. To address the exacerbated bone destruction in colitis+AP, we used a novel laser-induced cavitation system to locally deliver the immunosuppressant tacrolimus into the jawbone. This targeted approach effectively suppressed alveolar bone loss in the colitis+AP model. Our findings highlight the importance of the inflammatory interplay between IBD and AP. Systemic inflammation caused by IBD weakens local neutrophil function, leading to increased bone destruction and treatment-resistant AP. Furthermore, laser-activated local administration of tacrolimus significantly ameliorated bone destruction in AP associated with colitis.
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Nakano et al. (2026) studied this question.
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