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Updated: Sep 20, 2026
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
Systemic effects of experimental apical periodontitis in animal models: Does lesion burden modulate circulating
Almir Gabriel Bolonhez Rodrigues1, Ana Carla Thalez Ywabuchi Nobumoto2, Anna Clara Cachoni3
1School of Dentistry, São Paulo State University (UNESP), Araçatuba, Brazil; Graduate Program in Science, Brazil; Department of Restorative Dentistry and Endodontics (UNESP), Brazil.
Objective:
This systematic review and meta-analysis evaluated whether experimental apical periodontitis (AP) in rodents induces systemic inflammatory and metabolic alterations and whether lesion burden influences these responses.
Design:
The review followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines and was registered in PROSPERO. PubMed/MEDLINE, EMBASE, Web of Science, and LILACS/BIREME were searched through June 2026. Experimental rodent studies with AP induction, condition-matched controls without AP, and quantitative systemic biomarkers were included. Primary outcomes were circulating inflammatory cytokines; secondary outcomes included glycemic, insulin-related, and lipid parameters. Hedges' g was pooled using multilevel random-effects models, with effect sizes nested within studies. Meta-regression assessed lesion burden, experimental duration, comorbidity, and animal model when sufficient data were available.
Results:
Thirty studies were included in the synthesis. AP was associated with higher circulating tumor necrosis factor-α (g = 1.69), interleukin (IL)-6 (g = 0.96), and IL-1β (g = 1.84), whereas IL-10, IL-17, and IL-18 were not significantly altered. AP was also associated with higher insulin (g = 1.19) and homeostatic model assessment for insulin resistance (HOMA-IR) (g = 1.55), but not with glucose, total cholesterol, high-density lipoprotein, low-density lipoprotein, or triglycerides. Lesion burden did not significantly moderate the inflammatory or metabolic outcomes.
Conclusions:
The number of lesions did not significantly modify the magnitude of the systemic responses evaluated. Experimental AP was associated with selective alterations, including increased TNF-α, IL-6, IL-1β, insulin, and HOMA-IR. Among the moderators analyzed, only animal model influenced the IL-6 response, although this finding was exploratory.
