International endodontic journal · 2026
Integrative Computational and Experimental Approaches Reveal the Protective Role of Moderate Caffeine Intake Against Apical Periodontitis Induced Bone Loss.
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Rodrigues Matheus Ferreira Lima, Frazão Deborah Ribeiro, Souza-Monteiro Deiweson, Dos Santos Vinicius Ruan Neves, Nunes Felipe Oliveira, de Moura João Daniel Mendonça, Gomes Thamires Campos, Cruz Jorddy Neves, do Socorro Ferraz Maia Cristiane, Cunha Rodrigo A, Collares Fabrício Mezzomo, de Castilho Jacinto Rogerio, Lima Rafael Rodrigues
Аннотация
AIM: To investigate whether moderate systemic caffeine intake modulates the progression of apical periodontitis (AP) and associated alveolar bone loss, combining in vivo rat experiments with in silico molecular docking to explore potential mechanisms.
METHODOLOGY: Male Wistar rats were randomly assigned to four groups (n = 8 per group): control, caffeine, AP, AP + caffeine. AP was induced by pulp exposure of mandibular first molars and allowed to develop for 28 days. Animals in caffeine groups received 10 mg/kg/day by orogastric gavage during the experimental period. The antioxidant capacity of caffeine was assessed by DPPH• and ABTS• + assays. Systemic oxidative status was evaluated by blood reduced glutathione (GSH) and thiobarbituric acid reactive substances (TBARS). Histology, Picro-Sirius red staining for collagen, and micro-computed tomography (micro-CT) analysis of alveolar bone (BV/TV, Tb.N, Tb.Sp, porosity, lesion volume) were performed. Molecular docking against adenosine A1 and A2 A receptors was used to probe caffeine-receptor interactions.
RESULTS: Caffeine showed relevant radical-scavenging activity in vitro (DPPH• assay). AP induced systemic redox imbalance, marked inflammatory infiltration, collagen loss and increased lesion volume. Moderate caffeine intake restored redox markers (↑GSH, ↓TBARS), attenuated inflammatory infiltrate, preserved collagen content and reduced lesion volume (AP + caffeine vs. AP; p < 0.05). Micro-CT demonstrated improved alveolar bone microarchitecture in AP + caffeine group (increased BV/TV and Tb.N; reduced Tb.Sp and porosity). Molecular docking indicated stable hydrophobic and hydrogen-bond interactions of caffeine within A1 and A2 A receptor binding pockets, supporting an antagonistic effect on adenosine signalling consistent with reduced pro-inflammatory activation.
CONCLUSION: Moderate systemic caffeine (10 mg/kg/day) attenuates apical periodontitis progression and preserves alveolar bone quality in rats, associated with antioxidant activity and a probable modulation of adenosine receptor-mediated inflammatory pathways.
METHODOLOGY: Male Wistar rats were randomly assigned to four groups (n = 8 per group): control, caffeine, AP, AP + caffeine. AP was induced by pulp exposure of mandibular first molars and allowed to develop for 28 days. Animals in caffeine groups received 10 mg/kg/day by orogastric gavage during the experimental period. The antioxidant capacity of caffeine was assessed by DPPH• and ABTS• + assays. Systemic oxidative status was evaluated by blood reduced glutathione (GSH) and thiobarbituric acid reactive substances (TBARS). Histology, Picro-Sirius red staining for collagen, and micro-computed tomography (micro-CT) analysis of alveolar bone (BV/TV, Tb.N, Tb.Sp, porosity, lesion volume) were performed. Molecular docking against adenosine A1 and A2 A receptors was used to probe caffeine-receptor interactions.
RESULTS: Caffeine showed relevant radical-scavenging activity in vitro (DPPH• assay). AP induced systemic redox imbalance, marked inflammatory infiltration, collagen loss and increased lesion volume. Moderate caffeine intake restored redox markers (↑GSH, ↓TBARS), attenuated inflammatory infiltrate, preserved collagen content and reduced lesion volume (AP + caffeine vs. AP; p < 0.05). Micro-CT demonstrated improved alveolar bone microarchitecture in AP + caffeine group (increased BV/TV and Tb.N; reduced Tb.Sp and porosity). Molecular docking indicated stable hydrophobic and hydrogen-bond interactions of caffeine within A1 and A2 A receptor binding pockets, supporting an antagonistic effect on adenosine signalling consistent with reduced pro-inflammatory activation.
CONCLUSION: Moderate systemic caffeine (10 mg/kg/day) attenuates apical periodontitis progression and preserves alveolar bone quality in rats, associated with antioxidant activity and a probable modulation of adenosine receptor-mediated inflammatory pathways.