Background: Periodontitis is a chronic inflammatory disease influenced by host aging, yet the specific effects of aging on disease susceptibility remain unclear.
Objective: This study aimed to evaluate whether aging increases susceptibility to
Porphyromonas gingivalis (
P. gingivalis)-induced periodontitis in
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Background: Periodontitis is a chronic inflammatory disease influenced by host aging, yet the specific effects of aging on disease susceptibility remain unclear.
Objective: This study aimed to evaluate whether aging increases susceptibility to
Porphyromonas gingivalis (
P. gingivalis)-induced periodontitis in a murine model. We formulated the null hypothesis that age does not affect susceptibility to periodontal bone loss.
Methods: Young (8 weeks) and aged (78 weeks) male C57BL/6 mice were randomly assigned into four groups: young control, young infected, old control, and old infected (n = 8 per group, except for old control, where n = 7). Experimental periodontitis was induced by oral application of
P. gingivalis suspended in 5% carboxymethylcellulose (CMC), administered every other day, for a total of three applications. Alveolar bone loss was assessed 39 days after the last inoculation using histomorphometric measurement of buccal distance from the cemento-enamel junction to the alveolar bone crest (CEJ–ABC distance) and micro-computed tomography (μCT) at mesial and distal interdental sites. Bonferroni’s correction was applied to the Mann–Whitney U Test to determine statistical significance. A
p-value of less than 0.05 was considered statistically significant.
Results: Morphometric analysis showed significantly greater buccal bone loss in infected mice versus controls in both age groups (young: 0.193 mm vs. 0.100 mm,
p < 0.01; old: 0.262 mm vs. 0.181 mm,
p < 0.01). μCT analysis revealed that interdental bone loss was significant only in aged infected mice (mesial: 0.155 mm vs. 0.120 mm,
p < 0.05; distal: 0.185 mm vs. 0.100 mm,
p < 0.01), and not significant in young infected mice.
Conclusions: Aging significantly exacerbates
P. gingivalis-induced alveolar bone loss, particularly in interdental regions. These results allowed us to reject the null hypothesis. This study validates a clinically relevant murine model for analyzing age-related periodontitis and provides a foundation for investigating underlying molecular mechanisms and potential therapeutic interventions.
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