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Updated: Feb 6, 2026

Murine Model of Advanced Periodontitis Induced by Nylon Ligature in the Second Upper Molar
Published on: May 30, 2025
Porphyromonas gingivalis induces exacerbated periodontal disease during pregnancy
Xingyu Duan1, Aislinn Hays1, Wei Zhou1
1Department of Oral Immunology and Infectious Diseases, University of Louisville School of Dentistry, Louisville, KY, 40202, USA.
Although pregnant women are prone to gingival inflammation, its mechanism remains unclear. Animal models are ideal for investigating immunological mechanisms in the periodontal disease. A murine model for ligature-induced periodontal disease has been modified and utilized to determine the susceptibility to periodontal inflammation and tissue damage in pregnant mice. Expression of different inflammatory mediators in the gingivae was determined by quantitative real-time PCR (qPCR). Inflammatory bone loss was determined by measuring the distance from the cementoenamel junction to the alveolar bone crest (CEJ-ABC). Oral bacterial number was determined by the CFU (Colony Forming Units) count from anaerobic culture of oral swabs. In our experiments, ligation itself did not cause higher gingival inflammation and bone loss in pregnant mice than non-pregnant mice, while ligation combined with P. gingivalis infection led to increased gingival inflammation and periodontal bone loss, accompanied by lower gingival expression of anti-inflammatory cytokines in pregnant mice. Our results indicated that P. gingivalis infection was important in inducing more severe periodontal diseases during pregnancy, which might be attributed to the down-regulated anti-inflammatory mechanisms, but not be associated with higher oral bacterial burden.
Although pregnant women are prone to gingival inflammation, its mechanism remains unclear. Animal models are ideal for investigating immunological mechanisms in the periodontal disease. A murine model for ligature-induced periodontal disease has been modified and utilized to determine the susceptibility to periodontal inflammation and tissue damage in pregnant mice. Expression of different inflammatory mediators in the gingivae was determined by quantitative real-time PCR (qPCR). Inflammatory bone loss was determined by measuring the distance from the cementoenamel junction to the alveolar bone crest (CEJ-ABC). Oral bacterial number was determined by the CFU (Colony Forming Units) count from anaerobic culture of oral swabs. In our experiments, ligation itself did not cause higher gingival inflammation and bone loss in pregnant mice than non-pregnant mice, while ligation combined with P. gingivalis infection led to increased gingival inflammation and periodontal bone loss, accompanied by lower gingival expression of anti-inflammatory cytokines in pregnant mice. Our results indicated that P. gingivalis infection was important in inducing more severe periodontal diseases during pregnancy, which might be attributed to the down-regulated anti-inflammatory mechanisms, but not be associated with higher oral bacterial burden.
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