Proposal for a novel murine model of human periodontitis using Porphyromonas gingivalis and type II collagen antibody injections

INTRODUCTION: Periodontitis is a chronic disease in humans induced by several pathogens including Porphyromonas gingivalis (P. gingivalis). Although mouse models of human periodontitis have been developed for study using an oral gavage of P. gingivalis, existing models take over a month to develop in order to ensure adequate periodontal destruction. The aim of the present study is to determine if using an injection of a cocktail of type II collagen antibodies along with an oral gavage of P. gingivalis in mice induces adequate periodontal destruction in a shorter time so as to potentially serve as a more useful mouse model of periodontitis. METHODS: Twenty-eight DBA1/BO male mice were placed in four groups: Group A (antibody injection plus gavage), Group B (gavage only), Group C (antibody injection only), and Group D (neither antibody injection nor gavage, control). Between six and eight weeks old, all mice underwent antibiotic administration, and at eight weeks old, were given antibody injection (Groups A and C) and oral P. gingivalis gavage (Groups A and B). Fifteen days after gavage Groups A and B received gavage, all mice were euthanized. Histomorphometric, morphometric, and cell counting analyses were conducted using analysis of variance (ANOVA) and Kruskal Wallis analysis followed by pairwise t-tests using Bonferroni correction. RESULTS: For histomorphometric analysis, mean distance from the cemento-enamel junction to the alveolar bone crest (CEJ-ABC) and the mean epithelial downgrowth (ED) in μm was statistically significantly highest for Group A (CEJ-ABC 1.49.81 vs. Group B 101.46, Group C 78.74, and Group D 66.23, p < 0.0083; ED 66.76 vs. Group B 25.92, Group C 9.21, and Group D 9.10, p < 0.0083). Morphometric analysis also showed that Group A had a significantly higher mean CEJ-ABC in μm compared to all other groups (265.50 vs. Group B 195.77, Group C 150.33, and Group D 133.93, p < 0.0083). A similar pattern was seen in cell counting, in which Group A had a significantly lower mean count of fibroblasts per 45 × 50 μm field (8.02 vs. Group B 9.56, Group C 12.09, and Group D 11.02, p < 0.0083), and a significantly higher mean count polymorphonuclear leukocytes per 45 × 50 μm (4.59 vs. Group B 1.74, Group C 0.83, and Group D 0.68, p < 0.0083). CONCLUSION: The results of this study provide proof-of-concept for a mouse model that can be quickly developed for human periodontitis using a type II collagen antibody cocktail injection coupled with oral gavage of P. gingivalis in DBA1/BO male mice. Future studies should verify the results of this proof-of-concept, compare this new model to existing models, and evaluate the extent of this model’s usefulness.