Ecological network collapse and functional potential shifts in the canine oral microbiota associated with periodontal disease: a pilot study.

Periodontal disease is a highly prevalent disease in dogs; however, the underlying shifts in the oral microbiota remain unclear. Although dysbiosis is often associated with a loss of diversity, the ecological dynamics of canine periodontal disease remain poorly characterized. Therefore, we performed pilot study using a multi-angle comparison of the oral microbiota of healthy dogs and those with periodontal disease to identify the taxonomic, predicted functional, and structural signatures of the disease. Supragingival plaque samples were collected from five clinically healthy dogs and five dogs with periodontal disease. Microbial composition was analyzed by sequencing the 16S rRNA gene. Downstream bioinformatics analyses included alpha and beta diversity, differential abundance testing (DESeq2), functional prediction (Phylogenetic Investigation of Communities by Reconstruction of Unobserved States 2), and co-occurrence network analysis. Our results showed that the oral microbiota of the two groups were structurally distinct (permutational multivariate analysis of variance, p < 0.01), even after adjusting for age. Unexpectedly, the periodontal disease group exhibited significantly higher alpha diversity than the healthy group (p < 0.05). A high abundance of Pasteurellaceae characterized the healthy microbiota, whereas the periodontal disease microbiota was characterized by a convergent dysbiotic state dominated by pathogenic families, such as Porphyromonadaceae. Predicted functionally, this shift was associated with an enrichment of pathways with pro-inflammatory potential, specifically sulfur-containing amino acid metabolism. Additionally, a marked heterogeneity was observed in the composition of healthy microbiota, suggesting alternative stable states, while network analysis revealed a severe reduction in microbial inter-connectivity in periodontal disease. These preliminary findings generate the hypothesis that canine periodontal disease is characterized by "additive dysbiosis" with increased alpha diversity that converges into a uniform, pathogen-enriched structure with collapsed ecological interactions. The loss of potentially protective commensals, such as Pasteurellaceae, may act as an ecological trigger for this shift, whereas a healthy oral state may encompass multiple distinct compositional states. These findings provide a novel, hypothesis-generating ecological framework for understanding canine periodontal disease and for developing novel therapeutic strategies.