Periodontal disease is a chronic inflammatory disease affecting the structures supporting the teeth. It results from the interaction between a microbial biofilm on the tooth surface and a de‐regulated host response in the periodontal tissues of a genetically susceptible host. There are strong correlations between specific ‘red complex’ micro‐organisms within the subgingival biofilm and disease. Dysbiosis, a deleterious shift in the relative abundance of components of the microbiota in disease, is a recognised property of microbiomes at other sites of the GI tract in chronic diseases. Exploring dysbiosis in the oral commensal microbiota using a mouse model of periodontitis, we have shown that a ‘red complex’ organism (Porphyromonas gingivalis) caused significantly more periodontal bone loss in specific pathogen free (SPF) mice than controls and no bone loss in germ free (GF) mice. This confirms the oral commensal microbiota is fundamentally required for periodontal bone loss. In addition, low level colonisation of SPF mice with P. gingivalis led to qualitative and quantitative changes to the microbiota; dysbiosis. The oral commensal microbiota of the SPF mice was stable for our aging population of SPF mice and this led to increased alveolar bone loss with age. Through a series of co‐caging experiments we have shown that the oral commensal microbiota of different strains of mice was transmissible into GF mice and led to periodontal bone loss. We have also demonstrated that a dysbiotic oral commensal microbiota was transmissible into GF mice and led to increased periodontal bone loss. In conclusion, the oral commensal microbiota is fundamental in the pathogenesis of periodontal disease in this mouse model. Moreover, it is dysbiosis of this oral commensal microbiota, brought about by P. gingivalis, that drives accelerated alveolar bone loss. We propose that P. gingivalis be considered as a keystone species.

Thesis (M.S.)--University of Michigan, 1987.

Thesis (M.S.)--University of Michigan, 1987.

Diss. Stockholm : Karol. inst.