The Oral Virome-A New Driver in Periodontal Disease and "Periodontal Arthritis"
It’s been central dogma that Periodontal Disease is triggered by pathogenic bacteria that present as a bacterial dysbiosis of the oral microbiome.
Although viruses are also present within the oral cavity with differences observed between health and disease states, there is limited knowledge about their relationship to periodontal disease. Studies suggest that viruses, including herpes simplex virus-1,2, Epstein–Barr virus, and cytomegalovirus may play important roles in periodontal disease. Also, in recent studies, other different viruses have been associated with periodontal disease, however, a comprehensive evaluation of the oral virome in relationship to periodontal disease using shotgun sequencing has not been carried out in mice and to a limited extent in humans. For these reasons, we evaluated the entire oral microbiome in a mouse model of periodontal disease and discovered that the virome exhibits significant changes in diversity and total virome load more so than the bacteriome.
This leads to the following questions: What is really driving periodontal disease: bacteria (as always assumed) or viruses? Do they work together? Could bacteriophages alter the balance? Might bacteriophages be key mediators within this communication superhighway within the host.
Another long held tenet in the relationship between periodontal disease pathogenesis and bacterial plaque has been the concept of a close or proximal radius of effect or radius of action. This concept maintains that bacterial plaque can induce bone loss or mediate destructive effects on the periodontium only within a close radius of 1.5–2.5 mm, but beyond 2.5mm there is no effect. The current study, which shows a widening of the periodontal ligament space throughout the ligament and at a distance far removed from the site of bone loss and initial site of bacterial infection, supports a new concept—that the microbiome-mediated radius of effect on the periodontium is far greater than previously thought, and it effects deeper aspects of the periodontalligament space. This latter finding may have significant implications for the pathogenesis of periodontal disease and biomechanical properties of the periodontium.
Further, members of the oral microbiome are known to enter the systemic circulation and affect other organ sites; this may include joint tissues. Associations between periodontal disease and arthritis in humans and mouse models have been reported. Can we translate the findings from the current study, such that changes in the width of the periodontal ligament space mediated by changes in the virome/microbiome might also be reflected in other joints in the body? The current study provides a potential biomechanical mechanistic link between the microbiome and pathogenic alterations in ligament/joint physiology underlying arthritic conditions, including periodontal disease. Should we call this biomechanical feature “Periodontal Arthritis” or “OralVirome/Microbiome-Induced Arthritis”?
Read the paper here:
Polymicrobial periodontal disease triggers a wide radius of effect and unique virome: Li Gao, Misun Kang, Martin Jinye Zhang, M. Reza Sailani, Ryutaro Kuraji, April Martinez, Changchang Ye, Pachiyappan Kamarajan, Charles Le, Ling Zhan, Helene Range, Sunita Ho, Yvonne L. Kapila. NPJ Biofilms and microbiomes, 6(1), 10: https://doi.org/10.1038/s41522-020-0120-7