4.5 Article

Biome-microbiome interactions in peri-implantitis: A pilot investigation

Journal

JOURNAL OF PERIODONTOLOGY
Volume 93, Issue 6, Pages 814-823

Publisher

WILEY
DOI: 10.1002/JPER.21-0423

Keywords

genomics; host-microbial interactions; implantology; microbiology

Funding

  1. NIDCR [R01 DE022579]

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This study revealed that there is an active transcriptional activity of the peri-implant microbiome surrounding healthy implants. In disease conditions, an upregulation of microbial genes correlated with human genes, suggesting a potential role of commensals in maintaining epithelial integrity.
Background Dental implants replace missing teeth in at least 100 million people, yet over one million implants fail every year due to peri-implantitis, a bacterially induced inflammatory disease. Our ability to treat peri-implantitis is hampered by a paucity of information on host-microbiome interactions that underlie the disease. Here, we present the first open-ended characterization of transcriptional events at the mucosal-microbial interface in the peri-implant crevice. Methods We simultaneously sequenced microbial and human mRNA from five pairs of healthy and diseased implants from the same patient and used graph theoretics to examine correlations between microbial and host gene expression in the peri-implant crevice. Results We identified a transcriptionally active peri-implant microbiome surrounding healthy implants. Microbial genes encoding phenylalanine, tyrosine, and tryptophan biosynthesis, cysteine, methionine, arginine, proline, and histidine metabolism correlated to human genes encoding cell development, metabolism, morphogenesis, adhesion, gap junctions, cell-cell signaling, and immunoinflammatory pathways, suggesting a role for commensals in protecting epithelial integrity. In disease, we found 4- to 200-fold upregulation in microbial genes encoding biofilm thickness, heme transport and utilization, and Gram-negative cell membrane synthesis. These genes correlated with mucosal zinc finger proteins, apoptosis, membrane transport, inflammation, and cell-cell communication. Conclusions Within the limitations of a small sample size, our data suggest that microbial dysbiosis in the peri-implant sulcus might promote abandonment of host-bacterial transactions that dictate health and instead drive a move towards chronic programming of a non-healing wound.

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