Biome-microbiome interactions in peri-implantitis: A pilot investigation.
Biome-microbiome interactions in peri-implantitis: A pilot investigation.
复制标题
DOI：
10.1002/jper.21-0423
复制
发表时间：
2022-06
影响因子：
4.3
通讯作者：
Kumar, Purnima S.
中科院分区：
文献类型：
--
作者：
Ganesan, Sukirth M.;Dabdoub, Shareef M.;Nagaraja, Haikady N.;Mariotti, Angelo J.;Ludden, Christopher W.;Kumar, Purnima S.
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. 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. 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 immuno-inflammatory pathways, suggesting a role for commensals in protecting epithelial integrity. In disease, we found 4–200-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. 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 drives a move towards chronic programming of a non-healing wound. Microbial dysbiosis in the peri-implant sulcus promotes abandonment of homeostatic host-bacterial transactions and creates a scenario compatible with chronic programming of a non-healing wound
