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

Abstract

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.

Inflammasomes NLRP3 and AIM2 in peri‐implantitis: A cross‐sectional study

“…It is quite interesting that despite so many previously described similarities between periodontitis and peri-implantitis, as Rakic pathogenesis of periodontal disease (Marchesan et al, 2020). In peri-implantitis, Ganesan et al (2022) have reported the increased in NLRP2, NLRP8, and NLRP12. The current study has also identified NLRP3 inflammasome in peri-implantitis.…”

Impact of local predisposing/precipitating factors and systemic drivers on peri‐implant diseases

“…68 In biofilm surrounding implants, differences from normoglycemia were reported to regards mostly the deep pockets, 69 more yeasts were found in T2D, 69 and a 4-to 200-fold increase was reported in upregulated gene expression toward a non-healing wound by suppressing the commensals' protective effect enhancing epithelial integrity. 70 Similar mechanisms are found around implants where hyperglycemia causes changes in the composition of the microbiome that interrupts the homeostasis between the bacteria and the host defense system. In brief, chronic hyperglycemia (Figure 10):…”

“…Moreover, due to impaired metabolic and immune regulation, T2D patients are reported to be more susceptible to such microbiome shifts (dysbiosis) than health individuals 68 . In biofilm surrounding implants, differences from normoglycemia were reported to regards mostly the deep pockets, 69 more yeasts were found in T2D, 69 and a 4‐ to 200‐fold increase was reported in upregulated gene expression toward a non‐healing wound by suppressing the commensals' protective effect enhancing epithelial integrity 70 …”

The burden of diabetes on the soft tissue seal surrounding the dental implants

“…More pro-inflammatory macrophages implied increased expression of inflammatory cytokines (e.g., IL-1, IL-6, and IL-8) and MMP, which may lead to more prolonged inflammation ( Wilkinson et al, 2019 ). Genes involved in apoptosis, mucosal migration and intercellular communication were reported to be upregulated 4-fold–200-fold when inflammation around the implant increased, which simultaneously slowed the rate of wound healing ( Ganesan et al, 2022 ).…”