Mapping the omics landscape for peri-implant diseases: A scoping review.
TL;DR
Current omics evidence suggests that peri-implant disease follows a staged, implant-conditioned biological trajectory rather than a simple binary healthy/diseased model.
Abstract
Objectives
To map omics evidence across peri-implant health, peri-implant mucositis, and peri-implantitis, and to identify recurring molecular patterns and candidate biomarker signals relevant to diagnosis, monitoring, and treatment.
Materials And Methods
This scoping review included human studies using genomics, DNA methylation-based epigenomics, bulk and single-cell transcriptomics, non-coding RNA analyses (including miRNA, lncRNA, and circRNA), proteomics, metabolomics, and microbiome profiling. Findings were organized by clinical state (health, mucositis, peri-implantitis) and interpreted within an implant-conditioned niche shaped by microbial, host, and biomaterial-related influences.
Results
Of 319 records identified, 78 studies were included. Most focused on genomics, transcriptomics, and the microbiome, with fewer studies in DNA methylation-based epigenomics, proteomics, and metabolomics. Peri-implant health was generally associated with oxygen-tolerant, biosynthetically active microbial communities and a regulated host-response baseline. Peri-implant mucositis appeared to be an intermediate plaque-induced state marked by expansion of bridge anaerobes and early innate inflammatory activation, but it was under-represented in transcriptomic, proteomic, and epigenomic datasets. Peri-implantitis was associated with stronger coupling between dysbiosis and host-destructive responses, including recurrent innate inflammatory hubs, chemokine-driven myeloid recruitment, protease activity, osteo-immune imbalance, and catabolic metabolomic profiles enriched in polyamines and short-chain fatty acids. DNA methylation studies linked disease status, and in limited cohorts, titanium particle burden, with altered methylation patterns. Non-coding RNA studies suggested additional regulatory networks related to inflammation and bone-associated signaling. Treatment studies indicated that decontamination may reduce bacterial biomass on rough titanium surfaces, but it does not consistently eliminate residual biofilm, suggesting biological improvements may reflect ecological shifts rather than complete surface decontamination.
Conclusions
Current omics evidence suggests that peri-implant disease follows a staged, implant-conditioned biological trajectory rather than a simple binary healthy/diseased model.