Comparative Transcriptome Analysis of Gingival Immune-Mediated Inflammation in Peri-Implantitis and Periodontitis Within the Same Host Environment.

Objective: This investigation aimed to determine whether and to what extent there are transcriptional differences between periodontitis and peri-implantitis in the same susceptible host. Background: As an immune-mediated inflammatory disease resulting in aggressive bone resorption around dental implants, peri-implantitis constitutes a major threat to dental implants' long-term success. Compared to periodontitis, its etiological molecular mechanism remains elusive. Currently, there are few investigations on these two diseases at the transcriptional level within the same basal environment. Methods: Ligature-induced peri-implantitis and periodontitis were generated in the same mice. Gingival tissues of healthy, periodontitis, and peri-implantitis sites from the same oral cavity were collected and used for RNA sequencing. Differentially expressed genes (DEGs) were screened between periodontitis/peri-implantitis and healthy sites. Enrichment analysis of DEGs was performed. The comprehensive immune landscape was annotated by seq-ImmuCC. Hub genes from peri-implantitis-specific DEGs were filtered using the STRING database and Cytoscape. Validation of the selected hub genes was performed on the GEO106090 dataset (gingival tissues from six periodontitis patients, six peri-implantitis patients, and six healthy controls). Results: The results indicated that peri-implantitis and periodontitis exhibited significantly distinct transcriptional signatures, with the complement and coagulation cascade pathways and osteoclast differentiation predominating in peri-implantitis mucosa. Compared with periodontitis, peri-implantitis sites exhibited elevated macrophage proportions and relatively enriched macrophage activation and bone loss. Hub genes were selected, and IL1B, CCL3, and CLEC4E were significantly highly expressed in human peri-implantitis mucosa. Conclusion: The study suggests that the interplay between macrophages and bone resorption seems to be more robust than in periodontitis. IL1B, CCL3, and CLEC4E may be considered promising therapeutic targets for peri-implantitis. These critical biological processes and identified genes may contribute to the etiology of peri-implantitis, which is unique from periodontitis. This work may make way for deeper exploration and contribute significantly to the treatment and prevention of peri-implantitis.