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The severity of human peri‐implantitis lesions correlates with the level of submucosal microbial dysbiosis

Aim To cross‐sectionally analyse the submucosal microbiome of peri‐implantitis (PI) lesions at different severity levels. Materials and Methods Microbial signatures of 45 submucosal plaque samples from untreated PI lesions obtained from 30 non‐smoking, systemically healthy subjects were assessed by...

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Published in:Journal of clinical periodontology 2018-12, Vol.45 (12), p.1498-1509
Main Authors: Kröger, Annika, Hülsmann, Claudia, Fickl, Stefan, Spinell, Thomas, Hüttig, Fabian, Kaufmann, Frederic, Heimbach, André, Hoffmann, Per, Enkling, Norbert, Renvert, Stefan, Schwarz, Frank, Demmer, Ryan T., Papapanou, Panos N., Jepsen, Søren, Kebschull, Moritz
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Language:English
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Summary:Aim To cross‐sectionally analyse the submucosal microbiome of peri‐implantitis (PI) lesions at different severity levels. Materials and Methods Microbial signatures of 45 submucosal plaque samples from untreated PI lesions obtained from 30 non‐smoking, systemically healthy subjects were assessed by 16s sequencing. Linear mixed models were used to identify taxa with differential abundance by probing depth, after correction for age, gender, and multiple samples per subject. Network analyses were performed to identify groups of taxa with mutual occurrence or exclusion. Subsequently, the effects of peri‐implant probing depth on submucosal microbial dysbiosis were calculated using the microbial dysbiosis index. Results In total, we identified 337 different taxa in the submucosal microbiome of PI. Total abundance of 12 taxa correlated significantly with increasing probing depth; a significant relationship with lower probing depth was found for 16 taxa. Network analysis identified two mutually exclusive complexes associated with shallow pockets and deeper pockets, respectively. Deeper peri‐implant pockets were associated with significantly increased dysbiosis. Conclusion Increases in peri‐implant pocket depth are associated with substantial changes in the submucosal microbiome and increasing levels of dysbiosis.
ISSN:0303-6979
1600-051X
DOI:10.1111/jcpe.13023