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Subgingival Microbial Profiles at Peri-Implant and Adjacent Tooth Sites: A Cross-Sectional Quantitative PCR Study
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Background Peri-implant diseases are primarily driven by microbial biofilm accumulation on the implant surface, leading to inflammatory destruction of the soft and hard tissues supporting dental implants, with progressive marginal bone loss and potential implant failure. Objectives: To analyze the subgingival microbial profiles of peri-implant sites and adjacent teeth in peri-implantitis and to assess the modifying effects of smoking and periodontal status. Methods: In this cross-sectional study, 43 adults (mean age: 54.5 years) contributed 100 dental implants and 50 adjacent natural teeth. Implants were classified as healthy implants (HI; n = 74) or peri-implantitis sites (PI; n = 26), and sampled teeth (TT) were categorized as periodontally diseased (n = 19) or periodontally healthy (n = 31). Subgingival biofilm was collected with sterile paper points and analyzed by quantitative polymerase chain reaction using the Paro x panel (ADD Laboral), which reported qualitative and quantitative data for 22 bacterial taxa. Additional subgroup analyses were performed according to smoking and periodontal status. Results: Peri-implantitis sites showed a significantly greater bacterial load than adjacent teeth for 10 taxa after false discovery rate correction, including Campylobacter rectus (β = 1.292, 95% CI 0.773–1.811; adjusted p = 2.38 × 10−5) and Porphyromonas gingivalis (β = 1.374, 95% CI 0.730–2.019; adjusted p = 3.22 × 10−4). Additional significant increases at peri-implantitis sites were observed for the Streptococcus constellatus group, Fusobacterium nucleatum, Eubacterium nodatum, Filifactor alocis, Parvimonas micra, Tannerella forsythia, Actinomyces odontolyticus, and Treponema denticola. In contrast, no taxon differed significantly in bacterial load between HI and TT after multiple-testing correction, and no taxon remained significant in prevalence analyses for either PI versus TT or HI versus TT. Clinically, significantly higher proportions of bleeding on probing and suppuration were present in PI sites vs. HI sites (96.15% of PI sites compared with 28.38%, 2.7%, 18.00%, and 8.00% of TT sites, respectively). Subgroup analyses by smoking and periodontal status suggested additional variation in microbial overlap, but these findings should be interpreted with caution given the limited subgroup sizes, particularly among smokers. Conclusions: Peri-implant and adjacent tooth sites shared substantial microbiological overlap; however, peri-implantitis sites showed higher detection frequencies and bacterial loads for selected taxa, whereas comparisons between healthy implant and tooth sites were less consistent.
Title: Subgingival Microbial Profiles at Peri-Implant and Adjacent Tooth Sites: A Cross-Sectional Quantitative PCR Study
Description:
Background Peri-implant diseases are primarily driven by microbial biofilm accumulation on the implant surface, leading to inflammatory destruction of the soft and hard tissues supporting dental implants, with progressive marginal bone loss and potential implant failure.
Objectives: To analyze the subgingival microbial profiles of peri-implant sites and adjacent teeth in peri-implantitis and to assess the modifying effects of smoking and periodontal status.
Methods: In this cross-sectional study, 43 adults (mean age: 54.
5 years) contributed 100 dental implants and 50 adjacent natural teeth.
Implants were classified as healthy implants (HI; n = 74) or peri-implantitis sites (PI; n = 26), and sampled teeth (TT) were categorized as periodontally diseased (n = 19) or periodontally healthy (n = 31).
Subgingival biofilm was collected with sterile paper points and analyzed by quantitative polymerase chain reaction using the Paro x panel (ADD Laboral), which reported qualitative and quantitative data for 22 bacterial taxa.
Additional subgroup analyses were performed according to smoking and periodontal status.
Results: Peri-implantitis sites showed a significantly greater bacterial load than adjacent teeth for 10 taxa after false discovery rate correction, including Campylobacter rectus (β = 1.
292, 95% CI 0.
773–1.
811; adjusted p = 2.
38 × 10−5) and Porphyromonas gingivalis (β = 1.
374, 95% CI 0.
730–2.
019; adjusted p = 3.
22 × 10−4).
Additional significant increases at peri-implantitis sites were observed for the Streptococcus constellatus group, Fusobacterium nucleatum, Eubacterium nodatum, Filifactor alocis, Parvimonas micra, Tannerella forsythia, Actinomyces odontolyticus, and Treponema denticola.
In contrast, no taxon differed significantly in bacterial load between HI and TT after multiple-testing correction, and no taxon remained significant in prevalence analyses for either PI versus TT or HI versus TT.
Clinically, significantly higher proportions of bleeding on probing and suppuration were present in PI sites vs.
HI sites (96.
15% of PI sites compared with 28.
38%, 2.
7%, 18.
00%, and 8.
00% of TT sites, respectively).
Subgroup analyses by smoking and periodontal status suggested additional variation in microbial overlap, but these findings should be interpreted with caution given the limited subgroup sizes, particularly among smokers.
Conclusions: Peri-implant and adjacent tooth sites shared substantial microbiological overlap; however, peri-implantitis sites showed higher detection frequencies and bacterial loads for selected taxa, whereas comparisons between healthy implant and tooth sites were less consistent.
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