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Related Experiment Video

Updated: Oct 18, 2025

Experimental Model of Ligature-Induced Peri-Implantitis in Mice
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Transcriptome-wide Gene Expression Analysis in Peri-implantitis Reveals Candidate Cellular Pathways.

A Martin1, P Zhou1, B B Singh2

  • 1Translational Periodontal Research Lab, Department of Periodontics, School of Dentistry, UT Health San Antonio, San Antonio, TX, USA.

JDR Clinical and Translational Research
|September 29, 2021
PubMed
Summary

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Peri-implantitis involves distinct inflammatory mechanisms driven by implant particles and bacteria. Upregulated genes in the endosomal-lysosomal and oxidative stress pathways suggest receptor-driven inflammation plays a key role in this disease.

Area of Science:

  • Oral biology
  • Immunology
  • Genomics

Background:

  • Peri-implantitis is a destructive inflammatory condition affecting tissues around dental implants.
  • It differs clinically from periodontitis, suggesting unique inflammatory pathways.
  • Implant-derived titanium particles (i-TiPs) may alter the microenvironment and contribute to antibiotic resistance.

Purpose of the Study:

  • To investigate the genetic programs underlying oral peri-implant inflammatory disease.
  • To understand cellular responses to biomaterial degradation products and oral bacteria.

Main Methods:

  • Peri-implant tissues from healthy and diseased implants (N=10) were analyzed.
  • Next-generation transcriptome-wide microarray profiling was used to examine gene expression.
Keywords:
dental implantinflammationoxidative stressperi-implantitisphagocytosistitanium

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  • Global differential gene expression and pathway analysis were performed.

    • Main Results:

    • Genes in the endosomal-lysosomal pathway, including actin polymerization, were significantly upregulated in diseased tissues.
    • Cellular respiration pathways related to oxidative stress were highly transcribed in all samples.
    • These findings suggest increased intracellular activity and potential implant-induced oxidative stress.

    Conclusions:

    • Upregulation of endosomal-lysosomal and oxidative stress pathways indicates a crucial role for receptor-driven inflammation in peri-implantitis.
    • Extracellular signals like i-TiPs and pathogens likely trigger these inflammatory responses.
    • Further validation in external cohorts is warranted.