ArticleACS biomaterials science & engineering2025
3D Peri-Implant Epi-Mucosa-on-a-Chip Reveals Alterations in Epithelial Barrier Function Mediated by Host-Bacteria-Biomaterial Interactions.
Article in ACS biomaterials science & engineering, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- The immune-microbe-metal triad: a vicious cycle driving biomaterial corrosion in the oral inflammatory microenvironment.Bioactive materials · 2027Review
- TLR4-paxillin-Rac1 signaling mediates LPS-induced dysregulation of keratinocyte function.iScience · 2026Article
- Time-sequentially released bilayer sandwich cerium oxide nanoparticles on femtosecond laser-treated zirconia implant surface for enhanced antibacterial and osseointegration capacity.Materials today. Bio · 2026Article
- Impact of Zirconia and Titanium Implant Surfaces of Different Roughness on Oral Epithelial Cells.Dentistry journal · 2026Article
- Peri-implantitis: a systemic burden for our patients.Frontiers in dental medicine · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Peri-implantitis is characterized by disruption of the epithelial barrier at the implant-mucosa interface, driven by complex interactions between mechanical, microbial, and material factors. Histological and immunohistochemical analysis of human peri-implant and periodontal tissues revealed significant epithelial abnormalities specific to peri-implantitis, which indicated compromised barrier integrity. Specifically, peri-implant tissues had increased intercellular edema, inflammatory infiltration, and marked loss of junctional proteins E-cadherin and ZO-1. To further investigate these findings in a controlled environment, we developed a novel
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Registered trials
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