ArticleDental materials : official publication of the Academy of Dental Materials2023
Immunomodulatory IL-23 receptor antagonist peptide nanocoatings for implant soft tissue healing.
Article in Dental materials : official publication of the Academy of Dental Materials, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- Biomolecule-functionalized dental implant surfaces: Towards augmenting soft tissue integration.Bioactive materials · 2025Review
- Diagnostic accuracy of bone-related biomarkers on peri-implantitis: potential of A-proliferation-inducing ligand.BMC oral health · 2025Article
- Surface modification strategies to reinforce the soft tissue seal at transmucosal region of dental implants.Bioactive materials · 2024Review
- Immune dysregulation and macrophage polarization in peri-implantitis.Frontiers in bioengineering and biotechnology · 2024Review
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
objectivePeri-implantitis, caused by an inflammatory response to pathogens, is the leading cause of dental implant failure. Poor soft tissue healing surrounding implants - caused by inadequate surface properties - leads to infection, inflammation, and dysregulated keratinocyte and macrophage function. One activated inflammatory response, active around peri-implantitis compared to healthy sites, is the IL-23/IL-17A cytokine axis. Implant surfaces can be synthesized with peptide nanocoatings to present immunomodulatory motifs to target peri-implant keratinocytes to control macrophage polarization and regulate inflammatory axises toward enhancing soft tissue healing.
methodsWe synthesized an IL-23 receptor (IL-23R) noncompetitive antagonist peptide nanocoating using silanization and evaluated keratinocyte secretome changes and macrophage polarization (M1-like "pro-inflammatory" vs. M2-like "pro-regenerative").
resultsIL-23R antagonist peptide nanocoatings were successfully synthesized on titanium, to model dental implant surfaces, and compared to nonfunctional nanocoatings and non-coated titanium. IL-23R antagonist nanocoatings significantly decreased keratinocyte IL-23, and downstream IL-17A, expression compared to controls. This peptide noncompetitive antagonistic function was demonstrated under lipopolysaccharide stimulation. Large scale changes in keratinocyte secretome content, toward a pro-regenerative milieu, were observed from keratinocytes cultured on the IL-23R antagonist nanocoatings compared to controls. Conditioned medium collected from keratinocytes cultured on the IL-23R antagonist nanocoatings polarized macrophages toward a M2-like phenotype, based on increased CD163 and CD206 expression and reduced iNOS expression, compared to controls. SIGNIFICANCE: Our results support development of IL-23R noncompetitive antagonist nanocoatings to reduce the pro-inflammatory IL-23/17A pathway and augment macrophage polarization toward a pro-regenerative phenotype. Immunomodulatory implant surface engineering may promote soft tissue healing and thereby reduce rates of peri-implantitis.
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