Dataset Information

Immunomodulatory IL-23 receptor antagonist peptide nanocoatings for implant soft tissue healing.

ABSTRACT:

Objective

Peri-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.

Methods

We 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").

Results

IL-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.

SUBMITTER: Pizarek JA

PROVIDER: S-EPMC9899321 | biostudies-literature | 2023 Feb

REPOSITORIES: biostudies-literature

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Publications

Immunomodulatory IL-23 receptor antagonist peptide nanocoatings for implant soft tissue healing.

Pizarek John A JA Fischer Nicholas G NG Aparicio Conrado C

Dental materials : official publication of the Academy of Dental Materials 20230113 2

<h4>Objective</h4>Peri-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 nanocoati ...[more]

PMID: 36642687

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Project description:PurposeBiofilm-free implant surface is ultimate prerequisite for successful soft and bone tissue integration. Objective of the study was to estimate the effects of argon plasma healing abutment pre-treatment (PT) on peri-implant soft-tissue phenotype (PiSP), inflammation, plaque accumulation and the microbiome (PiM) between non-treated (NPT) and treated (PT) abutments following 3-months healing period. The hypothesis was that cell-conductive and antimicrobial properties of PT would yield optimal conditions for soft tissue integration.Material and methodsTwo months following second-phase surgery, microbiological and clinical parameters were assessed around thirty-six healing abutments with two types of microtopography, smooth surface (MACHINED) and ultrathin threaded microsurface (ROUGH). A two level randomization schema was used to achieve equal distribution and abutments were randomly divided into rough and machined groups, and then divided into PT and NPT groups. PiM was assessed using next-generation DNA sequencing.ResultsPiM bacterial composition was highly diverse already two months post-implantation, consisting of key-stone pathogens, early and late colonizers, while the mycobiome was less diverse. PT was associated with lower plaque accumulation and inflammation without significant impact on PiSP, while in NPT clinical parameters were increased and associated with periopathogens. NPT mostly harbored late colonizers, while PT exerted higher abundance of early colonizers suggesting less advanced plaque formation. Interaction analysis in PT demonstrated S. mitis co-occurrence with pro-healthy Rothia dentocariosa and co-exclusion with Parvimonas micra, Porphyromonas endodontalis and Prevotella oris. PiSP parameters were generally similar between the groups, but significant association between PiM and keratinized mucosa width was observed in both groups, with remarkably more expressed diversity in NPT compared to PT. PT resulted in significantly lower BOP and PI around rough and machined abutments, respectively, without specific effect on PiM and PiSP.ConclusionsPT contributed to significantly the less advanced biofilm accumulation and inflammation without specific effects on PiSP.

Dataset Information

Immunomodulatory IL-23 receptor antagonist peptide nanocoatings for implant soft tissue healing.

Objective

Methods

Results

Significance

Publications

Immunomodulatory IL-23 receptor antagonist peptide nanocoatings for implant soft tissue healing.

Similar Datasets

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