Project description:PURPOSE:To present a case series of zygomatic implants combined with bone regeneration and soft tissue enhancement techniques to reduce the risk of biological delayed complications such as maxillary sinusitis and soft tissue recession. MATERIALS AND METHODS:Zygomatic implants placed simultaneously with different bone regeneration techniques (buccal, palatal and buccal-palatal bone regeneration) and soft tissue enhancement techniques (pediculate and free connective tissue graft) were followed for at least 12 months. The following information was collected: patient age and sex, number of zygomatic implants, zygomatic implant success rate, zygomatic implant position according to classification of the Zygomatic Anatomy Guide Approach (ZAGA), sinus membrane perforation, type and outcome of the bone regeneration or the soft tissue enhancement technique, bone gain (width and length along the zygomatic implant) and keratinized buccal mucosa width, duration of follow-up, loading protocol (immediate or delayed) and biological complications (maxillary sinusitis and soft tissue recession). RESULTS:Thirty-one zygomatic implants placed in 19 patients were included. All implants were successful and none of the implants presented biological complications. The bone regeneration technique was successful in 30 of 31 cases with a mean palatal bone width of 3 mm, buccal bone width of 2.65 mm, palatal bone length of 6.5 mm and buccal bone length of 8.3 mm. The success rate of soft tissue enhancement was 100% and it established at least 2 mm of keratinized buccal mucosa width in all implants. CONCLUSIONS:Within the limitations of the present study, bone regeneration and soft tissue enhancement techniques were useful to establish more favorable conditions of the peri-implant tissues around zygomatic implants. This could prevent biological complications such as maxillary sinusitis and soft tissue recessions. Prospective and randomized controlled clinical trials with longer follow-up periods are advisable.

Project description: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.SignificanceOur 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.

Project description:Bone development and regeneration is associated with the Wnt signaling pathway that, according to literature, can be modulated by lithium ions (Li+). The aim of this study was to evaluate the gene expression profile during peri-implant healing of poly(lactic-co-glycolic acid) (PLGA) implants with incorporated Li+, while PLGA without Li+ was used as control, and a special attention was then paid to the Wnt signaling pathway. The implants were inserted in rat tibia for 7 or 28 days and the gene expression profile was investigated using a genome-wide microarray analysis. The results were verified by qPCR and immunohistochemistry. Histomorphometry was used to evaluate the possible effect of Li+ on bone regeneration. The microarray analysis revealed a large number of significantly differentially regulated genes over time within the two implant groups. The Wnt signaling pathway was significantly affected by Li+, with approximately 34% of all Wnt-related markers regulated over time, compared to 22% for non-Li+ containing (control; Ctrl) implants. Functional cluster analysis indicated skeletal system morphogenesis, cartilage development and condensation as related to Li+. The downstream Wnt target gene, FOSL1, and the extracellular protein-encoding gene, ASPN, were significantly upregulated by Li+ compared with Ctrl. The presence of β-catenin, FOSL1 and ASPN positive cells was confirmed around implants of both groups. Interestingly, a significantly reduced bone area was observed over time around both implant groups. The presence of periostin and calcitonin receptor-positive cells was observed at both time points. This study is to the best of the authors’ knowledge the first report evaluating the effect of a local release of Li+ from PLGA at the fracture site. The present study shows that during the current time frame and with the present dose of Li+ in PLGA implants, Li+ is not an enhancer of early bone growth, although it affects the Wnt signaling pathway. PLGA implants with +/- incorporated Li were inserted in rat tibia for 7 or 28 days, peri-implant bone was harvested and RNA extracted using Qiazol lysis reagent and TissueLyser followed by Qiagen's Rneasy Micro Kit. The microarray experiment was conducted at SCIBLU Genomics (www.lu.se/sciblu) according to Affymetrix guidelines (n=6).

Project description:Bone development and regeneration is associated with the Wnt signaling pathway that, according to literature, can be modulated by lithium ions (Li+). The aim of this study was to evaluate the gene expression profile during peri-implant healing of poly(lactic-co-glycolic acid) (PLGA) implants with incorporated Li+, while PLGA without Li+ was used as control, and a special attention was then paid to the Wnt signaling pathway. The implants were inserted in rat tibia for 7 or 28 days and the gene expression profile was investigated using a genome-wide microarray analysis. The results were verified by qPCR and immunohistochemistry. Histomorphometry was used to evaluate the possible effect of Li+ on bone regeneration. The microarray analysis revealed a large number of significantly differentially regulated genes over time within the two implant groups. The Wnt signaling pathway was significantly affected by Li+, with approximately 34% of all Wnt-related markers regulated over time, compared to 22% for non-Li+ containing (control; Ctrl) implants. Functional cluster analysis indicated skeletal system morphogenesis, cartilage development and condensation as related to Li+. The downstream Wnt target gene, FOSL1, and the extracellular protein-encoding gene, ASPN, were significantly upregulated by Li+ compared with Ctrl. The presence of β-catenin, FOSL1 and ASPN positive cells was confirmed around implants of both groups. Interestingly, a significantly reduced bone area was observed over time around both implant groups. The presence of periostin and calcitonin receptor-positive cells was observed at both time points. This study is to the best of the authors’ knowledge the first report evaluating the effect of a local release of Li+ from PLGA at the fracture site. The present study shows that during the current time frame and with the present dose of Li+ in PLGA implants, Li+ is not an enhancer of early bone growth, although it affects the Wnt signaling pathway.

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Hard and soft tissue healing around implants with a modified implant neck configuration: An experimental in vivo preclinical investigation.

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