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Interventions to augment the mucosal thickness around dental implants are indicated to optimize esthetics and maintain peri-implant health. However, there is a lack of clinical data on the long-term performance of soft tissue substitutes, such as volume-stable collagen matrix (VCMX), compared to autogenous grafts, such as subepithelial connective tissue grafts (SCTGs). This randomized controlled trial aimed to assess 5-year data on clinical and radiographic outcomes at implant sites previously augmented with VCMX or SCTG.Twenty patients were randomly assigned for soft tissue augmentation with VCMX or SCTG at single implant sites. Following abutment connection, final restorations were inserted (baseline; BL) and patients were reexamined up to 5 years (FU-5). Measurements included clinical data, marginal bone levels, mucosal thickness, and ridge contour changes. Nonparametric tests and estimates were applied for the statistical analysis.The median buccal mucosal thickness increased by 0.3 mm (Q1: -0.8; Q3: 1.0) in the VCMX group (P = 0.656) and 0.3 mm (Q1: 0.0; Q3: 1.0) in the SCTG group (P = 0.188) between BL and FU-5 (intergroup P = 0.752), while the ridge contour decreased by a median of -0.3 mm (-0.9; -0.1) (P = 0.078) for VCMX and -0.3 mm (-0.4; -0.2) (P = 0.039) for SCTG (intergroup P = 0.817). Peri-implant health was maintained in both groups with stable clinical and radiographic outcomes and without significant differences between the treatments.Despite the limited power and considerable dropout rate in the present study, soft tissue augmentation at implant sites with either VCMX or SCTG resulted in similar stable peri-implant tissues, favorable esthetics, and clinically negligible contour changes at 5 years post loading.

This study evaluates a newly developed titanium-zirconium implant (TiZr), comparing it to a commercially available pure titanium (Ti) implant subjected to the same surface treatment.In nine dogs, 12 implants (six TiZr and six Ti) were randomly placed in the mandible with the implant shoulder at the bone crest and subjected to submerged healing. Standardized radiographs were taken after implantation, and at the sacrifice of 2 weeks (three dogs), 4 weeks (three dogs), and 8 weeks (three dogs). Histologic and histomorphometric measurements were performed on non-decalcified histologic sections. The main outcome measures included the first bone-implant contact (fBIC) and BIC over time. For statistical analysis, Wilcoxon signed-rank test and mixed model regressions were applied.From baseline to 8 weeks, a mean bone loss of 0.09 ± 0.33 mm for TiZr and a gain of 0.02 ± 0.33 mm for Ti were calculated radiographically. The number of implants with the fBIC coronal to the reference point (implant shoulder) gradually increased over time, reaching 39% of all TiZr implants and 50% of all Ti implants at 8 weeks. The mean fBIC values for Ti and TiZr were 0.29 ± 0.42 mm and 0.26 ± 0.32 mm (2 weeks), -0.01 ± 0.20 mm and 0.10 ± 0.28 mm (4 weeks), and -0.06 ± 0.22 mm and 0.08 ± 0.30 mm (8 weeks), respectively. The mean BIC values peaked at 86.9% ± 6.8% (8 weeks) for TiZr and at 83.4% ± 5.9% (4 weeks) for Ti. No statistically significant differences were observed at any time point.TiZr and Ti bone level implants with chemically-modified, sandblasted, and acid-etched surfaces performed similarly in regards to osseointegration in this unloaded canine study.

A polyethylene glycol (PEG)-based hydrogel matrix covalently bound to a 35-amino acid peptide of parathyroid hormone cystein-PTH 1-34 (cys-PTH 1-34) was shown to enhance bone regeneration around implants. The aim of this study is to test if the addition of an integrin-receptor-binding arginine-glycine-aspartic acid (RGD)-containing peptide at early healing time points improves the performance of the PEG matrix supplemented with cys-PTH 1-34 (PTH) when applied in acute defects around implants at early healing time points (2 and 4 weeks).Six dogs received 48 implants. Each side of the mandible was randomly assigned for implantation at day 0 or 2 weeks. A circumferential critical-size defect was created at each site before implantation. Sites were randomly assigned to one of four groups: 1) PEG alone (PEG group), 2) PEG plus RGD (PEG/RGD group), 3) PEG plus PTH (PEG/PTH group), and 4) PEG plus RGD plus PTH (PEG/RGD/PTH group). Dogs were sacrificed 2 weeks after the second surgery, and specimens were obtained for histologic analysis. For the statistical analysis, mixed linear regression with repeated measurements was used, and a Dunnett-Hsu adjustment was made for multiple comparisons.At 2 weeks, the percentages of new bone formation within the defect were 12.43% for the PEG group, 15.95% for the PEG/RGD group, 15.32% for the PEG/PTH group, and 16.60% for the PEG/RGD/PTH group. At 4 weeks, the percentages of new bone formation within the defect were 30.01% for the PEG group, 27.90% for the PEG/RGD group, 29.89% for the PEG/PTH group, and 27.58% for the PEG/RGD/PTH group. A marginally significant difference (PEG/RGD/PTH group versus PEG group; P = 0.055) was found at 2 weeks but not at 4 weeks. The highest percentage of bone-to-implant contact (BIC) in the defect site at 2 weeks was observed for the PEG/RGD group (8.57%). The BIC after 4 weeks of healing ranged from 11.54% (PEG/RGD/PTH group) to 16.61% (PEG group). No statistically significant differences were observed in BIC.The effect of binding PTH covalently to a synthetic, RGD-modified PEG hydrogel marginally significantly improved bone formation at 2 weeks of healing compared to the use of PEG alone. Bone regeneration within the defects increased in all groups at week 4 of healing without statistically significant differences.

Porcine enamel matrix derivative (EMD) has a clinical use in facilitating periodontal healing by enhancing the regeneration of alveolar bone, cementum, and periodontal ligament. The mechanism of clinical use has not been elucidated, but in vitro studies suggest that EMD may enhance healing, in part, by stimulating angiogenesis. This study analyzes the effect of EMD on the production of blood vessels in the chorioallantoic membrane (CAM) of the developing chicken egg.Various amounts of EMD ranging from 15 to 125 ng/5 microl were pipetted onto a 3-mm diameter x 2-mm thick bioabsorbable hemostatic gelatin and placed onto the surface of the CAM. Recombinant human amelogenin and a purified 5-kDa protein fraction derived from EMD were also tested at various amounts ranging from 15 to 62 ng/5 microl. A mixture of fibroblast growth factor and vascular endothelial growth factor served as the positive control. The negative control was 0.9% saline. A histologic examination of the interface of the gelatin and CAM was performed, evaluating for new blood-vessel formation on an ordinal scale of 0 to 3. Non-parametric statistical analyses were applied to compare test groups with the negative controls.CAM treated with EMD displayed moderate vascularity as indicated by a maximal score of 3.0 +/- 0.05 (mean +/- SEM). This compared favorably to the degree of vascularity stimulated by the mixture of fibroblast growth factor and vascular endothelial growth factor, which had a score of 3.0 +/- 0.05. Interestingly, the stimulation of angiogenesis by EMD was significant only at the lowest amounts tested. At the higher amounts, vascularity was reduced and not significantly different from the negative control. Vascularity was also increased by recombinant human amelogenin as indicated by a maximal score of 2.9 +/- 0.14. By contrast, there was only mild vascularity in sections treated with the negative control as indicated by a score of 1.7 +/- 0.4. The vascularity of the 5-kDa EMD-protein fraction was not different from the negative-control group (2.5 +/- 0.5 versus 1.7 +/- 0.4, respectively).EMD stimulates angiogenesis in the CAM model. As a heterogeneous mixture of extracellular matrix components, EMD may have multiple biologic functions, but it is likely that at least part of the explanation for its observed positive clinical effects may be the stimulation of angiogenesis. The fact that vascularity was also increased by recombinant human amelogenin raises the possibility that this 28.9-kDa protein may be the source of the angiogenic activity because it is the predominant protein of the EMD mixture. These results, taken together with results from previously reported in vitro studies, suggest that EMD may increase angiogenesis directly and/or indirectly at the wound-healing site.